fordoctors

Allogeneic Stem Cell Transplant Effective for Younger Patients with Poor-prognosis AML

2009-02-02T18:38:00.000-08:00

According to an article recently published in the journal Blood, patients with AML who are at a high risk of cancer progression following standard therapy may benefit from an unrelated allogeneic stem cell transplant.

Acute myeloid leukemia (AML) is a cancer of the bone marrow and blood characterized by the rapid, uncontrolled growth of immature white blood cells known as myelocytes. The disease is more common in adults than in children; average age at diagnosis is more than 65 years.

Treatment of AML often begins with induction therapy (initial treatment) that includes chemotherapy to produce a complete remission (defined as the disappearance of leukemia cells in the bone marrow and normalization of the white blood cell, red blood cell, and platelet levels). After induction therapy, patients generally receive additional treatment (consolidation therapy) to reduce the likelihood of leukemia recurrence. Depending upon prognosis, age of the patient, and/or other existing medical conditions, consolidation therapy can range from extremely aggressive to less aggressive.

An allogeneic stem cell transplant, considered an extremely aggressive treatment option, involves the use of high doses of therapy, which kill a greater amount of cancer cells than standard doses. Unfortunately, the high doses of therapy also cause a significant reduction in blood cells, resulting in a patient's susceptibility to infection, bleeding, and the need for blood transfusions. Often, the infections caused by these high doses of therapy are life-threatening.

To restore levels of blood cellsstem cells, which are immature blood cells, are collected from a donor and infused into the patient following high-dose therapy. These donor stem cells can also mount an attack against the patient's cancer cells. Unfortunately, these donor cells can also attack a patient’s healthy cells, causing a potentially life-threatening condition called graft-versus-host disease (GVHD). Stem cells donated by a relative (related donor) tend to carry a lower risk of GVHD than those from an unrelated donor.

A drawback of an allogeneic stem cell transplant is that treatment-related mortality and side effects can be substantial; researchers have thus focused on curative options that are more easily tolerated. However, for patients with very aggressive AML and those who are younger, an allogeneic stem cell transplant still appears to provide optimal outcomes.

Researchers affiliated with the International Blood and Marrow Transplant Registry recently conducted a clinical study evaluating the use of allogeneic stem cell transplants with unrelated donors for patients with AML. This trial included 261 patients with AML in first remission (when disease is undetectable for the first time following treatment) or second remission (the second time following two different treatment courses that disease is undetectable) who were 60 years of age or younger. Patients in this trial were divided into three groups: those who had a high, intermediate, or low risk of developing a cancer recurrence following standard therapies.

The following results include patients in first remission:

• At five years overall survival was between 29–30% for all groups of patients.
• At five years mortality related to treatment was 47% for patients at a high risk of developing a recurrence, 53% for patients at an intermediate risk of developing a recurrence, and 63% for patients at a low risk of developing a recurrence.
• Cancer recurrence rates were 8%, 17%, and 26%, respectively for patients with low, intermediate, and high risks of developing a cancer recurrence.

The following results include patients in second remission:

• At five years overall survival was 45%, 37%, and 36%, respectively, among patients with a low, intermediate, and high risk of developing a cancer recurrence.
• At five years mortality related to treatment was 46%, 46%, and 30%, respectively among patients with a low, intermediate, and high risk of developing a cancer recurrence.
• Cancer recurrence rates were 12%, 18%, and 32%, respectively, among patients with a low, intermediate, and high risk of developing a cancer recurrence.

The researchers concluded that an unrelated allogeneic stem cell transplant can provide AML patients 60 years of age or younger who are in first remission and have a high risk of a cancer recurrence overall survival rates at five years that are comparable to those among patients with a lower risk of a recurrence. However, this trend did not seem to hold true for patients in second remission. Furthermore, mortality related to treatment was high.

Patients with AML who are at a high risk of developing a cancer recurrence and do not have a related donor for an allogeneic stem cell transplant may wish to speak with their physician regarding their individual risks and benefits of an unrelated stem cell transplant.

Reference: Tallman MS, Dewald GW, Sandham S, et al. Impact of cytogenetics on outcome of matched unrelated donor hematopoietic stem cell transplantation for acute myeloid leukemia in first or second complete remission. Blood. 2007; 110:409-417.

Vitamins During Pregnancy Decrease Childhood Cancer Risk

2009-02-02T18:33:00.000-08:00

According to an early online publication in the journal Clinical Pharmacology and Therapeutics, children of mothers who take vitamins during pregnancy have a decreased risk of pediatric brain tumors, neuroblastoma, and leukemia.

It is generally recommended that pregnant women receive vitamin supplementation during pregnancy to assure normal growth and development of the fetus. Several studies have suggested that vitamin supplementation during pregnancy can prevent birth defects. There have also been associations established between vitamin supplementation and the child’s risk of acute lymphoblastic leukemia and brain tumors. In addition, research has suggested that the widespread use of vitamin supplementation in pregnant women has helped decrease the incidence of childhood medulloblastoma and neuroblastoma.

In the current study, researchers
from the University of Toronto conducted a literature review of materials produced between 1960 and 2005. A meta-analysis was performed of data from seven studies to determine the relationship between maternal vitamin intake and childhood cancer incidence. All vitamins evaluated included folic acid. The following comparisons were made between children of women who received vitamin supplements containing folic acid during pregnancy and those who did not:

* There was a 36% reduction for pediatric leukemia; an 18% reduction in pediatric brain tumors; and a 47% reduction in neuroblastoma in children of women taking vitamin supplements.
* It was estimated that, in the U.S., vitamin supplementation during pregnancy could prevent 900 cases of pediatric leukemia and 300–400 cases of pediatric brain tumors annually.

These authors stated that it was not know specifically which vitamins were responsible for these effects. They did speculate, however, that folic acid may be responsible for this decreased risk pediatric brain tumors, neuroblastoma, and leukemia. Women who are pregnant may wish to speak with their physician regarding prenatal vitamin supplementation.

Reference: Goh YI, Bollano E, Einarson TR, et al. Prenatal multivitamin supplementation and rates of pediatric cancers: A meta-analysis. Clinical Pharmacology and Therapeutics [early online publication]. February 21, 2007. DOI: doi:10.1038/sj.clpt.6100100.

Copyright Brain Cancer Information Center on CancerConsultants.com

Copyright Leukemia Information Center on CancerConsultants.com

Neoadjuvant Radiation Improves Survival in Pancreatic Cancer

2009-02-02T18:26:00.000-08:00

Preoperative radiation nearly doubles the survival rate for patients with operable pancreatic cancer, according to the results of a study published in the November 15, 2008 issue of the International Journal of Radiation Oncology Biology Physics.[1]

The pancreas is an organ that is surrounded by the stomach, small intestine, bile ducts (tubes that connect the liver to the small intestine), gallbladder, liver, and spleen. The pancreas helps the body to break down food and also produces hormones, such as insulin, to regulate the body’s storage and use of food.

Pancreatic cancer has one of the highest mortality rates of all cancers. It accounts for approximately 2% of all newly diagnosed cancers in the United States each year but 5% of all cancer deaths. Pancreatic cancer is often called a “silent killer” because its symptoms are usually not recognizable until it has advanced and spread outside the pancreas. As a result the majority of pancreatic cancers are not diagnosed until they have reached advanced stages and are considered incurable.

If pancreatic cancer has not spread to surrounding or distant organs, it is usually considered operable. Historically, patients have been treated with surgery followed by chemotherapy and/or radiation to destroy any micrometastases (cancer cells that have spread outside the pancreas). New research indicates, however, that neoadjuvant radiation therapy (radiation delivered prior to surgery) might offer greater benefit to patients because it can potentially shrink the tumor prior to surgery, thereby ensuring a better chance of removal. Furthermore, because pancreatic surgery

is so invasive, many patients are in no condition to undergo radiation treatment after surgery, so neoadjuvant treatment allows them to receive radiation that they might not receive otherwise.

Researchers from the Weill Cornell Medical College used data from the Surveillance, Epidemiology, and End Results (SEER) registry database to perform a retrospective analysis on patients who had surgically resected (removed) pancreatic cancer between 1994 and 2003. The researchers compared the overall survival rates among patients who received neoadjuvant radiation, adjuvant radiation, or no radiation. Patients who received neoadjuvant radiation survived 23 months, compared with 12 months for patients who did not receive radiation and 17 months for those who received adjuvant radiation (following surgery).

The researchers concluded that neoadjuvant radiation therapy offers a significant benefit over surgery alone or surgery with adjuvant radiation therapy in treating pancreatic cancer. Research will likely be ongoing to further explore these findings.

Reference:
[1] Stessin AM, Meyer JE, Sherr DL. Neoadjuvant radiation is associated with improved survival in patients with resectable pancreatic cancer: An analysis of data from the Surveillance, Epidemiology, and End Results (SEER) Registry. International Journal of Radiation Oncology Biology Physics. 2008; 72: 1128-1133.

Company claims new 'mouth swab' gene test will lead to personalised breast screening

2009-02-02T18:21:00.000-08:00

A UK company has launched a new genetic risk assessment service which they claim will allow doctors to draw up personalised breast cancer screening and prevention programmes.

The test combines information about a woman's lifestyle with a DNA test. The results are combined to calculate her overall 'absolute risk' of breast cancer, according to the company, BreastHealthUK.

The gene test is provided by Icelandic company deCODE genetics and is carried out using a sample of DNA extracted from a mouth swab.

*With more and more commercial genetic screens emerging, there's an urgent need for well-designed studies evaluating these types of tests.*

- Dr Lesley Walker, director of cancer information, Cancer Research UK

It looks at seven gene variations - or SNPs - that are associated with an increased risk of breast cancer, several of which were discovered by Cancer Research UK scientists.

It combines these with results from a lifestyle risk calculation programme called the Tyrer-Cuzick model, also developed by Cancer Research UK-funded scientists.

Women are then presented with the results in consultation with an experienced breast surgeon or genetic counsellor, so thattheir genetic and lifestyle risk factors can be discussed and the implications fully explained.

The test is not available on the NHS but can be obtained privately for ?700.

Breast surgeon Professor Gordon Wishart, medical director of BreastHealth UK, commented: "Although genetic testing is still a relatively young technique, when combined with proven methods to elicit lifestyle and family history factors, it can provide breast surgeons with new insights into detection and prevention of this disease."

However, experts pointed out that there is still a long way to go before the genetics of breast cancer is fully understood, and that research is needed to prove that these commercial tests will actually reduce cancer death rates.

Dr Lesley Walker, Cancer Research UK's director of cancer information, commented: "Assessing your risk of cancer and interpreting the results of genetic tests is a very complex matter. With more and more commercial genetic screens emerging, there's an urgent need for well-designed studies evaluating these types of tests - we need to know more about their clinical and psychological impacts, and their current scientific value."

Dr Walker continued: "We've still only got a few pieces of the genetic puzzle. Genetic testing without this missing information means we risk worrying women who may never develop the disease. The commercial market for genetic testing should be properly regulated and appropriate information on the pros and cons should be conveyed to customers.

"At this stage, Cancer Research UK would recommend that women worried about their risk of cancer visit their GP or contact Cancer Research UK's information nurses on 0808 800 4040. Women with a strong family history of breast cancer will be offered genetic testing on the NHS."

Women with a strong family history of breast cancer are already eligible for genetic testing on the NHS. According to guidelines published by the National Institute for Health and Clinical Excellence (NICE), women can be referred to specialist genetics services if they have a high risk of developing breast cancer.

This risk is usually determined by looking at a number of factors, including the age at which close relatives were diagnosed with breast cancer; whether a relative had cancer in both breasts; and whether any men in the family have had breast cancer.

Study sheds light on cancer-causing gene

2009-02-02T18:11:00.000-08:00

US scientists have discovered a previously unknown way by which a cancer-causing version of the Myc gene speeds up the progression of the disease.

A faulty version of Myc is already known to interfere with the early stages of DNA activity in the nucleus of the cell. It prevents DNA from being 'transcribed' into RNA, which is an essential first step in making proteins for cell growth and function.

However, scientists at the University of California San Francisco (UCSF) have now found that the faulty Myc gene can also act directly on the final stage of protein production.

*Genes like Myc contribute to cancer in many different ways and every time we discover a new one, we give ourselves another potential avenue for beating the disease.*

- Ed Yong, health information manager, Cancer Research UK

Dr Maria Barna, a faculty fellow in the university's Biochemistry and Biophysics Department and one of the study's senior authors, explained that cancer-causing genes such as Myc regulate a number of distinct cellular processes.

"The key to our studies was the ability to generate novel genetic tools to halt Myc's action on protein production. This demonstrates how essential this process is for cancer formation," she revealed.

Co-senior author Dr Davide Ruggero, assistant professor of urology at the UCSF Helen Diller Family Comprehensive Cancer Centre, commented: "Control of protein production rapidly affects cell behaviour, and in a robust manner.

"The ability of the Myc oncogene to directly alter this process may well explain the rapid progression of cancer formation."

In order to find out whether Myc-induced protein production plays a role in cancer, the researchers bred two types of mice - one of which was prone to cancer and over-expressed the Myc oncogene, whilethe other had lowered protein production.

This resulted in mice which had the destructive Myc traits as well as an enhanced ability to suppress protein production.

The researchers found that in these mice, cell growth, division and death - which is required to counter cancer - were restored to near-normal levels.

This also helped to counter Myc-induced damage to chromosome function, indicating that Myc causes changes in the genetic integrity of cells through control of protein production and that it may disrupt a number of genes.

Dr Ruggero said: "We discovered a previously unrecognised link between alterations in protein synthesis and the mechanism by which cells maintain the integrity of the genome.

"We found that when Myc is overexpressed, this leads to changes in protein levels of a key gene that is essential for normal distribution of genetic material between daughter cells during cell division."

The discovery, which appears in Nature, suggests that existing drugs which counter increased protein production could slow down tumour growth in cancers where Myc is overactive.

Ed Yong, Cancer Research UK's health information manager, said: "Genes like Myc contribute to cancer in many different ways and every time we discover a new one, we give ourselves another potential avenue for beating the disease."

Ref: Barna et al. Nature 456, 971-975 (18 December 2008)

New Australian Study: Ovarian Cancer Not A 'Silent Killer'

2009-02-02T17:51:00.000-08:00

Ovarian cancer has often been referred to as a 'silent killer', but new preliminary findings from an Australian study show the disease is in fact not silent - these latest data show most women (83 per cent) experience at least one symptom of ovarian cancer in the year prior to their diagnosis.

The study also revealed 17 per cent of women waited more than three months after the onset of their symptoms before visiting their doctor, with 8 per cent waiting more than six months.

"The most common reason for the delay was an assumption that the symptoms were not serious, with many women attributing them to another medical condition or the natural process of ageing," said Dr Helen Zorbas, CEO, National Breast and Ovarian Cancer Centre.

The study by National Breast and Ovarian Cancer Centre in collaboration with the Queensland Institute of Medical Research, examined the pathways taken by 1500 Australian women to their diagnosis of ovarian cancer, strengthening the case for women to be aware of the symptoms of the disease.

"As there is no screening test for ovarian cancer, the first step to diagnosis is a woman identifying symptoms which are persistent and unusual for her and seeking medical attention. It is therefore vital that women are aware of the symptoms to look out for," said Dr Zorbas.

The symptoms of ovarian cancer include:

- abdominal bloating
- abdominal or back pain
- appetite loss or feeling full quickly
- changes in toilet habits
- unexplained weight loss or gain
- indigestion or heartburn
- fatigue

The most common symptoms, experienced by half of the study participants, were abdominal symptoms such as fullness and pain. Bloating, bowel or urinary symptoms were reported by approximately one third of participants.

"We know many women will experience these symptoms as part of everyday life," said Dr Zorbas. "But if any of these symptoms are unusual for you and they persist, it is important to see your doctor. No one knows your body like you do."

This year about 1300 women will be diagnosed with ovarian cancer in Australia. More than half of women diagnosed do not survive five years after their diagnosis. More than 70 per cent of women are diagnosed at an advanced stage, where the cancer has spread and is difficult to treat successfully.

National Breast and Ovarian Cancer Centre is funded by the Australian Government and works with consumers, health professionals, cancer organisations, researchers and governments to improve care and cancer control in breast and ovarian cancer. Queensland Institute of Medical Research coordinates the Epidemiology core of the Australian Ovarian Cancer Study. The Australian Ovarian Cancer Study is a collaborative research program between clinicians, scientists, patients and advocacy groups aimed at improving the prevention, diagnosis, and treatment of ovarian cancer.

Source
Bree Stevens
Senior Communications & Policy Officer
National Breast and Ovarian Cancer Centre
Level 1, Suite 103, 355 Crown Street SURRY HILLS NSW 2010
Telephone + 61 2 9357 9402 Mobile 0438 209 833 Facsimile + 61 2 9357 9477
http://www.nbocc.org.au

Breast Cancer Saliva Test to Make Dangerous Mammograms Obsolete

2009-01-31T12:04:00.000-08:00

Researchers are working to develop a saliva test for breast cancer that could vastly reduce the use of dangerous and invasive breast cancer screening techniques such as mammograms."This will be a noninvasive, quick means of detection," said lead researcher Charles Streckfus, a professor of diagnostic sciences at the Dental Branch of the University of Texas (UT) at Houston. "With it, dentists will be able to catch cancers before a woman can feel a lump."Researchers have discovered that the onset of breast cancer changes the density of different proteins excreted by the salivary glands. In the current study, published in the journal Cancer Investigation, Streckfus and other researchers from the UT-Houston Dental Branch and Medical School compared the protein levels found in the saliva of 10 women with breast cancer, 10 healthy women and 10 women with a type of tumor called fibroadenoma.Fibroadenoma is the most common kind of benign breast tumor."Saliva is a complex mixture of proteins," said researcher William Dubinsky. "We go through a process that compares different samples by chemically labeling them in such a way that we can not only identify the protein, but determine how much of it is in each sample. This allows us to compare the levels of 150-200 different proteins in cancerous versus non-cancerous specimens to identify possible markers for disease."The researchers identified 49 proteins that were present at different levels between the three groups. These proteins should hypothetically allow doctors to use such a saliva test to alert them when a woman has a tumor, and to determine whether it is cancerous or benign."This is a unique finding," Streckfus said, "as it targets both the benign and malignant tumor, which could potentially reduce the number of false positives and false negatives associated with current cancer diagnostics".Previously, the same team of researchers was able to correctly detect whether a woman had breast cancer 85 percent of the time, using only one saliva protein as a marker. With 49 different markers, Streckfus says that the accuracy of the test should be closer to 95 percent.In the current method, the saliva sample is placed onto a hand-held, gold-plated chip or lab dish, developed by UT-Austin biochemists. A laser analyzes the protein content of the sample."I see this as a future public health service by dentists," Streckfus said. "Most folks, especially women and children, visit the dental office way more often than they ever see the physician. Saliva is a non-invasive, quicker way for detection."Many obstacles remain before this test could be available, however. The first step is more studies to confirm the effectiveness of the protein markers as diagnostic tools in a larger group of patients. Streckfus and colleagues hope to launch a large, multicenter clinical trial of the test within the next two years, and to apply for FDA approval within five.The only saliva test currently approved by the FDA is one for HIV/AIDS.A saliva test for breast cancer has many advantages over current diagnostic methods such as ultrasounds, mammograms, biopsies and blood tests. It would be far less invasive and expensive than most such tests, and have a much higher accuracy rate than blood tests, which are not currently favored for breast cancer diagnosis due to their poor accuracy.The higher accuracy of a saliva test comes in part from the fact that saliva proteins are much easier to detect than the proteins in blood, Dubinsky said."In the case of breast cancer, saliva analysis has been used to monitor patient response to chemotherapy or surgical treatment of the disease," said Professor Damien Walmsley, scientific adviser for the British Dental Association. "The mouth itself is a good indicator of an individual's overall health, and dentists already play an important role in diagnosing and detecting oral cancers."Streckfus said that a saliva test would be particularly valuable in places where mammography centers are rare, such as in many Third World countries, or in breast cancer survivors who need to be regularly monitored for potential cancer recurrence.Regular use of mammograms is not only expensive and emotionally distressing, but can also be dangerous. Because women are exposed to X-ray radiation as part of the mammogram procedure, regular mammogram use actually increases women's risk of developing various cancers. For this reason, mammograms are not normally performed for women under the age of 40, in whom the risk of breast cancer is relatively low unless symptoms are present.But Streckfus warned that a saliva test cannot utterly replace mammograms, because the saliva test is unable to determine which breast contains the tumor.Nonetheless, cancer patient advocates have greeted the new research as promising. According to Leonard Lichtenfeld, deputy chief medical officer for the American Cancer Society, the saliva test will one day be "a terrific advance.""I think advances like this test portend the day when we'll be able to diagnose disease that would be invisible using today's technologies," Lichtenfeld said. "[Patients will] be able to be diagnosed and treated before they would otherwise know they have the disease."Streckfus and colleagues are also researching whether saliva tests can be used to diagnose other cancers, including of the cervix, uterus, head, neck and ovaries. Another group of researchers, at Johns Hopkins Kimmel Cancer Center, is also working on a saliva test for head-and-neck cancer. According to Lichtenfeld, the Johns Hopkins team is farther along than the UT-Houston team, because their test relies on genetic rather than protein markers.

Bras Shown to Cause Cancer

2009-01-31T12:03:00.000-08:00

Is it possible that wearing a bra can actually cause cancer? Studies show that this is a very real possibility. The reason is that regularly wearing a bra prevents lymph drainage and circulation, which can greatly increase the possibility of developing breast cancer.The lymphatic and circulatory systems are responsible for both delivering vital nutrients and clearing out toxins. When the body does not have access to nutrients or when it is under the attack of toxins, cancer may develop.A study published in the European Journal of Cancer studied factors for breast cancer such as breast size and handedness. They discovered that premenopausal women who do not wear bras are less than half as likely to get breast cancer that those who regularly wear a bra. A study conducted by researcher David Moth revealed that even the lightest bras place pressure on the lymphatic system.Other research published in Chronobiology International in 2000 discovered that regular bra wearing decreases the production of melatonin, which is a potent natural antioxidant and the hormone that regulates sleep, boosts the immune system and, incredibly fights aging. Balanced melatonin levels are essential for the body to fight many types of cancer, including breast cancer.Researchers Singer and Grismaijer observed 4,500 women and their bra wearing practices. An amazing 3 out of 4 women who wore their bras 24 hours per day developed breast cancer. Women who wore their bras more than 12 hours per day had a 1 in 7 chance of getting breast cancer. 1 out 152 women who wore their bra less than 12 hours a day got breast cancer and an incredibly low 1 out of 168 women who rarely or never wear a bra developed breast cancer.These same researchers studied the indigenous populations of New Zealand and Australia. The Maoris, who are indigenous to New Zealand, are basically fully integrated into mainstream New Zealand life and interestingly have the same chances of developing breast cancer. The aboriginals of Australia on the other hand have not integrated into regular western society and do not regularly wear bras, and have practically no breast cancer. Japanese, Fijians, and many women from other cultures were found to have a significantly higher chance of developing breast cancer when they began wearing bras.It may be interesting to note that a very small proportion of men do develop breast cancer, exactly the same amount as women who go braless!European, Journal of Cancer 1991 ;27(2): 131-5.Cancer is Not a Disease by Andreas Moritz

Brussels Sprouts Defend against All Types of Cancer

2009-01-31T11:59:00.000-08:00

Plant phytonutrients found in Brussels sprouts boost the body`s natural defense systems to protect against cancer and other diseases. Brussels sprouts and other cruciferous vegetables disarm cancer causing chemicals and encourage the body`s detoxification enzymes.Evidence in the Netherlands suggests that Brussels sprouts keep the body free from cancer by promoting healthy DNA. DNA is responsible for cell division in the body. When DNA gets damaged, cells may begin to replicate much more rapidly than normal, which can cause a cancerous tumor to begin to form. Several studies reveal that Brussels sprouts have the ability to help protect DNA from damage.Researchers compared two groups of healthy men. Half of these men ate 300 grams of Brussels sprouts daily, while the other men didn`t have any cruciferous vegetables in their diet. After three weeks, the men who ate their daily dose of Brussels sprouts had a 28% decrease in measured DNA damage.Diminish Digestive Cancers with Brussels SproutsThe phytonutrients in Brussels sprouts have been shown to protect against heterocyclic amines, which are the carcinogenic compounds found in grilled and charbroiled meat. These carcinogens are particularly associated with colon cancer. The study, published in Carcinogenesis, found that animals that were given Brussels sprout juice and heterocyclic amine carcinogen were less likely to develop the cancer.The animals given Brussels sprouts had a reduction in pre-cancerous cells in the colon of 41-52% in the colon and 27-67% in the liver, and drastically diminished the size (85-91%) of pre-cancerous lesions in the liver. These amazing results seem to be a result of Brussels sprouts potent ability to detoxify the body and clear out the colon.Brussels sprouts are also packed with fiber, which nourishes the cells lining the walls of the colon and prevents colon problems including cancer.Brussels Sprouts Fight Bladder CancerResearch published in the International Journal of Cancer shows that Brussels sprouts protect against bladder cancer. The diets of 697 people who were recently diagnosed with bladder cancer were compared with 708 people with the same age, gender and ethnicity who were healthy. The average daily intake of Brussels sprouts and other cruciferous vegetables was significantly lower in those with bladder cancer than in their healthy counterparts. Those who had the highest intake of Brussels sprouts and cruciferous vegetables had a 29% lower risk of bladder cancer that those who ate the least.The benefits of these vegetables were highest in those who have the highest risk of bladder cancer, including men, smokers and older individuals.Brussels sprout`s bladder cancer properties appear to come from their high levels isothiocyanates, which are potent anti-carcinogens. Isothiocyanates travel through the bladder to be excreted, making them particularly powerful against this form of cancer.Breast Cancer ProtectionSulforaphane is released by Brussels sprouts and has been proven to trigger the liver to produce enzymes that detoxify the body of cancer-causing chemicals They have been shown to inhibit chemically-induced breast cancers in animal studies. Research published in the Journal of Nutrition shows that sulforaphane can halt the proliferation of breast cancer cells, even in the later stages of their growth.Defend Against Prostate CancerResearch at Fred Hutchinson Cancer Research Center in Seattle studied 1,000 men. It was shown that eating 28 servings of different vegetables a week reduced their risk of prostate cancer by 35%. But those who ate 3 or more servings of cruciferous vegetables each week had a 44% lower prostate cancer risk.Many people claim to not enjoy eating Brussels sprouts. If you are not a fan of this incredible food, try chopping them up into tiny peices and sprinkling them over a salad. You won`t even be able to taste them but you will still get the health enhancing benefits and defend your body against disease.http://www.whfoods.com http://www.drbriffa.com

Apple Pectin Helps Prevent Colorectal Cancer

2009-01-31T11:56:00.000-08:00

The pectin from apple peels and extracts of apple juice appear to increase the production of a chemical associated with protection from colon cancer, according to a new study conducted by German researchers and published in the journal Nutrition.

The researchers fermented fecal slurry from healthy volunteers with either apple pectin, apple juice extract, or a combination of the two. They found that the concentrations of a short chain fatty acid (SCFA) known as butyrate were higher in the samples that had been fermented with apple pectin. Concentrations of other SCFAs were also elevated.

"Butyrate not only serves as a major nutrient for the colon epithelia [lining] but is also thought to play an important role in the protective effect of natural fiber against colorectal cancer," the researchers wrote.

Butyrate appeared to inhibit the production of histone deacetylases (HDAC), which have been linked to the development of precancerous cells and tumors. When the researchers tested the fermented fecal slurries on both healthy and cancerous colon cells, they found that the production of HDAC was significantly inhibited.

The slurries fermented with apple juice did not have butyrate levels as high as those fermented with pectin, but they inhibited HDAC production just as effectively. A combination of pectin and apple juice, however, was no more effective than pectin alone. This led the researchers to hypothesize that while apple juice contains still-unknown HDAC inhibitors other than butyrate, butyrate is the most significant inhibitor for the human body.

The study is part of a growing interest in the cancer-suppressing qualities of fruits and vegetables. Another recent study found that freeze-dried grape powder appears to hamper the development of colorectal cancer cells. This effect is believed to arise from the chemical resveratrol, rather than from pectin. But researchers have noted that the cancer-fighting properties of fruits and vegetables often arise from complex interactions between different ingredients.

Sources for this story include: www.foodnavigator-usa.com.

Breast Cancer Gene-Free Baby Is Dangerous Sign of New Era of Eugenics, Genetic Class Wars

2009-01-28T07:03:00.000-08:00

The era of pre-birth genetic screening of babies has commenced. Doctors at University College in London have produced what they called the "world's first breast cancer gene-free baby" by screening a baby for the BRCA1 gene, which they claim causes breast cancer. (http://news.bbc.co.uk/2/hi/health/7...)That announcement is saturated with so many medical myths, it's difficult to know where to begin. For starters, the idea that the BRCA1 gene causes cancer is pure hogwash. There's no such thing as a gene that causes cancer by itself. The truth is that environmental factors such as exposure to cancer-causing chemicals in foods, medicines, personal care products, pesticides or other industrial chemicals causes the expression of the cancer gene. Without all that toxic chemical exposure, the gene never gets expressed in the first place.And it gets even better: You can eat raw broccoli sprouts or other cruciferous vegetables and suppress the BRCA1 gene so that you never grow cancer tumors at all. Thus, the patient has complete control over the expression of their genes based on their diet and environment, and there are literally hundreds of different foods that have an anti-cancer effect: Cruciferous vegetables, onions, garlic, red wine, green tea, raw cacao, omega-3 oils, and of course a whole universe of anti-cancer herbs and superfoods.This doesn't even mention the effects of vitamin D and exercise on the BRCA1 gene, both of which also suppress cancer.But modern medicine -- which is largely based on marketing-motivated quackery -- wants women to believe they have no control over breast cancer and that it all comes down to your genes, not your choices. That's the little trap they set for women, stripping them of their power and condemning them to a lifetime of medical "treatment" that just happens to earn outrageous profits for the drug companies.
Welcome to the new era of eugenicsSo now we have a new era being unleashed where babies born with the BRCA1 gene are going to be considered "defective" while babies born without the gene will be considered "superior."This is leading us into a dangerous new mindset where babies will be condemned as second-class citizens from the moment they're born simply because they carry a gene that the corrupt medical system mistakenly believes is a causative factor for some disease.The relevant movie to watch here is GATTACA (http://www.imdb.com/title/tt0119177/), a film that depicts a future society where your genes determine every opportunity you have in life: Your job, you income, your social standing and much more.GATTACA is a smart movie that sends a highly relevant warning message: If we begin to profile babies for their genes, then we are heading down a slippery slope of defunct medical ethics that could ultimately lead to a new division between the "genetic upper class" and the "genetic lower class."The next class war could very well be based on genetics, and parents will fret over the genetic makeup of their children, choosing to abort babies that don't have the "right" genes, even if those babies are perfectly healthy. And then we'll have medical companies offering to manipulate the genes of the fertilized egg, promising to give parents a baby with blond hair, or a high IQ, or a thin physique...It's just what we need, huh? A whole society of genetically-selected supermodels running around society, thinking they're superior because they've been genetically designed by scientists who think they're God.These gene-pushing doctors mistakenly think they can determine the future of a human being by manipulating the genes of the fetus. It's no surprise, after all: Most conventionally-trained physicians believe in outright determinism, thinking that there is no such thing as a soul, or free will, or a spiritual reality of any kind. You're born with genes, you "play out" your predetermined fate recorded in those genes, and then you die and that's the end of everything. It's a deeply pessimistic, deterministic point of view, and yet it's the view that's held by the vast majority of western doctors.The real truth is that while genes certainly have potential influence over a person's health, it is the environment (foods, health habits, exercise, exposure to chemicals, etc.) that is the far more important factor in determining what happens to an individual's health. I can take a room full of a thousand BRCA1 gene carriers and show every one of them how to live a life 100% free of breast cancer through simple, safe and low-cost methods that are available to everyone.Modern medicine refuses to do that. Because despite all the grand technology, the manipulation of human life and the arrogant playing God that takes place daily in the minds of western doctors, there's one thing they still haven't figured out how to do: Tell the truth to a patient about how they can prevent cancer, regardless of their genes.Modern medicine is a huge technical success and a complete humanistic failure. It offers the most impressive technology in the world and puts it into the hands of the most ethically-deficient professionals who are so pessimistic about the nature of reality that they don't even believe in the existence of their own souls.And do you really want scientists who don't even believe in the existence of the human soul to be playing God with your baby's genes?Disturbing.It should also be noted, by the way, that this whole process of "gene screening babies" involves testing the embryo at the eight-cell stage (when conception has already taken place and the baby is beginning to grow), and then throwing away any embryos that don't fit the desire genetic profile.In effect, the gene screening of babies involves the systematic destruction of viable human embryos that could grow into full-fledged babies. This opens up a whole new debate on the issue of abortion, of course, and I'd like to hear your comments on all this. Simply post your thoughts in the comment section below.The key issues are: At what point is the genetic screening of a baby going too far? Most people might agree, for example, that screening for major birth defects is acceptable, but is it acceptable to screen for things like blue eyes and then toss out the embryos that don't carry that gene?What will happen in the future of society if the gene screening of embryos becomes socially acceptable and is embraced by parents?What are the risks posed by a race of beings that engages in routine genetic selection? (For example, might be lose biodiversity? Might the BRCA1 gene have another positive purpose that doctors haven't identified yet?)Should humans be genetically engineered to insert new traits? Larger brains? Stronger muscles? Bigger boobs? (Parents could actually order up a boob job on their daughter before she's born!)Think carefully about this one. It's a hugely complex sociomedicalethical issue

Vigorous Activity Lowers Risk of Breast Cancer in Women

2009-01-28T06:59:00.000-08:00

Recent research published in the journal Breast Cancer Research has found that vigorous activities, which include chores such as digging in the garden and heavy housework, lower the risk of women getting breast cancer. This protective effect, however, only applied to women who were in the normal weight range.About Breast CancerIn 2004, over 185,000 women and more than 1,800 men in the United States alone were diagnosed with breast cancer, while almost 41,000 women and 362 men succumbed to the disease.In that year, breast cancer was the number two cancer killer of American women, ranked only after non-melanoma skin cancer, while also being their number five killer overall. In addition, for Hispanic women, breast cancer was the number one cancer killer.In Canada, the picture isn't much better either. Among Canadian women, breast cancer is the most common form of cancer. The Canadian Cancer Society has estimated that some 22,400 women will be diagnosed with it this year, while about 5,300 will succumb to the disease.Details of StudyExercise has already been heavily linked with the prevention of many chronic diseases. Also, previously, other studies had suggested that women who went through more physical activity had lower risks of getting breast cancer. But this time, the researchers dug deeper.In this study, conducted by the National Cancer Institute of the US National Institutes of Health, more than 32,000 women from across the United States were tracked for a period of 11 years. The average age of the subjects was 61, and all of them were free from chronic diseases at the start of the study. The participants were made to fill out a detailed questionnaire regarding their physical activity.The survey asked the participants to estimate the typical number of hours which they spent each day carrying out various physical activities. These included moderate activities such as bowling, gardening, hiking, jogging lightly, mowing the lawn, vacuuming the floor and walking.They also included vigorous activities such as aerobics, chopping wood, competitive tennis, cycling on hills, digging in the garden, fast dancing, heavy housework, heavy yard work, jogging quickly, running, scrubbing the floors and washing the windows.Findings of StudyOverall, the participants of the study spent an average of 5.9 hours each day taking part in non-vigorous activities, and an average of 1.2 hours doing vigorous activities. By the end of 11 years, 1,506 of the women had been diagnosed with breast cancer.The study found that the women who were the most active had a 13% lower risk of getting post-menopausal breast cancer, when compared with their least active counterparts.A significant finding is that this difference was a lot more pronounced in women in the normal weight range (body mass index below 25). For this group, the difference in risk between the most active and least active women was 30%.On the other hand, for women who were overweight or obese, there was no difference in risk between the most active and least active women."The association with physical activity was essentially limited to the leaner women," said Dr Michael Leitzmann, leader of the study.The ImplicationsOne limitation of the study was that it only measured the level of physical activity once, which would not have given a very accurate reflection of the women's level of physical activity over the whole period of the study. Even then, the study team still felt that physical activity in mid to late adulthood had an important influence on the risk of breast cancer.And, from the findings of the study, we can probably draw two conclusions. Firstly, even for women who are in the normal weight range, a sedentary lifestyle is still a risk factor for breast cancer. Further, for overweight women, being physically more active did not seem to help.The bottomline? If you are serious about averting breast cancer, you may want to watch your weight, and make sure you are getting enough vigorous exercise.Main SourceIntense activity curbs breast cancer risk (http://www.canada.com/calgaryherald...)

Conventional Prostate Cancer Treatment Contributes to Cognitive Decline

2009-01-28T06:55:00.000-08:00

Through many cancer regiments, the results of the treatments leave the patients with debilitating and most of time deadly side effects such as hair loss, vomiting, weight loss, edema, immune dysfunction, etc. For prostate cancer, another consequence of the treatment can be added to the list: the degeneration of cognitive abilities.Typically, prostate cancer patients go through a treatment known as androgen deprivation therapy (ADT) or hormone deprivation therapy that blocks testosterone production and can slow the growth of the tumor.Though a recent MSNBC article presents the type of cognitive decline as miniscule and limited to functions such as spatial ability and the ability to multitask (and other such actions), can we be certain that the effects of this treatment are as minimal as the mainstrem media make it out to be? I do not think anyone can accurately know the answer to that question, unless there are those who know these effects to be more serious than what is reported here; however, what is sure is that these cognitive decline effects can certainly be avoided through natural means.One way to treat prostate cancer is to cut out low-fat dairy products. Low-fat dairy products are callously promoted under the misconception that saturated fat is unhealthy and "bad" for you. A study conducted by the Cancer Research Center of Honolulu last year found that, after collecting data from 1993-2002 of 82,483 male participants forty-five years old and over, there was a twelve percent decrease in the risk of developing prostate cancer for the whole milk drinkers: there was a sixteen percent increased chance for developing the illness for those who drank 2% milk or skim milk.Another way to treat prostate cancer is to increase the intake of broccoli and tomatoes together. Sheryl Waters of Natural News wrote, when quoting Professor John Erdman of University of Illinois food science and human nutrition, that, "When tomatoes and broccoli are eaten together, we see an additive effect. We think it's because different bioactive compounds in each food work on different anti-cancer pathways," These documented effects demonstrate the wonderful, yet simple, solution to better health that broccoli and tomatoes provide.Unfortunately, there is another added side effect to the purported treatment for prostate cancer; however, that does not have to be the undue fate of the illness's sufferers. There are natural treatments that can help to restore the physical and mental health of the afflicted.Sources:1. (www.msnbc.msn.com/id/25887520)2. (www.dietdetective.com/content/view/...)3. (http://www.naturalnews.com/023125.html)4. (http://www.naturalnews.com/021446.html)

Seven Good Reasons to Avoid Cow's Milk

2009-01-28T06:46:00.000-08:00

Drink all of your milk is a phrase many people grew up hearing. Yet evidence increasingly suggests that milk is not as healthy as it has been believed to be. Health concious people are giving up milk and turning to alternatives. Here are 7 reasons why all of us can consider avoiding cow's milk:1) Milk doesn't keep our bones healthy, preventing fractures and osteoporosis. In fact, according the Nurse's Health Study, dairy may actually increase the risk of fractures rather than protecting our bones. Countries such as those in Africa and Asia who don't consume large amounts of dairy actually have the lowest rates of osteoporosis.2) Milk is not the great source of calcium that most people believe it is. First of all, pasteurizing milk kills all of the nutrients, including calcium. Second, spinach, tahini, kale and other green leafy vegetables are the best sources of calcium on the planet.3) Milk is has been linked with acne by at least three large-scale studies reported in the American Journal of Dermatology. Research shows that there is up to 44% more chance of developing acne in those who drink milk.4) Dairy may raise cancer risk. Research has revealed that a higher intake of dairy products may increase a man's risk of prostate cancer by 30 to 50 percent. In addition, the body's insulin-like growth factor-1 (IGF-1), which is a known cancer promoter is increased by drinking milk.5) Approximately 75 percent of the world's population is lactose intolerant, which means that they are unable to fully digest dairy. Lactase is the enzyme needed to digest lactose, and most people stop producing it around the age of 5.6) Dairy is full of saturated fat and is linked to heart disease. Like cancer, countries such as Japan have a very low level of heart disease, and research commissioned by the New Zealand company A2 shows that there could be a link between a protein in milk.7) People with many different healthy complaints notice a significant improvement when they avoid dairy. Health complaints associated with dairy intolerance include irritable bowel syndrome, allergies, sinus problems, and ear infections.So what is the first step in giving up milk?*Get loads of sunshine to ensure plenty of vitamin D.*Start eating masses of green leafy vegetables so you can ensure you are getting your calcium.*Try substituting milk with nut milk.*Many studies show that raw milk (unpasteurized) is far better because the nutrients have not been destroyed. Raw goat's milk and raw sheep's milk are both increasingly popular.*Avocado is a wonderful butter substitute. It offers a creaminess that is people who have given up milk miss. Many vegans and raw foodists find that avocado is one of the most essential transition foods.*Coconut butter is another buttery, creamy substitute for those that want to give up milk. Coconut butter is the healthiest oil in cooking. It can also replace butter as a spread and cream in healthy cakes and desserts.http://www.womenrepublic.co.uk www.mercola.com

Common food additive may increase lung cancer risk

2008-12-31T15:25:00.000-08:00

A diet high in inorganic phosphates, which are found in a variety of processed foods-including meats, cheeses, beverages, and bakery products-can increase the risk and spread of lung cancer, according to a new study.
Washington, Dec 30 : A diet high in inorganic phosphates, which are found in a variety of processed foods-including meats, cheeses, beverages, and bakery products-can increase the risk and spread of lung cancer, according to a new study.
The study, using a mouse model, indicated that inorganic phosphates might speed growth of lung cancer tumours, and even contribute to the development of those tumours in individuals predisposed to the disease.
Conducted by Myung-Haing Cho, D.V.M., Ph.D., and his colleagues at Seoul National University, the study also suggested that dietary regulation of inorganic phosphates might play an important role in lung cancer treatment.
"Our study indicates that increased intake of inorganic phosphates strongly stimulates lung cancer development in mice, and suggests that dietary regulation of inorganic phosphates may be critical for lung cancer treatment as well as prevention," said Cho.
The study revealed that high levels of inorganic phosphates can stimulate non-small cell lung cancer (NSCLC) pathways.
"Lung cancer is a disease of uncontrolled cell proliferation in lung tissue, and disruption of signaling pathways in those tissues can confer a normal cell with malignant properties. Deregulation of only a small set of pathways can confer a normal cell with malignant properties, and these pathways are regulated in response to nutrient availability and, consequently, cell proliferation and growth," explained Cho.
He added: "Phosphate is an essential nutrient to living organisms, and can activate some signals. This study demonstrates that high intake of inorganic phosphates may strongly stimulate lung cancer development by altering those (signaling) pathways."
For the study, the researcher analysed lung cancer-model mice for four weeks.
The mice were randomly assigned to receive a diet of either 0.5 or 1.0 percent phosphate, a range roughly equivalent to modern human diets.
After four-weeks, the lung tissue was analysed to determine the effects of the inorganic phosphates on tumours.
"Our results clearly demonstrated that the diet higher in inorganic phosphates caused an increase in the size of the tumours and stimulated growth of the tumours," said Cho.
"The results of this study suggest that dietary regulation of inorganic phosphates has a place in lung cancer treatment, and our eventual goal is to collect sufficient information to accurately assess the risk of these phosphates," he said.
The study has been published in the January issue of the American Journal of Respiratory and Critical Care Medicine.
ANI

Lack of Sleep Greatly Increases Breast Cancer Risk

2008-12-30T10:21:00.000-08:00

A study on almost 24,000 Japanese women recently published in the British Journal of Cancer has found that lack of sleep can greatly increase the risk of breast cancer, with women who slept 6 hours or less every night having a significantly higher risk.Breast Cancer StatisticsBreast cancer is the most common cancer to hit women worldwide. In Japan, when age-standardized to the world population, the incidence rate was 28.3 per 100,000 in 1991, and rose to 39.5 in 2001.In the United States in 2004, the disease hit more than 185,000 women and over 1,800 men, with almost 41,000 women and 362 men dying from it that year. In that year, after non-melanoma skin cancer, breast cancer was the next highest cancer killer of American women. It was also their fifth highest killer overall.Next up, over to Canada, where, among the women, breast cancer is the most common type of cancer to strike. According to Canadian Cancer Society estimates, about 22,400 women will be diagnosed with the disease this year, with about 5,300 dying from it.With such grim statistics, every little thing which can be done to prevent and combat the disease becomes all the more critical.Details of StudyThe Ohsaki National Health Insurance (NHI) Cohort Study started in 1994 and involved 28,515 women in northeastern Japan. The questionnaire used included information on sleep duration and other lifestyle habits.Participants who had withdrawn from the NHI study before follow-up, had a history of cancer, did not provide information on their sleep duration, and who reported having slept for less than 4 hours or more than 12 hours every night were omitted. This left the data for 23,995 women to be analyzed. An 8-year period, from 1995 to 2003, was used, during which 143 women were hit with breast cancer.Findings of StudyThe women who slept 7 hours each night was used as the reference group. It was then found that women who slept 6 hours or less each night had a 62% higher risk of getting breast cancer. On the other hand, those who slept 9 hours or more every night had a 28% lower risk of getting the disease.It would follow, then, that those who slept 6 hours or less every night had 2.25 times the risk of getting breast cancer when compared to those who slept 9 hours or more each night.The results remained largely consistent even when participants who were diagnosed with breast cancer within 3 years from the start of the study were excluded, or when the data was analyzed by age and menopausal status.Previous StudiesThe findings of this study validates the findings of two previous prospective cohort studies relating breast cancer and sleep duration (Verkasalo et al, 2005, Wu et al, 2008). Those two studies had also shown a significant decrease in breast cancer risk for those who slept the longest.It must be noted, though, that another such study (Pinheiro et al, 2006) did not find any such association. The study team pointed out, however, that that study had looked at residential nurses, who underwent rotating-shift work and had varying sleep timings. The findings of that study thus might not be applicable to the general population.Strengths and Limitations of StudyAccording to the study team, their research had a couple of strong points. Firstly, it used study subjects from the general population, thus allowing for overall generalization of its findings. In addition, it used the Miyagi Prefectural Cancer Registry, which the study team said is “one of the earliest and most accurate population-based cancer registries in Japan”.There were also, however, several limitations. Firstly, self-reported sleep data was used, and assessment was also only carried out once. In addition, and probably very significantly, no information on sleep quality, sleep timing, use of sleep medication, or presence of sleep disorders were available. These factors, of course, are very important as they can directly or indirectly affect cancer risk.Further, the researchers added that they had no information with regard to rotating-shift work or night work, but they felt that would not have affected their findings greatly as more than half of the study subjects were housewives, farmers or retired.The Sleep Duration – Breast Cancer LinkWhy is breast cancer risk linked to sleep duration? The answer could lie in melatonin, which is secreted during night sleep. When a person sleeps fewer hours, less melatonin is secreted, and lower levels of the chemical had previously been associated with increased breast cancer risk.In addition, melatonin may possess an inhibitory effect on gonadal function, which includes synthetizing and secreting sex hormones. It had also been found to have an antiproliferative effect on breast cancer cells.The Bottom LineIf the findings from this study are indeed accurate, then there is an immense difference in breast cancer risk between sleeping 4 to 6 hours every night, and just sleeping 1 to 3 hours more each night. In fact, it is more than likely that the protective effects of sufficient sleep also extend to other forms of cancer. 7 hours of sleep a night may thus be a good number to aim for.Hopefully, in time to come, further research will reveal more information relating sleep and disease risk, with sleep quality and sleep timing being two of the main possibilities.Main SourceSleep duration and the risk of breast cancer: the Ohsaki Cohort Study (http://www.nature.com/bjc/journal/v99/n...)

Talcum powder as dangerous as asbestos

2008-12-30T10:18:00.000-08:00

Back in 1973 the evidence about the dangers of talc prompted the FDA to think about steps to reduce the level of the asbestos-like fibers in cosmetic talc. The dangers are that talc is related to asbestos – a known carcinogen – and that the presence of talc particles is linked to tumors. However, the FDA did not regulate cosmetic talc even after 1993 when the National Toxicology Program reported that cosmetic talc, which had no fibers, was the cause of tumors in animals.Talc is a soft green-gray colored mineral produced from rocks and processed into a powder. Pure talc mineral is a hydrous magnesium silicate. Some trace minerals are removed in processing but very small fibers remain which are similar to those that occur in asbestos.Most talc is formed from altered dolomite or magnesite when there is excess dissolved silica. A number of minerals associated with talc include: tremolite, serpentine, anthophyllite, magnesite, mica and chlorite. Note that there are six minerals are defined as asbestos and two of these are also talc – tremolite and anthophyllite.Commercial talc may contain impurities and contaminates such as asbestos and crystalline silica. In fact asbestos may occur in talc.Talc is used in diverse industries and for a wide variety of purposes. It is commonly used in cosmetics and body powders, including those for babies. It has hydrophobic surface properties helping to keep skin dry.In the paper industry, talc is used as a filler which enhances the quality of the paper for printing and appearance of opacity. It is used in ceramic tiles, and in paints and coatings. Did you know that the dust on some chewing gums contains talc? Talc is also used in in flea and tick powder, deodorants, chalk and crayons, textiles and soap.Now we have another study (published in the Cancer Epidemiology, Biomarkers and Prevention journal) that shows that women who use talcum powder around their genital areas are 40% more likely to develop ovarian cancer. The study led by Dr Maggie Gates of Harvard Medical School analyzed 3,000 women. The risk of ovarian cancer for those who used talcum powder once a week was found to be 36%, while those using it every day the risk went up to 41%.In a recent separate incident a group of doctors at the Harvard Medical School found talc particles in the pelvis of a woman diagnosed with ovarian cancer. She had used talcum powder every day for around 30 years.In 1982 in Cancer magazine the conclusions from a study recommend that the lifetime use of talcum powder increases the risk of ovarian cancer by more than three times. Consequently, various cancer organizations warn against the use of talcum powder. For many people this warning is a bit late.Talc also causes poisoning due to accidental exposure. The website preventcancer.com (see link below) state that from the early 1980’s accidental inhalation of talc (baby powder) has caused the death or serious illness of several thousands infants.Talc is used in some medications such as some antiacids and in some antiseptics. So the question is is talc dangerous when used as medications? Actually there are so many questions we need to ask. What guidelines should be available and what regulations exist that protect people? Why do so many children suffer needlessly because of lack of care demonstrated by authorities? Why weren’t women protected against the use of talcum powder 30 years ago?Over and over again when there is a choice about caring for our fellow human beings and about earning profits, selfishness wins. And the authorities lack the care and the compassion required to serve us well.Reference: www.preventcancer.com/consumers/cosmeti...

Selenium Curbs AIDS Virus, may Fight Cancer

2008-12-30T10:14:00.000-08:00

After decades of attempting to fight AIDS with experimental vaccines and drugs, scientists have recently discovered how several natural substances could be powerful weapons against the disease. For example, in mid-November, UCLA AIDS researchers published research concluding that the herb astragalus contains a substance with the potential to possibly replace the side-effect plagued HAART (highly active antiretroviral therapy) currently used to treat AIDS patients. http://www.naturalnews.com/024799.htmlNow Penn State immunologists say they’ve documented how a micronutrient could help battle AIDS. Their findings, just published in the Journal of Biological Chemistry, show how selenium could dramatically put the brakes on the replication of HIV, the virus that causes AIDS.Selenium is needed by the body to maintain normal metabolism. It’s also increasingly being studied for its anti-cancer properties. Although other nutrients usually bind to proteins, selenium actually becomes incorporated into proteins, forming what are called selenoproteins. These selenium-containing proteins are believed to slow the spread of infections. However, when HIV infects a person, the virus manages to degrade selenoproteins, probably due to a protein, dubbed Tat, produced by the HIV virus. In particular, Tat seems to target a selenoprotein known as TR1.But there may be a way to get around this degradation of selenoproteins -- supplementation with selenium. "Since HIV targets the selenoproteins, we thought that the logical way to deal with the virus is to increase the expression of such proteins in the body," K. Sandeep Prabhu, assistant professor of immunology and molecular toxicology at Penn State, said in a statement to the press.To test their idea, the scientists isolated blood cells from human volunteers who did not have HIV. Then they infected those cells with the virus and added a form of selenium called sodium selenite to the cell culture.The result? The added selenium inhibited the replication of HIV at least 10-fold, in comparison to cell cultures with no added selenium. The scientists also selectively reduced the production pf the selenoprotein TRI. When there was less selenium-containing protein,HIV replication soared 3.5 times. Bottom line: The research confirms that an increase in selenium in cells zaps replication of HIV while a reduction in the amount of selenium-containing TR1 protein gives the virus a boost."We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV. Once we fully understand the function of these selenium proteins, it will give us a handle to come up with more effective drugs," said Dr. Prabhu in the prepared statement for the media.Two more new studies offer additional evidence that selenium may impact the immune system. German scientists from St. Josefs-Hospital in Wiesbaden recently published a study in the Swedish medical journal Acta Oncologica that suggests the micronutrient could help prevent prostate cancer and prostate enlargement. The researchers found that whole blood selenium levels were significantly lower in all men tested who had prostate cancer or benign prostate hypertrophy (which can cause difficulty with urination) and concluded, “our findings may support the recommendation of selenium supplementation” to help prostate health. What’s more, a study just published in the journal Molecular Nutrition and Food Research suggests enzymes that contain selenium have anti-oxidative and anti-inflammatory effects that could make them important in preventing prostate and colorectal cancers.Too much selenium in can cause a condition called selenosis, resulting in loss of hair, nail problems, nausea, irritability, fatigue, and mild nerve damage. However, selenium toxicity is extremely rare. A lack of selenium may, in fact, be far more common and potentially more dangerous to health. According to the National Institutes of Health, people age 14 and older should take in about 44 micrograms of selenium a day. Good sources of the micronutrient include Brazil nuts, eggs, brown rice, whole wheat bread and pasta, walnuts and oatmeal.

Cancer Doc Issues Warning About Cell Phone Use

2008-12-30T10:09:00.000-08:00

The director of the University of Pittsburgh Cancer Institutes and the Cancer Centers at the University of Pittsburgh Medical Center has issued a warning to all 3,000 faculty and staff under his supervision, warning them to limit cellular phone use in order to avoid adverse health effects."Recently I have become aware of the growing body of literature linking long-term cell phone use to possible adverse health effects including cancer," the memo from Dr. Ronald Herberman reads. "Although the evidence is still controversial, I am convinced that there are sufficient data to warrant issuing an advisory to share some precautionary advice on cell phone use."Herberman advises keeping mobile phone conversations as short as possible and using headsets, text messages or speaker phone settings to keep the phone away from the head. He also warns that children should only you cellular phones in emergencies, because their still-developing organs "are the most likely to be sensitive to any possible effects of exposure."The doctor noted that similar warnings have been issued by the governments of several European countries, and that Toronto's public health agency has called on children to avoid using the phones.Herberman is believed to be the first director of a U.S. cancer center to issue such a warning.Among the studies referenced by the memo is a still-ongoing study of cell phone users in 13 European countries. Preliminary data suggest that long-term users are significantly more likely to develop brain tumors, especially on the side of the head with the phone is most often held. Similar results have been found in other long-term studies."From a public health perspective, it makes sense to limit risks," said Dr. Dan Wartenberg of the University of Medicine and Dentistry of New Jersey.Along with Herberman and roughly 20 other international experts, Wartenberg has signed a letter calling for precautions on cell phone use, and for manufacturers to make phones "with the lowest possible risk" and to "encourage consumers to use their devices in a way that is most compatible with preserving their health."Sources for this story include: www.post-gazette.com.

Study Shows How Meat Spurs Cancer Growth

2008-12-30T10:05:00.000-08:00

Like to eat meat? Consider this unappetizing truth: When you gulp down a nice juicy steak or hamburger, you are contributing to tumor-fueling inflammation in your body.In fact, eating a diet rich in red meat has long been linked to a host of ills including an increased risk of several types of cancer. But what is it about meat consumption that could impact cancer growth? Now scientists at the University of California, San Diego School of Medicine, have found a mechanism that explains how eating red meat, as well as milk, could spur the growth of malignancies. The new study, headed by Ajit Varki, M.D., suggests that inflammation resulting from a molecule introduced through eating these foods could make cancer grow. The research is set for upcoming publication in the Proceedings of the National Academy of Sciences (PNAS).Dr.Varki, UC San Diego School of Medicine distinguished professor of medicine and cellular and molecular medicine and co-director of the UCSD Glycobiology Research and Training Center, and his research team studied a non-human glycan, or sugar molecule, known as N-glycolylneuraminic acid (Neu5Gc). Although this molecule is not produced naturally in the human body, it’s incorporated into human tissues if you eat red meat. The body then develops antibodies against Neu5Gc – and this immune response could potentially trigger a low-grade chronic inflammation, spurring the growth of cancer. In a statement prepared for the media, Dr. Varki explained it has been recognized by scientists for some time that chronic inflammation can stimulate cancer progression."We've shown that tumor tissues contain much more Neu5Gc than is usually found in normal human tissues. We therefore surmised that Neu5Gc must somehow benefit tumors,” Dr. Varki said in the press statement. So the scientists came up with this hypothesis: The fact that Neu5Gc accumulates in human tumors despite circulating anti-Neu5Gc antibodies suggests a low-grade, chronic inflammation has developed, and caused the tumor to grow. To test this idea, the researchers worked with specially bred mice. The animals lacked the Neu5Gc molecule , just as humans do before they eat red meat and the molecule is absorbed into their bodies, and they had tumors.Anti-Neu5Gc antibodies were given to half of the mice . In those animals, the antibodies induced inflammation and their cancers started growing faster. In the control group comprised of mice that were not treated with antibodies, their tumor growth was far less aggressive.Building on previous research that has shown that humans who take non-steroidal anti-inflammatory drugs (commonly known as NSAIDs) have a reduced risk of cancer, the researchers tried giving NSAIDs to the mice with cancerous tumors fueled by anti-Neu5Gc antibodies. The result? The anti-inflammatory treatment blocked the effect of the Neu5Gc antibodies and the tumors became smaller."Taken together, our data indicate that chronic inflammation results from interaction of Neu5Gc accumulated in our bodies from eating red meat with the antibodies that circulate as an immune response to this non-human molecule – and this may contribute to cancer risk," Varki said in the media statement.For anyone interested in reducing inflammation through natural, non-drug methods, here are seven top strategies to incorporate into your lifestyle:1. Stop eating meat and dairy products.2. Concentrate on a Mediterranean flavored style of eating with lots of fruits, vegetables, whole grains , olive oils and nuts. Research has shown these foods lower inflammation levels.3. Don’t smoke and avoid those who do – second hand smoke can contribute to inflammation.4. Know your oils. Avoid all inflammation-causing trans-fats, hydrogenated and partially hydrogenated oils as well as saturated animal fats. Instead, add inflammation-fighting omega-3 oils like flaxseed, canola and walnut oil to your diet.5. Lose weight if you need to. Research has shown that a waist that measures over 40 inches in a man or over 35 inches in a woman is a sign of probable high inflammation.6. Don’t skimp on sleep. Previous studies have concluded less than six hours of sleep can result in inflammation .7. De-stress. Try yoga, meditation, walking and other forms of exercise. Staying continually stressed out means your body is releasing excess, inflammation-promoting stress hormones . Schedule a minimum of 20 minutes a day to let your worries go.

Fruits and Vegetables Regulate the Cell Cycle to Prevent Cancer

2008-12-30T10:03:00.000-08:00

It’s amazing that more than 2000 years ago we realized many universal truths, and we did it without the scientific method. One person who really knew what he was talking about was Hippocrates, who said “Let food be thy medicine and medicine be thy food”.We lost our common sense for awhile and fell in love with a disease establishment that claimed science was on its side. Apparently we are now coming to earth again in a new age where science and sense meet. Scientists are now explaining the finer points of the truth Hippocrates was trying to tell us -- nature has provided us with all the tools we need to stay healthy. An example of this type of research is a study published in the January, 2008 edition of Frontiers in Bioscience that deals with the importance of regulation of the cell cycle in prevention of cancer.What is the cell cycle?The growth and maintenance of plants, animals and humans is the result of an ordered series of events which constitute the cell cycle. During this cycle, chromosomes are duplicated and one copy of each duplicated chromosome is transferred from the mother cell to the daughter cell. Proper regulation of this cycle is essential for the normal development of multi-cellular organisms. If control of this cycle is lost for any reason, cancer or other degenerative diseases may be the result.Successful cell replication depends on two critical processes: the replication of DNA, and mitosis -- the nuclear division of the daughter cell from the mother cell. The master controllers of these processes are protein kinases that regulate the proteins involved in this DNA replication and mitosis.The researchFor this study, scientists reviewed the sequence of events that regulate cell cycle progression with an eye towards the check points and mechanisms that cells employ to insure DNA stability during this cell cycle even in the face of genotoxic stress.They noted that key transitions in the cell cycle are regulated by the activities of the various protein kinase complexes composed of cyclin and cyclin-dependent kinase (CDK) molecules. These cyclins are CDK binding partners which are required for kinase activity and are intimately linked to the cell cycle stage. CDK activity can be controlled by other mechanisms, such as the addition of a phosphate group, resulting in deregulation of the cell cycle. This is the process that leads to cancer.Although diets rich in fruits and vegetables are increasingly being recommended for the prevention of cancer, their active ingredients and mechanisms of action have not been well understood. This research presents evidence that dietary agents identified from fruits and vegetables can act to modulate the effects of deregulated cell cycle checkpoints. It is through this mechanism that cancer may be prevented by dietary choice.Compounds from fruits and vegetables that appeared particularly noteworthy were apigenin (celery, parsley), curcumin (turmeric), epigallocatechin-3-gallate (green tea), resveratrol (red grapes, peanuts and berries), genistein (soybeans), and silymarin (milk thistle).

How to Protect Yourself From Cancer-Causing Acrylamides in the Foods You Love

2008-12-30T10:00:00.000-08:00

Can you eat the foods you love occasionally without compromising your health? A new study shows that adding certain compounds to your diet can protect you from the harmful effects of acrylamides found in many of American’s favorite foods.Acrylamides are cancer causing agents created when foods are grilled, fried, baked or roasted. They are a byproduct of cooking starchy foods at high temperatures. Acrylamides are found in the highest levels in foods that become browned in the cooking process such as french fries, potato chips, and grilled meats and vegetables that have grill marks on them. Toasted bread and cereals, and baked foods such as sweet potatoes and browned meats also contain substantial amounts, as does dried fruit.The danger of acrylamides was first revealed in 2002, when researchers found that women who consumed 40 micrograms or more of acrylamides each day had twice the risk of endometrial and ovarian cancer risk of women who ate substantially smaller amounts. This would be the amount of acrylamides contained in a small portion of potatoe chips. The FDA has been slow to acknowledge the threat of acrylamides. Food manufacturers have not been required to publish data on the levels of acrylamides in their products.Research reveals the way for consumers to protect themselvesAs published in the July 15, 2008 edition of the Journal of Agriculture and Food Chemistry, researchers found that three dietary constituents, tea polyphenols, resveratrol, and diallyl trisulfide, inhibit damage to DNA from acrylamides at levels typically found in human exposure. Results of analysis of the compounds with accelerator mass spectrometry demonstrated that all three significantly inhibited the formation of acrylamide damage to liver DNA, whereas tea polyphenols and diallyl trisulfide reduced DNA damage to protamines and hemoglobin as well.Further biochemical studies showed that acrylamides could significantly inactivate creatine kinase and glutathione S-transferase and deplete glutathione. When the inhibitors were treated with acrylamide, all of them could effectively recover the activities of creatine kinase. In addition, tea polyphenols and diallyl trisulfide could increase glutathione S-transferase at a remarkably high level. Creatine kinase is an enzyme essential in biochemical reactions and energy generation. Glutathione S-transferase is a family of enzymes that play key roles in the detoxification of substances such as carcinogens, drugs, and byproducts of oxidative stress.Acrylamides are formed when carbohydrate containing foods are baked, fried or roasted. They have been shown to cause cancer in animals exposed to high doses, as well as nerve damage. Acrylamides are not added to foods but occur naturally in the cooking process. Because of this, information on them is not required on food labels.Any starchy food cooked at high temperatures will contain acrylamides. Potatoes that are fried may be the worst offenders, with potato chips fried to a golden brown containing the highest levels. Boiled or mashed potatoes will contain acrylamides as will cooked sweet potatoes. It can also be found in toasted or roasted cereal grains and bread products -- again with the highest levels contained in those baked to a golden brown, and corn roasted on a grill, or popped in oil. Pretzels are promoted as healthy snacks, but that golden brown color is your tip that they contain high levels of acrylamides. Coffee creates acrylamides during its roasting.Acrylamides were discovered by Swedish scientists in 2002, and made headlines across America when they were first reported. Since then, there has been little interest by the FDA to keep people abreast of the dangers of eating acrylamide containing foods. The method by which acrylamides form in food remains unknown.What we do know from this study is that by taking steps to protect ourselves from acrylamides, we don’t have to be boorish sticks when we go out with our friends. We can eat foods containing acrylamides without suffering their effects if we also make sure we are fortified with tea polyphenols, resveratrol and diallyl trisulfide.Numerous studies have demonstrated the anti-cancer properties of tea polyphenols, with recent studies adding gastric, esophageal and skin cancers to the list of those inhibited by polyphenols from tea consumed in high amounts. Another study showed ovarian cancer risk reduced by 46 percent in women drinking 2 cups of tea daily. Researchers have found tea polyphenols to lower cholesterol levels, prevent blood clots, and help prevent heart disease. All types of tea contain polyphenols, with green and white tea having the highest levels due to their minimal processing.Resveratrol is turning out to be so good for us that red wine may end up on the superfood list. It is found in the skin of red or purple grapes, and in peanut products that contain the skins, such as Spanish peanuts. Resveratrol has also been shown to help prevent cardiovascular disease and cancer. A glass of tea or red wine during a meal containing foods that have produced acrylamides will offer you protection.Diallyl trisulfide is a compound found in garlic that has been roasted, smashed or otherwise processed. Shown particularly effective in the prevention and treatment of prostate cancer, this compound is also a potent immune system booster.All three of these compounds are extremely effective antioxidants.If you plan to be eating foods that contain acrylamides, you can protect yourself by having supplements of theses compounds on hand. Each offers an array of other health benefits.

Study Shows Link Between Diet and Stress Induced Cancer

2008-12-30T09:55:00.000-08:00

Will the stress in your life cause you to develop cancer? The answer to this question may depend on what you eat according to a study published in the August, 2008 edition of the International Journal of Oncology.Researchers examined the possible growth promoting effects of the stress-associated hormone norepinephrine on immortalized human pancreatic duct epithelial cells. The results suggested that norepinephrine can increase proliferation of these cells. They then evaluated the ability of norepinephrine to induce interleukin-6, and vascular endothelial growth factor, both believed to promote cancer of pancreatic duct epithelial cells. They found that norepinephrine can indeed increase the interleukin-6 and vascular endothelial growth factor in the cells.Based on theses results, the researchers performed further testing to see if dietary agents sulforaphane and resveratrol can inhibit norepinephrine-mediated increases in cell proliferation. Results indicated that sulforaphane but not resveratrol inhibits the norepinephrine-mediated increases in cell proliferation. Sulforaphane also inhibited norepinephrine-mediated increase of the interleukin-6 levels of the cells.We are living through an extremely stressful period of history. Hundreds of studies have documented how stress impacts our immune systems and ability to fight off invading organisms. This study goes a long way toward documenting the link between stress and cancer. The implications for further research are huge.Inhibiting norepinephrine is no small feat. Norepinephrine is a neurotransmitter that is similar to adrenaline. These hormones act together to produce heart rate and blood pressure increases among other biochemical actions to launch us into our natural defense mode, described as fight or flight. Chronic high levels of stress result in chronic high levels of norepinephrine and adrenaline.Sulforaphane is a compound that can be obtained by eating cruciferous vegetables such as Brussels sprouts, broccoli, cabbage, cauliflower, bok choy, kale, collards, kohlrabi, mustard, turnip, radish, rocket, and watercress.The compound’s anticancer activity is thought to be related to the induction of phase-II enzymes such as quinone reductase and glutathione S-transferase, and the enhanced transcription of tumor suppressor proteins.Sulforaphane is particularly abundant in broccoli sprouts. Researchers at Johns Hopkins University School of Medicine have been dedicated in their efforts to provide us with a broccoli sprout that guarantees a consistent level of sulforaphane. According to Johns Hopkins, eating just one ounce of their broccoli sprouts provides as much sulforaphane as more than a pound of cooked broccoli. Their product, called Brocco Sprouts, is available at many traditional supermarkets.If eating healthy amounts of cruciferous vegetables does not appeal to you, try adding broccoli sprouts to a sandwich or salad. Broccoli sprouts don’t have to be eaten daily to provide their full effect. A one ounce serving is good for three days worth of full spectrum antioxidant protection from sulforaphane comparable to the best antioxidant supplements on the market. A box of sprouts contains four of these servings and retails for about 4 dollars.Juicing is another good way to consume cruciferous vegetables, particularly if you have digestive difficulties. You can add cruciferous vegetables to your vegetable juice recipes. One large stalk of broccoli makes only about an inch of power packed juice in a glass, so it doesn’t have a huge impact on the taste of the recipe.Supplements of broccoli sprouts are available at health food stores and online health retailers such as Vitacost or Lucky Vitamin. The best known is called Broccoliv. Vitacost has a less costly house brand.

Smoking Linked to Bladder Cancer

2008-12-30T09:49:00.000-08:00

Smoking strongly increases a person's risk of developing bladder cancer - a risk that the majority of the population seems to be unaware of, according to a new analysis conducted by researchers from the University of Michigan Comprehensive Cancer Center."The general public understands that cigarette smoking can lead to lung cancer, but very few people understand that it also can lead to bladder cancer," study co-author James E. Montie said.The researchers compiled data from all studies in the MEDLINE database that had been conducted on the connection between bladder cancer and smoking between 1975 and 2007. The correlation between smoking behavior and bladder cancer risk, they found, was strong. For example, one study found that a person's risk of developing bladder cancer goes down by 40 percent within the first four years of quitting smoking.Yet the general population remains unaware of this connection, the researchers also found, as are patients who have been diagnosed with bladder cancer. Only 22 percent of bladder cancer patients surveyed knew that smoking increases the risk of developing the disease."A big gap exists between patient knowledge and their actual risk," co-author Seth A. Strope said. "Our study suggests that physicians must do a much better job of communicating the risk to our patients, and directing them toward smoking cessation programs."Bladder cancer is one of the most expensive forms of cancer to treat. In the United States, it is the fourth most common cancer in men in the ninth most common in women, with more than 47,000 new cases diagnosed in men and 16,000 in women each year. The higher prevalence in men is believed to be due to the fact that male sex hormones play a role in the development of the disease.Other than smoking, risk factors include being African-American or Hispanic and having a family history of the cancer. Exposure to secondhand smoke is also a suspected risk factor.

Saw Palmetto Keeps Prostates Healthy and Helps Prevent Baldness

2008-12-30T04:16:00.000-08:00

Saw palmetto may be a man’s best friend. It's the primary herb helping men maintain prostate health that’s very popular throughout Europe for its ability to relieve symptoms associated with benign prostatic hyperplasia (BPH), otherwise known as enlargement of the prostate. In the U.S. where pharmaceuticals are the standard of care for prostate problems, saw palmetto is gaining popularity following several recent studies showing it provides relief from short-term urinary symptoms and other symptoms of BPH, as well as relief from inflammation of the prostate and cell proliferation. It also promotes hair growth in men with thinning hair or baldness. It provides these benefits safely, naturally and with no noted side effects.Saw palmetto, botanically known as Serenoa repens or as sabal palm in Europe, is a magnificent palm tree that grows naturally in Florida, Georgia and Mississippi. The therapeutic compound comes from the berries of the plant. Historical use of the herb can be traced in the Americas to the Mayans who used it as a tonic and to the Seminoles who took it as an expectorant and antiseptic.Saw Palmetto prevents conversion of testosterone to DHTThe herb possesses several mechanisms of action, with the primary action relating to prostate health being its ability to inhibit the 5-alpha reductase enzyme which converts testosterone, the male sex hormone, to a more potent metabolite, dihydrotestosterone (DHT). In addition, it blocks receptor sites on cell membranes required for cells to absorb DHT. An excess of DHT is believed one of the primary causes of prostate problems as well as the cause of male baldness.Recent research documents the health benefits of saw palmettoIn a study reported in the Journal of Urology, men with BPH obtained significant short-term symptom relief with saw palmetto. Ninety-two men between the ages of 49 and 75 with lower urinary tract symptoms were divided into two groups, one treated with two soft gels of saw palmetto, and the other treated with a placebo. Both groups were treated for a twelve week period. Maximum urinary flow was significantly higher in the treatment group compared to the placebo group, and urinary resistance was significantly lower. Yet mean prostate volume was comparable in the two groups.The American Family Physician journal reported a diagnosic and management review of BHP. They found that through its ability to inhibit 5-alpha reductase, saw palmetto as well as rye grass pollen extract, and pygeum relieved symptoms such as urinary hesitancy, weak stream, nocturia, incontinence, and recurrent urinary tract infections.A review of literature published in Archivio Italiano di Andrologia found that saw palmetto, lycopene and selenium, the three most widely used compounds in treatment of the prostate, have a common feature which may be a dual activity on proliferative disorders as well as on inflammatory conditions at the level of the prostate gland.A study reported in Anticancer Research investigated the effect of an extract of saw palmetto on hormone sensitive and insensitive prostate and breast cancer cells, and urinary bladder, colon and lung cancer cells in order to assess its growth inhibitory abilities. They found that saw palmetto extract induced a dose-dependent anti-proliferative effect on all the human malignant cells tested.Saw Palmetto reduces male pattern hair lossMale hair loss can often be attributed to the conversion of testosterone to DHT promoted by the 5-alpha reductase enzyme. DHT causes hair thinning by shrinking the follicles in the scalp, which results over a period of time in the follicles being far too small for hair to grow, resulting in baldness.The link between DHT and hair loss has been well established, with numerous clinical studies and surveys concluding that this hormone can be directly linked as a cause of as many as 95% of all cases of hair loss. The studies have shown that this condition is genetically linked, with excessive production of DHT being passed from generation to generation. It is this condition that is targeted by pharmaceutical products such as propecia (finasteride), and rogaine (minoxidil).While the testosterone to DHT conversion creates hair loss on the head, it also promotes the growth of hair in places where it is not wanted. By preventing this hormonal conversion, saw palmetto is showing in research to be effective in the treatment of male hair loss. It is able to get the hair off men’s backs and back on their heads. Some studies have shown it to be as effective as Propecia and Rogaine. This aspect of saw palmetto was discovered by people using it for prostate issues who started reporting the regrowth of hair on their heads.Shampoos and lotions containing saw palmetto are available at health food stores and on line. Saw Palmetto is available as a supplement. The dosage amount for men is 300 to 500 mg. per day. Saw palmetto has been shown in research to be non-toxic and safe for extended use.Saw Palmetto is not the only herb able to influence prostate healthSeveral other herbs and plant compounds are potentially useful in maintaining prostate health, including pygeum, nettle, beta sitosterol, and carotenoids such as lycopene. Health of the prostate gland is heavily influenced by the overall health of the body. It’s hard to find a sick prostate gland in a body otherwise possessing excellent health. Following the basics for general health will go along way in promoting prostate health.Pygeum is an African plum tree found in tropical Africa. An extract from the bark of pygeum has been used in Europe as a prevention and treatment of prostate disorders including BPH. More recently in the U.S. pygeum has been marketed along side saw palmetto for prostate health and cancer prevention and treatment.An interesting study reported in Endocrine tested the anti-cancer potential of pygeum in vitro and in vivo. In tissue culture, pygeum extract inhibited the growth of cancerous cells, induced appropriate programmed cell death and altered cell kinetics, down regulated ER-alpha and PKC-alpha protein, and demonstrated the ability to bind with estrogen and androgen receptors. Mice fed with pygeum showed a significant reduction in prostate cancer incidence of 35% compared to controls. Researchers concluded pygeum is a useful supplement for men at high risk of developing prostate cancer.

Raw Cruciferous Vegetables Defend Against Bladder Cancer

2008-12-30T04:04:00.000-08:00

Eating raw cruciferous vegetables can reduce the risk of bladder cancer, according to studies conducted by researchers from the Roswell Park Cancer Institute.The cruciferous vegetable family includes broccoli, cabbage, cauliflower, arugula, Brussels sprouts, collard greens, daikon, garden cress, horseradish, kale, kohlrabi, mustard, radish, rape (canola), rapini, rutabaga, tatsoi, turnip, wasabi and watercress.In one study, Roswell Park researchers found that the risk of bladder cancer in rats decreased as the amount of freeze-dried broccoli sprout extract in their diets increased. In another study, people who ate as little as three servings of cruciferous vegetables per month had a 40 percent lower risk of bladder cancer than those who ate less. No benefit was found, however, in those who ate the vegetables cooked.Much of the vegetables' cancer-fighting effect is attributed naturally occurring plant compounds known as isothiocyanates. Isothiocyanates have been linked to decreased risk of both cancerous and noncancerous tumors, and at least one variety has been observed to induce cell death even in chemotherapy-resistant cancer lines.Cooking can destroy 60 to 90 percent of a meal's isothiocyanate content.Isothiocyanates and other components of cruciferous vegetables are believed to help regulate an enzyme response that helps the body protect itself against cancer. In addition to bladder cancer, cruciferous vegetables and their chemical components have been found to protect against cancers of the breast, cervix, colon, endometrium, liver and lung."When they are eaten raw, they induce a kind of enzyme that may detoxify carcinogens," said Roswell Park's James Marshall. A press release from the institute cited the case of Katie Herdlein, who boosted her intake of fruits and vegetables to help her get through chemotherapy.

Aromatase Inhibitors Improve Outcomes in Early Breast Cancer

2008-12-18T03:19:00.000-08:00

According to a combined analysis of previous studies, adjuvant (post-surgery) treatment with an aromatase inhibitor results in fewer recurrences than treatment with tamoxifen (Nolvadex®) among postmenopausal women with early, hormone receptor-positive breast cancer. These results were presented at the 2008 annual San Antonio Breast Cancer Symposium (SABCS).
Each year more than 180,000 U.S. women are diagnosed with breast cancer. Many of these breast cancers will be hormone receptor-positive, meaning that they are stimulated to grow by the circulating female hormones estrogen and/or progesterone.
Treatment of hormone receptor-positive breast cancer often involves hormonal therapies that suppress or block the action of estrogen. These therapies include tamoxifen as well as agents known as aromatase inhibitors. Tamoxifen acts by blocking estrogen receptors, whereas aromatase inhibitors suppress the production of estrogen in postmenopausal women.
Several large trials comparing aromatase inhibitors to tamoxifen have established the efficacy and safety of aromatase inhibitors for the treatment of hormone receptor-positive breast cancers among postmenopausal women. Follow-up of these trials continues.
To further explore the effects of aromatase inhibitors, researchers affiliated with the Aromatase Inhibitors Overview Group conducted a combined analysis of previous studies, including the following six randomized trials:
Arimidex, Tamoxifen, Alone or in Combination (ATAC)
Breast International Group (BIG) 1-98/International Breast Cancer Study Group (IBCSG) 18-98
Austrian Breast and Colorectal Cancer Study Group (ABCSG)
German Austrian Breast Cancer Group (GABG)/Arimidex-Nolvadex (ARNO)
Intergroup Exemestane Study (IES)/BIG 2-97
Italian Tamoxifen Anastrozole (ITA)
Some of these studies compared five years of treatment with an aromatase inhibitor to five years of treatment with tamoxifen, and others evaluated the effect of switching to an aromatase inhibitor after two to three years of tamoxifen.
The aromatase inhibitors that were evaluated were Femara® (letrozole), Arimidex® (anastrozole), and Aromasin® (exemestane).
In the studies that compared five years of tamoxifen to five years of an aromatase inhibitor, the following results were reported:
Over the course of five years, 9.6% of women treated with an aromatase inhibitor experienced a cancer recurrence compared with 12.6% of women treated with tamoxifen.
There was no statistically significant difference in survival between the two groups.
In the studies that evaluated a switch from tamoxifen to an aromatase inhibitor, the following results were reported:
Over the course of six years, 12.6% of women who switched to an aromatase inhibitor experienced a cancer recurrence compared with 16.1% of women who remained on tamoxifen.
Women who switched to an aromatase inhibitor also had modestly improved survival compared with women who remained on tamoxifen.
The researchers concluded that these results provide clear evidence that aromatase inhibitors significantly reduce recurrences in early, hormone receptor-positive, postmenopausal breast cancer. There was also some evidence that switching to an aromatase inhibitor after two to three years of tamoxifen improved survival compared with continued treatment with tamoxifen. The duration of follow-up in these studies is still somewhat short, however; longer follow-up may provide additional information about effects on survival.
Reference: Ingle J, et al. Aromatase inhibitors versus tamoxifen as adjuvant therapy for postmenopausal women with estrogen receptor positive breast cancer: meta-analysis of randomized trials of monotherapy and switching strategies. San Antonio Breast Cancer Symposium. December 10-14, 2008. Abstract 12.

Stem cells may 'ignite' bowel cancer development

2008-12-18T03:18:00.000-08:00

Cancer Research UK scientists have discovered for the first time that stem cells could be the root cause of bowel cancer, according to a study published in Nature* today (Wednesday).
Scientists at Cancer Research UK's Beatson Institute for Cancer Research in Glasgow, Cardiff University and the Hubrecht Institute in the Netherlands – isolated stem cells in the bowels of mice and 'knocked out' a gene called APC from them. These damaged stem cells then rapidly started to multiply out of control and to form tumours.
Bowel cancer** is the third most common cancer in the UK affecting more than 36,500 people each year. This research could pave the way for new treatments to target damaged stem cells and quench their ‘ignition’ of the disease.
A stem cell is one that, when it divides, produces two 'daughter' cells. One remains a stem cell, while the other multiplies into the sorts of cells required by its organ to keep it functioning. Previously scientists could not be sure if the cancer causing faults occurred directly to stem cells, or whether ‘daughter’ cells were the route cause of the tumour. This study provides extremely strong evidence to suggest that most bowel cancers start from stem cells.
Study author Dr Owen Sansom, from Cancer Research UK's Beatson Institute, said: "When we studied the effect of blocking the APC gene in the 'parents' – or stem cells – the results were striking and the cells started to transform within days. It was clear the 'ignition point' for the disease was to be found in the stem cells. Using the same experiment, the daughter cells also developed into tumours, but not nearly as often as the stem cells changed. We are now looking to understand how we can use these results to seek out and destroy stem cells that are lacking the APC gene."
Lead author Professor Hans Clevers, from the Hubrecht Institute said: "We are very excited by these findings but we need to establish whether the stem cells behave the same way in human cancers as they do in mice – and this will form the basis of the next stage of our research. We only looked at the APC gene to understand its onset of bowel cancer – it’s likely that other genes also play a role in the progression of the disease."
Dr Lesley Walker, Cancer Research UK's director of cancer information said: "As in most cancers, the cell that the cancer originates from has remained elusive in bowel cancer. So this work is a big leap forward in our understanding of the origins of the disease.
"Bowel cancer is one of the most common forms of cancer so anything that adds to our understanding of the disease is very important work."

Scientists to study feasibility of lung cancer screening

2008-12-18T03:15:00.000-08:00

The National Institute for Health Research Health Technology Assessment (NIHR HTA) programme has commissioned a study to assess the feasibility of a lung cancer screening programme in the UK.
The NHS currently has established national screening programmes for breast cancer, cervical cancer and bowel cancer.
Experts now want to know whether a programme using computerised tomography (CT) to scan high-risk people - such as ex-smokers - would be beneficial in the UK.
We await the results of this important study with interest. - Professor Tim Eisen, Cancer Research UK
Lead researcher Professor John Field, director of the Roy Castle Lung Cancer Research Programme at the University of Liverpool, revealed that the number of lung cancer deaths has fallen in recent years thanks to a decline in smoking and greater public awareness.
"However, there is a large ex-smoking population who remain at high risk of developing lung cancer," he noted.
"Screening to detect the disease before patients develop any symptoms is a method that urgently requires evaluation as surgical resection at an early stage of the disease remains the only realistic option for a cure."
If the feasibility study suggests a lung cancer screening programme might be effective, a pilot study would then be conducted followed by a large-scale clinical trial.
"Only then would evidence be available to show whether a National Lung Cancer Screening Programme should be considered," said Professor Field.
He added: "We are delighted that the HTA has decided to invest in this first stage, which will help inform whether it is feasible to conduct a full trial."
Professor Tim Eisen, Cancer Research UK clinician and chair of the National Cancer Research Institute's lung cancer clinical studies group, said: "We know that most people - around 80 per cent - who get lung cancer only find out about it once the cancer has gone past the point where it can be cured.
"This trial aims to assess the proportion of people who are diagnosed at a time when it can still be successfully treated. We await the results of this important study with interest."

New research moves us one step closer to personalised breast cancer treatment

2008-12-18T03:11:00.000-08:00

New research moves us one step closer to personalised breast cancer treatment

The research shows that women who have a duplication of chromosome 17 in their tumour will benefit from anthracycline drugs, while others can be spared the side-effects of the treatment. This group of chemotherapy drugs includes epirubicin which has already been shown to improve women's survival by a third.
This research is important as both the chemotherapy drugs and the test are already available, so a change in clinical practice could happen in the very near future.
The results of the British study are being presented at the San Antonio Breast Cancer Symposium today.Professor John Bartlett, a Cancer Research UK funded scientist from the University of Edinburgh, said: "We were looking for markers to help decide when to give women this type of chemotherapy using a test that is already part of patients' treatment.
"From previous trials we know that women who are treated with these drugs do better and are less likely to relapse. But, unless we know the drugs will be of benefit, we don’t want to give them to everyone because of the unpleasant side effects."
The researchers took small sections of tumours from over 2,500 women who had taken part in one of a number of studies, including the UK NEAT (National Epriubicin Adjuvant Trial)*. They tested the tumours to identify which markers could predict whether the chemotherapy treatment would be successful.
The results of the trial provide evidence that the marker – a duplication of Chromosome 17 – could be used to predict which women will benefit from chemotherapy and could go on to be introduced as a routine test in treatment**.
Professor Bartlett said: "This study gives us a key in the door to personalised chemotherapy treatment. Until now we haven't been able to predict which women are likely to benefit from this type of chemotherapy.
"We are now close to being able to use this new marker in the clinic to select appropriate therapies in early breast cancer."
Kate Law, director of clinical trials at Cancer Research UK, said: "These results are really encouraging and have the potential to change the way we treat women with breast cancer.

(free book)World_Without_Cancer

2008-12-11T06:38:00.000-08:00

The_Story_of_Vitamin_B17..G._Edward_Griffin

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Physician's Cancer Chemotherapy Drug Manual 2008

2008-12-11T06:16:00.000-08:00

* Publisher: Jones and Bartlett Publishers

* Number Of Pages: 552

* Publication Date: 2007-12-28

* ISBN-10 / ASIN: 0763755621

Product Description:

Completely revised and updated for 2008, this practical handbook is an up-to-date guide to all aspects of cancer chemotherapy. The book provides a comprehensive, easy to use catalogue of over 100 drugs-both on- and off-label-commonly used in cancer treatment. A section on Common Chemotherapy Regimens provides a quick reference to management of specific cancers, arranged alphabetically.

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Early breast cancer(text book)

2008-12-11T06:10:00.000-08:00

Product Description:

This book discusses the principles and practice of breast cancer management within the context of multidisciplinary team working and places emphasis on pragmatism. The text provides a comprehensive and contemporary account of the subject and should permit the reader to develop a firm understanding of the disease from epidemiology, genetics and screening, to pathology, diagnosis, treatment, and prevention. This in turn will enable healthcare personnel to deliver a high quality and up-to-date service to breast cancer sufferers.

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Encyclopedia of Cancer, 2nd edition

2008-12-11T06:03:00.000-08:00

By Manfred Schwab

* Publisher: Springer

* Number Of Pages: 3235

* Publication Date: 2008-10

* ISBN-10 / ASIN: 3540368477

Product Description

:The Encyclopedia of Cancer provides rapid access to focused information on all topics of cancer research for clinicians, research scientists and advanced students. Given the overwhelming success of the first edition, which appeared in 2001, and fast development in the different fields of cancer research, it has been decided to publish a second fully revised and expanded edition, following the principal concept of the first edition that has proven so successful.Recent developments are seeing a dynamic merging of basic and clinical science, with translational research increasingly becoming a new paradigm in cancer research. The merging of different basic and clinical science disciplines towards the common goal of fighting against cancer has long ago called for the establishment of a comprehensive reference source both as a tool to close the language gap between clinical and basic science investigators and as a platform of information for students and informed laymen alike.While the First Edition featured scholarly contributions from approximately 300 scientists/clinicians in one Volume, the Second Edition includes more than 1.000 contributors in 4 Volumes with an A-Z format of more than 7.000 entries. It provides definitions of common acronyms and short definitions of related terms and processes in the form of keyword entries. In addition, there are detailed essays, which provide comprehensive information on syndromes, genes and molecules, and processes and methods. Each essay is well-structured, with extensive cross-referencing between all entries.A panel of Field Editors, each an eminent international expert for the corresponding field, will ensure the presentation of timely and authoritative Encyclopedia entries. These new traits will meet the expectance that a wide community has towards a cancer reference works.The Encyclopedia of Cancer will be accessible both in print and online, and this information source will be of value to both the clinical and basic scientific community as well as to the public.

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Removal of More Lymph Nodes May Improve Survival in Gastric and Pancreatic Cancers

2008-12-06T06:15:00.000-08:00

Researchers recommend that at least 15 lymph nodes be removed and examined in patients with early gastric or pancreatic cancers. These results were recently published in the Archives of Surgery.
For accurate staging, or determination of extent of spread of gastric and pancreatic cancers, surgeons remove lymph nodes near the cancer. The lymph nodes are examined under a microscope to assess whether the cancer has spread to the lymph nodes, and if so, the extent of spread. Because treatment options are determined by the stage of the disease, an accurate assessment of spread to lymph nodes (nodal metastases) is imperative for optimal therapeutic choices.
Medical institutions that treat a high volume of patients with this disease or institutions affiliated with the National Comprehensive Cancer Network (NCCN) or National Cancer Institute (NCI), which follow strict guidelines, often tend to remove a larger number of lymph nodes during surgery than community centers or centers that treat a lower volume of patients with these diseases. It is currently not clear whether the removal of more nodes is associated with improved outcomes; however, patients treated at NCCN or NCI-designated centers or treated at medical centers that experience a high volume of these patients tend to have improved outcomes.
To further explore the possibility that the removal of more lymph nodes is associated with improved outcomes for patients diagnosed with gastric or pancreatic cancers, researchers evaluated outcomes among patients with gastric and pancreatic cancers who were treated at either high-volume or community medical centers (lower-volume centers). Included was data from the National Cancer Data Base from 2003-2004, which included more than 4,000 patients.
Patients undergoing surgery at National Comprehensive Cancer Network (NCCN) or National Cancer Institute (NCI)-designated institutions had more lymph nodes removed and examined than those treated at a community medical center.
Patients undergoing surgery at medical centers treating high volumes of patients with either gastric or pancreatic cancers also had more lymph nodes removed than those undergoing treatment at medical centers treating low volumes of these patients.
The researchers concluded that NCCN and NCI-designated centers and medical centers that treat a high volume of patients with pancreatic and gastric cancers tend to surgically remove more lymph nodes than community centers or medical centers that treat a low volume of patients with these diseases. The authors state: “Examination of at least 15 lymph nodes is an appropriate quality surveillance measure for gastric and pancreatic cancer because it is a feasible, achievable, and modifiable factor that is associated with improved outcomes.”
Patients diagnosed with gastric or pancreatic cancers may wish to speak with their physician regarding the status of the center at which they are receiving surgery. They may also wish to discuss their individual risks and benefits of greater removal of lymph nodes at the time of surgery.
Reference: Bilimoria K, Talamonti M, Wayne J, et al. Effect of hospital type and volume on lymph node evaluation for gastric and pancreatic cancer. Archives of Surgery. 2008;143:671-678

EndoTAG™-1 Shows Promise in Treatment of Pancreatic Cancer

2008-12-06T06:12:00.000-08:00

According to the results of a Phase II clinical trial, the addition of the investigational drug EndoTAG™-1 to chemotherapy with Gemzar® (gemcitabine) may improve survival among patients with inoperable pancreatic cancer. These results were presented at the 33rd Congress of the European Society for Medical Oncology (ESMO).
Pancreatic cancer has one of the highest mortality rates of all cancers. It accounts for approximately 2% of all newly diagnosed cancers in the United States each year but 5% of all cancer deaths. Pancreatic cancer is often called a “silent killer” because its symptoms are usually not recognizable until it has advanced and spread outside the pancreas. As a result the majority of pancreatic cancers are not diagnosed until they have reached advanced stages and are considered incurable.
Chemotherapy is a common treatment for advanced pancreatic cancer. However, due to the poor long-term survival achieved with chemotherapy alone, researchers continue to evaluate novel ways to improve outcomes for these patients.
EndoTAG™-1 is an investigational drug that is intended to “starve” cancer by destroying blood vessels that supply the tumor. It binds to cells that line new blood vessels and then releases the chemotherapy drug paclitaxel.
To evaluate EndoTAG™-1 in the treatment of pancreatic cancer, researchers conducted a Phase II clinical trial among 200 patients with inoperable, locally advanced or metastatic pancreatic cancer. In addition to treatment with the chemotherapy drug Gemzar® (gemcitabine), patients were assigned to receive one of three doses of EndoTAG™-1 or a placebo.
12-month survival was 17% among patients treated with Gemzar alone. Among patients treated with both Gemzar and EndoTAG™-1, survival was 22% among patients treated with the low dose of EndoTAG™-1, 36% among patients treated with the medium dose of EndoTAG™-1, and 33% among patients treated with the high dose of EndoTAG™-1.
During the latter part of the study, patients who responded to EndoTAG™-1 had the opportunity to continue treatment with EndoTAG™-1 for a longer period of time. Among these patients 12-month survival was 25% among patients treated with the low dose of EndoTAG™-1, 52% among patients treated with medium dose of EndoTAG™-1, and 40% among patients treated with the high dose of EndoTAG™-1.
This study suggests that EndoTAG™-1 may improve survival among patients with inoperable pancreatic cancer. Dr. Mathias Löhr, the principal investigator on the study, noted that “These study data demonstrate a noticeably higher efficacy from EndoTAG™-1 treatment compared to currently available treatments for pancreatic cancer.” These results will need to be confirmed in other studies.
Patients with pancreatic cancer may wish to discuss with their physician the risks and benefits of participating in a clinical trial further evaluating this or other promising therapeutic approaches. Two sources of information about ongoing clinical trials are the National Cancer Institute (www.cancer.gov) and www.eCancerTrials.com.
Reference: MediGene press release. MediGene reports positive 12-month survival data for EndoTAG™-1 from Phase II pancreatic cancer study. Available at: http://www.medigene.de/englisch/pressemitteilungen.php?ID=2599 (Accessed September 17, 2008).

Neoadjuvant Radiation Improves Survival in Pancreatic Cancer

2008-12-06T06:05:00.000-08:00

Preoperative radiation nearly doubles the survival rate for patients with operable pancreatic cancer, according to the results of a study published in the November 15, 2008 issue of the International Journal of Radiation Oncology Biology Physics.[1]
The pancreas is an organ that is surrounded by the stomach, small intestine, bile ducts (tubes that connect the liver to the small intestine), gallbladder, liver, and spleen. The pancreas helps the body to break down food and also produces hormones, such as insulin, to regulate the body’s storage and use of food.
Pancreatic cancer has one of the highest mortality rates of all cancers. It accounts for approximately 2% of all newly diagnosed cancers in the United States each year but 5% of all cancer deaths. Pancreatic cancer is often called a “silent killer” because its symptoms are usually not recognizable until it has advanced and spread outside the pancreas. As a result the majority of pancreatic cancers are not diagnosed until they have reached advanced stages and are considered incurable.
If pancreatic cancer has not spread to surrounding or distant organs, it is usually considered operable. Historically, patients have been treated with surgery followed by chemotherapy and/or radiation to destroy any micrometastases (cancer cells that have spread outside the pancreas). New research indicates, however, that neoadjuvant radiation therapy (radiation delivered prior to surgery) might offer greater benefit to patients because it can potentially shrink the tumor prior to surgery, thereby ensuring a better chance of removal. Furthermore, because pancreatic surgery is so invasive, many patients are in no condition to undergo radiation treatment after surgery, so neoadjuvant treatment allows them to receive radiation that they might not receive otherwise.
Researchers from the Weill Cornell Medical College used data from the Surveillance, Epidemiology, and End Results (SEER) registry database to perform a retrospective analysis on patients who had surgically resected (removed) pancreatic cancer between 1994 and 2003. The researchers compared the overall survival rates among patients who received neoadjuvant radiation, adjuvant radiation, or no radiation. Patients who received neoadjuvant radiation survived 23 months, compared with 12 months for patients who did not receive radiation and 17 months for those who received adjuvant radiation (following surgery).
The researchers concluded that neoadjuvant radiation therapy offers a significant benefit over surgery alone or surgery with adjuvant radiation therapy in treating pancreatic cancer. Research will likely be ongoing to further explore these findings.

Scientists Identify Genes That Lift Lung Cancer Risk

2008-12-06T06:03:00.000-08:00

An international research team has identified two genetic variations that appear to increase a person's risk of developing lung cancer by up to 60 percent, they reported on Sunday.
In April the same researchers identified another gene that raised lung cancer risk and they said their latest finding was relevant for both smokers and non-smokers.
"We are looking at differences in the DNA that makes you more or less likely to develop lung cancer," said Paul Brennan, a cancer epidemiologist at the World Health Organisation's International Agency for Research on Cancer.
"The idea is if you can identify genes then that might indicate why people develop lung cancer."
Lung cancer is the leading cause of cancer death in men and the second leading cause of cancer death among women worldwide, according to the American Cancer Society, with about 975,000 men and 376,000 women forecast to die annually.
Smoking is the leading risk factor but increasingly scientists are looking to genetics to help explain why some long-time smokers never develop the disease and why some non-smokers do.
The study published in the journal Nature Genetics included researchers from 18 countries who analyzed genetic mutations in more than 15,000 people -- 6,000 with lung cancer and 9,000 without the disease.
The researchers discovered a region on the fifth chromosome containing two genes -- TERT and CRR9 -- where they believe variations can boost the likelihood of lung cancer by as much as 60 percent.
"We are looking at versions of genes that everybody has," Brennan said in a telephone interview.
Not much is known about CRR9 but pinpointing the TERT gene is promising because it activates an enzyme called telomerase which is key to aging and cancer, Brennan said.
Cancer is caused by defects in DNA, the basic genetic material. All chromosomes, which carry the DNA, also have little caps on each end called telomeres.
Each time a cell divides, these telomeres become a little more frayed. When they are too worn out, the cell dies.
But when cells become cancerous, they produce telomerase, which can renew the telomeres and lets the cells reproduce out of control, eventually to form a tumor.
So implicating the TERT gene in a specific cancer can help lead to a better understanding of how cancer develops and boost the design of new drugs to stop tumors, Brennan added.
"The principle is there," he said. "If one can identify what goes wrong, it may be possible to identify targeted drugs." (Reporting by Michael Kahn; Editing by Maggie Fox and Matthew Jones)

BRCA1 Influences Lung Cancer Chemotherapy

2008-12-06T05:57:00.000-08:00

NEW YORK DEC 02, 2008 (Reuters Health) - Carriers of certain haplotypes of the BRCA1 gene, which plays a central role in the DNA repair system, do not appear to respond to platinum-based chemotherapy for non-small-cell lung cancer, Korean researchers report in the Journal of Clinical Oncology published online ahead of print.
"Results from this study," senior investigator Dr. Jeong-Seon Ryu told Reuters Health, "show that lung cancer patients with two copies of AACC of BRCA1 do not benefit from platinum doublets -- gemcitabine/platinum, docetaxel/platinum or paclitaxel/platinum -- that are standard regimens worldwide for locally advanced or metastatic non-small-cell lung cancer."
Dr. Ryu of Inha University Hospital, Inchon, and colleagues came to this conclusion after studying the relationship of 4 tagging single-nucleotide BRCA1 polymorphisms and their haplotypes on the outcome of treatment in 300 patients. The five haplotypes studied were AACC, AACA, GCTC, GATC and AATC.
Median survival was 13 months and the researchers did not find any significant associations between any of the tagging polymorphisms and overall survival.
However, patients with two copies of the AACC (wild type) haplotype had significantly shorter survival than those with one or no copy (8.47 versus 14.57 months). This continued to be true after adjustment for factors including weight loss and second-line treatment (hazard ratio, 2.097).
This effect on survival was seen in patient with squamous cell carcinoma but not in those with adenocarcinomas.
"Therefore," concluded Dr. Ryu, "this result suggests that a new strategy is needed for these patients, especially in squamous cell carcinoma."

Family history may have role in brain cancer

2008-12-06T05:53:00.000-08:00

US and Israeli scientists have found evidence that a family history of brain cancer may increase a person's chances of developing the disease.
Researchers at the University of Utah and Tel Aviv University analysed the medical records of nearly 1,500 people from Utah and tracked back for between three and ten generations of family members.
Their findings are published in the journal Neurology.
They found that a family history of brain tumours - including the aggressive glioblastoma - increases a person's likelihood of developing the disease, sometimes as much as fourfold.
Dr Deborah Blumenthal, co-director of Tel Aviv University's Neuro-oncology Service and an affiliate associate professor at the University of Utah Huntsman Cancer Institute, said that the study is unique as it was able to track genealogy records back so far.
She recommended that people with a family history of brain cancer should report this to their family doctor at routine medical checks.
"Until now, brain tumours were not thought to be an inheritable disease," said Dr Blumenthal. "A few earlier studies did find an increased risk in immediate relatives, but in such cases it is hard to distinguish between the effects of a shared environment and heredity."
However, Dr Blumenthal emphasised that the risks of having a hereditary brain tumour are still "very low" as the majority of primary brain tumours are not inheritable.
Less than five per cent of rare primary brain tumours are hereditary and the risk of inheriting genes that may increase the risk of a brain tumour is therefore low.
She explained: "Reporting to your family doctor that brain cancer runs in the family just gives a more comprehensive picture of your medical history. It may provide doctors and family members with useful information."
The researchers now hope to use blood and tissue samples from high-risk families to try to identify genes associated with brain tumours so that, in future, it may be possible to screen people with a family history of the disease and identify those whose genes place them at greater risk

Non-melanoma skin cancer linked with increased risk for other cancers

2008-12-06T05:39:00.000-08:00

Non-melanoma skin cancer linked with increased risk for other cancers

People who have previously had non-melanoma skin cancer appear to face a higher risk of other cancers, US scientists have found.
Researchers at the Medical University of South Carolina analysed data on 769 people with non-melanoma skin cancer - basal cell and squamous cell carcinoma - and a further 18,405 people with no previous history of cancer for 16 years.
They found that the rate of cancer in people with a history of non-melanoma skin cancer was 293.5 cases per 10,000 people per year, while in people with no previous history of cancer it was just 77.8 cases per 10,000 people per year.
This interesting study adds weight to the possibility that non-melanoma skin cancer may somehow increase a person's future risk of developing other types of cancer. - Dr Alison Ross, science information officer, Cancer Research UK
After other risk factors - such as age, sex, body mass index, smoking and education level - had been taken into account, people with a history of non-melanoma skin cancer were found to face a two-fold increase in the risk of subsequent cancers.
Previous research has suggested that non-melanoma skin cancer survivors are at increased risk of developing melanoma in the future, but the researchers found that the disease also increases the risk of other forms of cancer.
The association was strongest in young people between the ages of 25 and 44.
Commenting on the findings, which are published in the Journal of the National Cancer Institute, Dr Anthony Alberg of the Medical University of South Carolina said: "This pattern of associations, with earlier age of [non-melanoma skin cancer] diagnosis being linked more strongly to the risk of developing subsequent malignancies, is consistent with the pattern that one would expect for a marker of inherited predisposition to cancer."
Dr Alison Ross, science information officer at Cancer Research UK, said: "This interesting study adds weight to the possibility that non-melanoma skin cancer may somehow increase a person's future risk of developing other types of cancer.
"The next steps will be for scientists to investigate the biology behind this link, so they can piece together what's really happening in the body and how."

Gene-based Test Available to Detect Prostate Cancer

2008-12-05T11:34:00.000-08:00

A gene-based molecular diagnostic test used to detect prostate cancer has completed the clinical trials process and is ready for commercial use in patients who are at a high risk for the disease. These results were recently released in a press release by Health Discovery Corporation.
Prostate cancer is a common cancer among men in the United States. More than 1 million biopsies for prostate cancer (tissue removed from the prostate for laboratory analysis) are performed in this country each year, with 75% of the biopsies being “negative” (no evidence of prostate cancer). However, one-third of these negative results actually contain cancer that is not accurately identified.
The new test produced by Health Discovery Corporation utilizes gene signatures, a concept used in Oncotype DX® for breast cancer, to identify the presence of prostate cancer. The intent of the test is for use among men who have an initial negative reading on their prostate biopsy.
The latest results leading to the clinical availability of the test revealed that the gene-based test correctly identified 90% of all clinically significant prostate cancers, while correctly identifying 97% of non-prostate cancers; these findings represent an overall accuracy of 93%.
The test will initially be performed at Clarient’s Clinical Laboratory in Aliso Viejo, California, and is available for patients with an increased risk of developing prostate cancer.
Patients who are at an increased risk of developing prostate cancer may wish to speak with their physician regarding their individual risks and benefits of this gene-based molecular test.
Reference: Health Discovery Corporation. New Prostate Cancer Test is Ready for Commercialization Following Successful Completion of Final Clinical Trials [press release].

Initial Radical Prostatectomy Reduces Prostate Cancer Deaths

2008-12-05T11:26:00.000-08:00

Patients with early prostate cancer who are treated with initial surgery appear to have reduced death from prostate cancer compared with those who undergo watchful waiting as initial therapy. These results were recently published in the Journal of the National Cancer Institute.
Early prostate cancer refers to prostate cancer that has not spread from the prostate to distant sites in the body but is limited to the prostate and nearby lymph nodes. Standard therapy for early prostate cancer may include surgery (radical prostatectomy), radiation therapy, watchful waiting (also referred to as conservative management, in which there is no treatment until disease progression), and hormone therapy. Optimal treatment for early prostate cancer is still under debate, though it appears that individualized approaches may provide the best outcomes. Several variables are considered when selecting treatment options for early prostate cancer; these include age, aggressiveness of cancer, extent of spread, other existing medical conditions, and side effects of therapy.
Researchers from Scandinavia recently conducted a clinical trial that compared initial therapy with a radical prostatectomy with watchful waiting among men with early prostate cancer. This trial included 695 men who had been diagnosed between 1989 and 1999 and were followed for a median of nearly 11 years.
13.5% of men who received an initial radical prostatectomy had died of prostate cancer compared with 19.5% of men who underwent initial watchful waiting.
After approximately 10 years, the rate of death caused by prostate cancer stabilized between the two groups of men.
At 12 years 19.3% of men who received an initial radical prostatectomy and 26% of men who underwent initial watchful waiting had distant spread (metastasis) of their cancer.
Among the group of men who underwent an initial radical prostatectomy, those whose cancer extended outside the capsule of the prostate had 14 times the increased risk of death from the disease than those whose cancer had not extended outside the capsule of the prostate.
The researchers concluded that, when compared with watchful waiting as initial therapy for men with early prostate cancer, “Radical prostatectomy reduces prostate cancer mortality and risk of metastases with little or no further increase in benefit 10 or more years after surgery.” However, it is important for patients with early prostate cancer to discuss their individual risks and benefits of all treatment options with their healthcare provider.
Reference: Bill-Axelson A, Holmberg L, Filen F, et al. Radical Prostatectomy Versus Watchful Waiting in Localized Prostate Cancer: the Scandinavian Prostate Cancer Group-4 Randomized Trial. Journal of the National Cancer Institute [early online publication]. August 11, 2008. doi:10.1093/jnci/djn255

Green tea phytochemicals shown to prevent breast cancer, colon cancer, lung cancer and more

2008-12-05T11:24:00.000-08:00

New research shows just how powerful the phytochemicals in green tea are turning out to be: they are now known to prevent breast cancer, pancreatic cancer, colon cancer, lung cancer and other forms of cancer.
In fact, if green tea were a prescription drug, it would be called a "miracle cancer cure" drug, no doubt. (And it would be sold for $200 a pill, if not more.) But it's not a drug, and it's available to you right now for mere pennies. Green tea is simply one of the most powerful medicinal herbs known. It is especially useful for preventing cancer, and the research keeps on coming.
Every person suffering from cancer (or at risk of being diagnosed with cancer) should be taking green tea nutritional supplements. It has zero negative side effects, and yet delivers powerful anti-cancer compounds

Daily calcium supplements can help prevent colon polyps, study suggests

2008-12-05T11:20:00.000-08:00

A study published in the Jan. 17 issue of the Journal of the National Cancer Institute suggests that people can protect themselves from a type of polyp that leads to cancer -- recurrent colorectal adenomas -- for up to five years after discontinuing a daily calcium supplement regiment maintained for four years.
A previous study had shown a link between daily calcium supplementation and reduced colorectal adenoma risk, and the recent follow-up study showed that the supplements continue to offer protection after patients discontinue use.
Data from 587 patients who previously had at least one colonoscopy was analyzed for seven years after the conclusion of the previous study. At the five-year-mark, the former calcium users showed a 31.5 percent rate of adenoma formation, while the group who never used calcium supplements showed 43.2 percent growth, but no apparent effect on either group was noted after that time. The study also showed that the prior use of calcium supplements reduced advanced adenoma risk, but not in a way that was statistically significant.
In an interview with Reuters, study co-author Dr. John A. Baron of Dartmouth Medical School in Lebanon, New Hampshire, said he would like to see future researchers duplicate the results of his study, but noted it was too early to say calcium supplements were a viable way to prevent colorectal cancer. He added that the study turned up evidence that prostate cancer risk might be increased by calcium supplementation.
"I would urge consumers to supplement only with high-grade calcium sources, and avoid products like Tums which actually reduce stomach acid, interfering with the assimilation of minerals like calcium," said Mike Adams, author of "The 7 Laws of Nutrition" and a consumer health advocate. Adams said that calcium carbonate is a poor source of calcium, and that calcium citrate is better. The best sources, he said, include things like calcium malate, and he recommended consumers visit WellnessResources.com for "very high-grade calcium."
"The best way to take calcium is with acidic natural foods such as citrus or strawberries," he said. "A little vinegar, taken with calcium supplements, can also boost absorption and assimilation."

Eating blueberries slashes colon cancer risk by 57 percent, animal study finds

2008-12-05T11:17:00.000-08:00

A compound found in blueberries shows promise of preventing colon cancer, according to a new study. Scientists at Rutgers University and the U.S. Department of Agriculture conducted a joint study on animals, and found that the compound -- called pterostilbene -- lessened pre-cancerous lesions and inhibited genes involved in inflammation. Researchers presented the study at the American Chemical Society's annual meeting in March. "This study underscores the need to include more berries in the diet, especially blueberries," said study leader Bandaru Reddy, Ph.D., a professor in the chemical biology department at Rutgers. Although the blueberry compound won't cure colon cancer, it represents a strategy for preventing the disease naturally, said Reddy, who specializes in studying the relationship between nutrition and colon cancer.The researchers studied 18 rats in which colon cancer had been induced in a manner similar to human colon cancer development. All of the animals were placed on a balanced diet, with half of the animals' diets supplemented with pterostilbene. After eight weeks, the rats fed pterostilbene had 57 percent fewer pre-cancerous colon lesions compared to the control group. The researchers also noted that pterostilbene inhibited certain genes involved in inflammation, considered a colon cancer risk factor. Colon cancer is the second leading cause of cancer death in the U.S. It has been linked to a high intake of saturated fats and calories common in Western diets. Pterostilbene may be able to reverse this process, possibly by lowering lipids, Reddy said. Reddy cited a recent study by co-author Agnes Rimando of the Department of Agriculture. Rimando demonstrated that blueberries, particularly their skins, can lower cholesterol when fed to animals. Some thirty different species of blueberries are native to North America. The berries are rich in anthocyanins, widely recognized for their antioxidant qualities. Blueberries are also a good source of ellagic acid, which blocks metabolic pathways that can lead to cancer

Western diet boosts colon cancer risk by 300 per cent

2008-12-05T11:14:00.000-08:00

The rates of recurrence or death from colon cancer were nearly 3.5 times higher among patients who ate a typical Western diet than among those who followed it least closely, in a study published in the Journal of the American Medical Association.Researchers collected data on 1,009 people who had undergone surgery and chemotherapy for colon cancer in the two years between April 1999 and May 2001. In all cases, the cancer had metastasized to the lymph nodes but had not spread to other organs. The participants filled out standardized surveys about their dietary preferences and habits during chemotherapy and the six months following. They were then tracked for five years.Of the 1,009 patients who began the study, 324 experienced cancer recurrence during those five years, and 223 of those died. Only 28 of the people who did not experienced recurrence died in the same period.The dietary habits of the cancer patients fell into two basic patterns: The "Western" diet was characterized by the consumption of large amounts of red and processed meats, refined grains and sugars; the "prudent" diet was characterized by consumption of large amounts of fruits, vegetables and relatively higher amounts of poultry and fish relative to red meat.The researchers found that cancer recurrence and death were almost 3.5 times more common among people who adhered most closely to the Western diet than among those who ate the lowest amounts of red and processed meats, refined grains and sugars."Doctors who treat colon cancer patients need to have the conversation about diet," said researcher Jeffrey Meyerhardt. "From my own experience I know that patients ask about this a lot. They want to know what they should be eating and whether they should be exercising."The researchers warned that the study only demonstrates a correlation, and not causality between diet and colon cancer. According to Michael Thun, a spokesperson for the American Cancer Society, however, there are already many other health reasons for eating higher amounts of fruits and vegetables and avoiding the foods associated with the "Western" diet.But consumer health advocate Mike Adams has no doubt about the causes of colorectal cancer. "There's no question that eating dead, processed and chemically-treated foods promotes the development of colon cancer," he said. "Preventing colon cancer is as simple as adopting a diet primarily based on raw plants and living foods. Colon cancer simply disappears, and cancer risk throughout the body plummets on a raw foods diet

Fish Oil Protects Against Colon Cancer

2008-12-05T11:13:00.000-08:00

Fish Oil Protects Against Colon Cancer

Higher consumption of fish oil may lead to a significant reduction in the risk of colorectal cancer, according to a meta-analysis conducted by researchers from Wageningen University in the Netherlands and published in the American Journal of Epidemiology.In a review of 14 prior studies examining the connection between fish consumption and rates of colorectal cancer, the researchers determined that those with the highest consumption of fish oil had a 12 percent lower risk of contracting colorectal cancer than those with the lowest consumption. Every extra 100 grams (10 ounces, or three-quarters of a serving) of fish consumed each week reduced the cancer risk by 3 percent.Women appeared to derive a greater benefit from fish oil than men did, but the researchers said that the studies did not allow them to draw any firm conclusions about a sex difference.According to the World Health Organization, approximately 655,000 people die from colorectal cancer each year.Fish oil is high in omega-3 fatty acids, which are becoming more popular as research suggests that such fats provide a number of health benefits, such as reducing cancer risk, protecting against cardiovascular disease and improving cognitive function. The study authors noted that a recent study published in the journal Carcinogenesis found that supplementation with omega-3s led to a reduction in colorectal inflammation that could be associated with up to a 15 percent reduction in tumor formation.Omega-3 fatty acids primarily occur in fish, which acquire them from algae. Other dietary sources include flaxseeds and certain other oilseeds, and a number of companies have begun synthesizing omega-3s from other sources in order to supplement foods with them.The European market in omega-3s was estimated at approximately €160 million ($230 million) in 2004. It is expected to grow by approximately 8 percent yearly until at least 2010.

Family History of Breast Cancer

2008-12-05T09:48:00.000-08:00

Increases Risk Regardless of BRCA Status

Women with a significant family history of breast cancer but no BRCA mutation are four times more likely to develop breast cancer than women in the general population. These results were presented at the American Association for Cancer Research’s Seventh Annual International Conference in Washington, D.C. on November 17, 2008.[1]
Breast cancer is the second leading cause of cancer death in women in the United States, with approximately 180,000 cases diagnosed each year. Progress in the areas of screening and treatment has allowed for earlier detection and higher cure rates. Researchers continue to study the incidence rates and patterns of this disease with the hopes of further improving screening, prevention, and treatment.
Inherited mutations in two genes—BRCA1 and BRCA2—have been found to greatly increase the lifetime risk of breast and ovarian cancer in women. Mutations in these genes can be passed down through either the mother’s or the father’s side of the family. Women with BRCA mutations have an 85% lifetime risk of developing breast cancer and typically undergo more vigilant screening, chemoprevention with tamoxifen (Nolvadex®), and sometimes even prophylactic surgery. However, many women with a family history of this disease undergo genetic testing only to find that they do not have BRCA mutations. While this may be comforting in one sense, it does pose an interesting conundrum for screening and prevention in this group because the increased level of risk is unclear.
Researchers in Canada recently evaluated families with a significant history of breast cancer, which they defined as two or more breast cancers among close relatives under the age of 50 or three cases of breast cancer among close relatives at any age. They followed 1,492 women from 365 families for five years. None of the women included in the analysis had BRCA mutations. They then compared the rates of breast cancer with rates found in local breast cancer registries. The results indicated that women with a significant family history of breast cancer had a fourfold increase in breast cancer incidence. The elevation in risk was even higher among women under 40; who had a 15-fold increased risk compared with women under 40 in the general population.
Based on the results of this study, the researchers concluded that women with a significant family history of breast cancer have a 30 to 40% lifetime risk of developing breast cancer. There was no elevated risk for ovarian, colon, or any other form of cancer. These results provide new insight for screening women with a significant family history of breast cancer, but no BRCA mutation. The researchers observed that women in this population might benefit from intensified screening as well as chemoprevention.
Reference:
[1] Metcalfe K, Finch A, Poll A, et al. Breast cancer risks in women with a family history of breast or ovarian cancer who have tested negative for a BRCA1 or BRCA2 mutation. Proceedings from American Association for Cancer Research Annual Meeting. Abstract #B7.

Xeloda® and Eloxatin® Evaluated in Esophageal and Gastric Cancers

2008-12-05T09:30:00.000-08:00

Xeloda® and Eloxatin® Evaluated in Esophageal and Gastric Cancers

According to the results of a Phase III clinical trial published in the New England Journal of Medicine, it may be possible to replace 5-FU (5-fluorouracil) with Xeloda® (capecitabine) and to replace cisplatin (Platinol®) with Eloxatin® (oxaliplatin) in the treatment of advanced esophageal and gastric cancers.
For patients with advanced cancer of the esophagus, stomach, or esophagogastric junction (area where the esophagus joins the stomach), chemotherapy has been shown to improve survival. Chemotherapy drugs that are commonly used for these cancers include cisplatin and 5-FU.
Xeloda is an oral chemotherapy drug that offers a more convenient approach to treatment than 5-FU. Xeloda is currently approved for certain patients with breast and colorectal cancers. Eloxatin is also approved for colorectal cancer, and appears to offer advantages over cisplatin in this setting.
To explore the role of Xeloda and Eloxatin in advanced esophageal and gastric cancers, researchers conducted a Phase III clinical trial. The study enrolled 1,002 patients with locally advanced (inoperable) or metastatic cancer of the esophagus, esophagogastric junction, or stomach.
Patients were assigned to one of four treatment groups:
ECF (Ellence® (epirubicin), cisplatin, and 5-FU)
ECX (Ellence, cisplatin, and Xeloda)
EOF (Ellence, Eloxatin, and 5-FU)
EOX (Ellence, Eloxatin, and Xeloda)
One-year survival was 37.7% for ECF, 40.8% for ECX, 40.4% for EOF, and 46.8% for EOX.
Progression-free survival and response rates did not differ significantly across treatment groups. Overall survival was longer with EOX than with ECF.
Toxic effects of Xeloda and 5-FU were similar. Compared to cisplatin, Eloxatin was less likely to cause grade 3 or 4 neutropenia, hair loss, kidney problems, and blood clots, but slightly more likely to cause grade 3 or 4 diarrhea and neuropathy.
The researchers conclude that Xeloda is as effective as 5-FU and that Eloxatin is as effective as cisplatin. Xeloda and Eloxatin may be able to replace 5-FU and cisplatin in the treatment of advanced esophageal and gastric cancers.
Reference: Cunningham D, Starling N, Rao S et al. Capecitabine and oxaliplatin for advanced esophagogastric cancer. New England Journal of Medicine.

Esophageal Cancer Can Tolerate Chemoradiotherapy

2008-12-05T09:26:00.000-08:00

Esophageal Cancer Can Tolerate Chemoradiotherapy

Chemoradiotherapy (CRT) is an effective treatment and does not present major toxicity for elderly patients with esophageal cancer, according to the results of a study released in an early online publication of the November issue of the British Journal of Cancer.[1]
The esophagus is a tube that carries food from the mouth to the stomach. Esophageal cancer is relatively uncommon, but is one of the most aggressive and deadly forms of cancer. It is the eighth most common cancer, but the sixth cause of cancer death worldwide. Standard treatment for esophageal cancer may include chemotherapy, radiation therapy, and/or surgery.
Historically, treatment of elderly patients with esophageal cancer has been challenging because it is believed that the elderly cannot tolerate the side effects associated with treatment. However, there is very little data regarding the outcomes and side effects associated with CRT in elderly patients with locally advanced esophageal cancer.
Researchers in the UK conducted a study in 109 patients over the age of 70 with locally advanced esophageal cancer. The patients received CRT, consisting of radiation plus cisplatin-based chemotherapy. In this study, 38.5% of patients received the planned treatment, while 53.2% required a dose adjustment. Severe side effects (grade 3) occurred in 23.8% of patients, with 16.5% of patients being hospitalized.
Six to eight weeks after completing CRT, patients underwent endoscopy (examination of the esophagus through a long, lighted tube) and computed tomography scan (a series of detailed pictures of areas inside the body taken from different angles). The results indicated that 57.8% of patients experienced a complete response (total disappearance of cancer in response to treatment) and the two-year survival was 35.5%
The researchers concluded that CRT was an effective treatment for elderly patients, with no major side effects. In addition, they noted that their results showed that CRT in elderly patients produced similar response rates and overall survival as typically reported in younger patients treated with the same regimen

Guidelines Do Not Recommend Endoscopy for GERD

2008-12-05T09:22:00.000-08:00

Guidelines Do Not Recommend Endoscopy for GERD

The American Gastroenterological Association (AGA) has released a medical position statement that recommends against using endoscopy for the screening of patients with gastroesophageal reflux disease (GERD). These results were recently published in the journal Gastroenterology.
GERD, also referred to as heartburn, is a condition in which the acidic contents of the stomach back up into the esophagus (the tube that connects the throat to the stomach). GERD may be responsible for the irritation of tissues of the esophagus, a condition referred to as Barrett’s esophagus. Ultimately, chronic GERD and Barrett's esophagus may be associated with an increased risk of esophageal cancer.
The AGA is a medical association comprised of physicians that specialize in gastroenterological disorders, which include conditions of the esophagus, such as GERD and esophageal cancer. Researchers have been evaluating ways in which to screen for esophageal cancer so that the disease may be caught and treated early, in its most curable stages.
Members of the AGA recently evaluated data involving patients with GERD and screening for esophageal cancer, including the use of endoscopy. Endoscopy is a procedure in which a lighted tube is advanced through the mouth, esophagus and stomach. The data evaluated was obtained from literature searches regarding screening practices and outcomes among patients with GERD.
Overall, no survival was demonstrated among patients undergoing screening endoscopy.
The majority of patients diagnosed with esophageal cancer had not received a prior diagnosis of GERD. As a result, the AGA concluded that screening endoscopy is not a necessary precaution for individuals with GERD. Guidelines for the management of GERD consisted mainly of pharmaceutical drugs, surgery and/or lifestyle modification.
Patients with GERD should speak with their physician regarding their individual risks and benefits of screening and treatment for their condition, as guideline recommendations are not tailored to the individual.
Reference: Hiltz S, et al American Gastroenterological Association Medical Position Statement on the Management of Gastroesophageal Reflux Disease. Gastroenterology

Confirms Increased Incidence of Adenocarcinoma of the Esophagus in White Americans

2008-12-05T09:17:00.000-08:00

Confirms Increased Incidence of Adenocarcinoma of the Esophagus in White Americans

Researchers from the National Institutes of Health have reported that between 1975 and 2004, the incidence of adenocarcinoma of the esophagus increased by 463% in White males and 335% in White females. The details of this study appeared in an early online publication in the Journal of the National Cancer Institute on August 11, 2008.
The esophagus is the tube that connects the back of the mouth to the stomach. Esophageal cancer is relatively common and is very deadly. It 1998 there were approximately 12,300 new cases of esophageal cancer diagnosed in the United States and nearly 12,000 esophageal cancer deaths, making esophageal cancer one of the most deadly of all cancers. Most cancers of the upper two-thirds of the esophagus arise from a type of cell called squamous cells. Cancers of the lower esophagus most often arise from cells called columnar epithelium and are referred to as adenocarcinomas of the esophagus.
In the recent past, squamous cell cancers made up more than 80% of all esophageal cancers. Over the past two decades, there has been a dramatic increase in the incidence of adenocarcinomas, which now account for one-third to one-half of all esophageal cancers. Thus, the recent increase in the overall incidence of esophageal cancer is almost entirely due to the increase in adenocarcinomas.
Environmental factors such as smoking, drinking, and obesity have long been known to be associated with an increased incidence of gastric and esophageal cancers. It is also well recognized that gastroesophageal reflux plays a role in causing esophageal cancer.
The current study is the best documentation of the increased incidence of adenocarcinomas of the esophagus. Using data from the Surveillance, Epidemiology, and End Results (SEER) program, these authors compared the incidence of adenocarcinoma of the esophagus in the 1975-1979 period with the most recent data from 2000-2004.
Between 1975 and 2004 the incidence increased 463% among White males and 335% among White females.
The incidence rose in all age and stage groups and was not due to increased surveillance.
The researchers concluded that the incidence of esophageal cancer has risen significantly over the past 30 years, specifically adenocarcinoma of the esophagus. Although the exact causes of the increased incidence are unclear, a significant factor may be the increasing obesity of the U.S. population

Significantly Increase Risk of Developing Esophageal Cancer

2008-12-05T09:07:00.000-08:00

According to an article recently published in the journal Gut, individuals who are obese and have frequent symptoms of acid reflux have a significantly increased risk of developing esophageal cancer compared with the general population.
The esophagus is the tube through which food and liquid travel from the back of the throat to the stomach. There is a muscular ring at the bottom of the esophagus (the point where the esophagus and stomach meet) that allows material to pass into the stomach. This muscular ring also stops stomach acid from coming back into the esophagus. This muscle, however, does not entirely close in some individuals, resulting in acid coming back into the esophagus; this condition is referred to as acid reflux or gastro-esophageal reflux. It is thought that acid reflux may increase the risk of developing esophageal cancer as stomach acid damages the lining of the esophagus.
Researchers from Australia recently explored the relationship between obesity, acid reflux, and the risk of esophageal cancer. This study included approximately 700 individuals with esophageal cancer who were compared with 1,580 individuals who did not have esophageal cancer.
Individuals who were obese and had frequent symptoms of acid reflux had more than a 16-fold increase in the risk of developing esophageal cancer compared with individuals who were either obese without symptoms of acid reflux or those with symptoms of acid reflux who were not obese.
Obesity itself was associated with a significantly increased risk of developing esophageal cancer in all patients, but males and patients under 50 years of age had the greatest risks of esophageal cancer associated with obesity.
Acid reflux itself was also significantly associated with an increased risk of developing esophageal cancer.
The researchers concluded: “From a clinical perspective, these data suggest that patients with obesity and frequent symptoms of gastro-oesophageal reflux are at especially increased risk of [esophageal cancer].”
Patients who are obese and have frequent symptoms of acid reflux may wish to speak with their physician regarding screening for esophageal cancer.
Reference: Whiteman D, Sadeghi S, Pandeya N. Combined effects of obesity, acid reflux and smoking on the risk of adenocarcinomas of the oesophagus. Gut. 2008;57:173-180.

Study suggests some breast cancers may naturally regress

2008-12-05T06:48:00.000-08:00

A Norwegian study has raised the possibility that some breast cancers detected by routine screening may have regressed of their own accord if they had not been discovered and treated.
Research published in the Archives of Internal Medicine looked at rates of breast cancer among 119,472 women between the ages of 50 and 64, all of whom were screened three times between 1996 and 2001.
When compared with breast cancer rates in 1992 - when routine breast screening was not available - researchers from the Norwegian Institute of Public Health found that rates of the disease increased significantly following the introduction of routine mammography.
This work highlights the importance of scientific research for the development of effective breast screening programmes. - Dr Kat Arney, science information officer, Cancer Research UK
The study authors noted that, if all of these newly detected cancers had developed and been diagnosed over time, there would soon have been a fall in incidence among older women.
However, breast cancer rates among regularly screened women remained higher, suggesting that a small minority of cancers would have spontaneously regressed without treatment.
For every 100,000 screened women there were 1,909 who developed breast cancer during the six-year period, compared with just 1,564 for every 100,000 women in the control group.
The study authors noted that the 'cumulative' incidence of breast cancer remained 22 per cent higher in the screened group, with screened women more likely to have breast cancer at every age.
"Because the cumulative incidence among controls never reached that of the screened group, it appears that some breast cancers detected by repeated mammographic screening would not persist to be detectable by a single mammogram at the end of six years," the researchers wrote.
"This raises the possibility that the natural course of some screen-detected invasive breast cancers is to spontaneously regress."
The scientists conceded that many experts are sceptical about the idea of spontaneous regression, but insisted that the idea merits "careful" consideration, particularly as 32 cases of spontaneous regression of invasive breast cancer were reported in a recent literature review.
"This is a relatively small number given such a common disease. However, as some observers have pointed out, the fact that documented observations are rare does not mean that regression rarely occurs."
Dr Kat Arney, science information officer at Cancer Research UK, said "This work tells us that there is much we still don't understand about the development and progression of breast cancer.
"It also highlights the importance of scientific research for the development of effective breast screening programmes."

England on course to reduce cancer death rates by one fifth

2008-12-05T06:45:00.000-08:00

The Department of Health has published its first annual report on the Cancer Reform Strategy in which it reveals progress on several key priorities.
The strategy - Maintaining momentum, building for the future - was published in December 2007 and outlined a five-year plan for England's cancer services.
Professor Mike Richards, the national cancer director, revealed that there has been a considerable amount of progress during the first year.
It is vital that we carry on the progress we have made in the last year - Professor Mike Richards, National Cancer Director
Long-term treatment for cancer survivors is being improved, with the National Cancer Survivorship Initiative aiming to ensure that survivors receive integrated, high quality services.
The National Awareness and Early Detection Initiative was successfully launched, which should lead to more cancers being detected earlier.
Other achievements include the introduction of the HPV vaccine, which is designed to protect against the two strains of HPV responsible for more than 70 per cent of cervical cancer cases, and further rollout of the bowel cancer screening programme.
Professor Richards said that cancer treatment has improved "vastly" in recent years and that England is on course to reduce cancer death rates by at least 20 per cent by 2010.
"The proposals that I set out last month in 'Improving access to medicines for NHS patients' will also help to ensure that a greater range of more expensive drugs are made available to more cancer patients on the NHS, reducing their need to seek private drugs," Professor Richards said.
"Together with new proposals from NICE (the National Institute for Health and Clinical Excellence), this will enable patients to have faster access to more lifesaving cancer drugs.
"It is vital that we carry on the progress we have made in the last year and I have identified with the Cancer Reform Strategy board our key priorities for the coming year, including tackling delays in diagnosing cancer and improving the quality and safety of chemotherapy services."
Harpal Kumar, Cancer Research UK's chief executive, said that while it is good to see so much improvement in cancer treatment, there is still a "great challenge" ahead.
"We know that cancers are often being picked up too late and we could make an enormous difference if we could speed the process up," he noted.
"We hope that the range of measures we're launching with the national cancer director through the National Awareness and Early Diagnosis Initiative will go a long way towards redressing the balance

Deprivation doubles cervical cancer risk

2008-12-05T06:39:00.000-08:00

National Cancer Intelligence Network Press Release
Women living in the most deprived areas of England are nearly twice as likely to be diagnosed with cervical cancer than their affluent counterparts – according to a report presented by national cancer director Professor Mike Richards at the Britain Against Cancer conference today (Tuesday).
The report, published by the National Cancer Intelligence Network (NCIN), reveals a 'deprivation gap' that researchers believe is mainly fuelled by a lower uptake of cervical screening in deprived areas.
All cases of cancer diagnosed between 1995 and 2004 were included in this nation-wide analysis of the effect of deprivation on cancer incidence, including more than 25,000 cases of cervical cancer.
In the most deprived areas* of England, there were 12 women per 100,000 diagnosed with cervical cancer between 2000 and 2004. In the most affluent areas, only 6 per 100,000 women were diagnosed with the disease during the same time period.
Professor David Forman, NCIN information lead who is based at the University of Leeds, said: "These striking figures show there is still much more that needs to be done to tackle cancer in low-income communities.
"Cervical cancer is a largely preventable disease – the national screening programme will pick up most cases before they even develop into cancer. Our figures suggest that women living in poorer areas are less likely to attend cervical screening than women who are better-off, so they are more likely to develop the disease.
"Higher rates of smoking in most deprived areas and the earlier onset of sexual activity also contribute to the higher rates of cervical cancer."
Currently, women in England aged 25 to 64 are invited for cervical screening every three to five years. In 2006, around 20 per cent of women in England invited for cervical screening did not attend, and previous research** has shown that women in deprived areas are around 40 per cent less likely to attend. Screening can pick up on important changes to cells before cervical cancer develops.
Sara Hiom, director of health information at Cancer Research UK, said: "It's extremely worrying that your income and where you live can have such a significant effect on your risk of cancer. It's clear that much more needs to be done to encourage women from low-income communities to attend cervical screening."
Women living in deprived areas were 129 per cent more likely to be diagnosed with cervical cancer between 1995 and 1999. This figure was 106 per cent between 2000 and 2004. Although this drop is not statistically significant, doctors hope this downwards turn will continue.
Professor Mike Richards, who will present the report on behalf of the NCIN, said: "Reducing inequalities in cancer incidence and uptake of cancer services is a key aim set out in the Cancer Reform Strategy. Collecting and understanding data like this is a crucial first step in achieving this goal. The NHS Cancer Screening Programme is working with the Improvement Foundation, to improve the uptake of cervical screening in poor areas through targeted pilot programmes. The lessons learnt from this work due in 2009, will be shared with Strategic Health Authorities and local screening programmes to develop best practice."
Professor Julietta Patnick CBE, director of NHS Cancer Screening Programmes, said: "This is a helpful report shedding light on the relationship between cancer and deprivation. Over recent years we have seen a downward trend in women taking up their screening invitation, especially younger women and those in deprived inner city areas, and the reasons for this are difficult to determine. Cervical screening saves around 4,500 lives a year, and it is important for women to consider this when deciding whether or not to accept their invitation."
Sara Hiom added: "Most cases of cervical cancer are caused by HPV – a sexually transmitted virus – and smoking increases the chances of the virus causing cancer. Greater awareness of the link with smoking and, most importantly, of cervical screening are all key to reducing the risk of cervical cancer in deprived areas. Cancer Research UK is investing in research to understand how to improve public health and cervical screening coverage in low-income groups."
ENDS
For media enquiries please contact the NCIN press office on 020 7061 8300 or, out-of-hours, the duty press officer on 07050 264 059.
Notes to editors:
* The report separated England into five groups, graded from the least deprived to the most deprived. Each cancer patient was put into a group based on their postcode of residence, using a standard national measure of deprivation.
** Time dependent response to invitation for cervical screening. Richardson et al. NHS Cervical Screening Publications, Publication No 29. March 2007
In September 2008, the rollout of the Human Papillomavirus (HPV) vaccination programme – which protects against two strains of HPV that cause over 70 per cent of cases of cervical cancer – began for girls aged 12-13. For more information, visit CancerHelp UK.
In the UK, around 2,800 women are diagnosed with cervical cancer each year, and around 1,000 women die from the disease.
For more information on cervical screening, visit CancerHelp UK.
The report looked at the association of all of the common cancers with deprivation. Overall, people living in deprived areas were 19 per cent more likely to be diagnosed with any type of cancer between 1995 and 1999. This figure was 15 per cent between 2000 and 2004. The difference between figures was not statistically significant. Apart from cervical cancer, several others showed a similarly strong association with deprivation, including head and neck, lung, stomach and liver cancer.

NICE expected to lift ban on kidney cancer drugs

2008-12-05T06:32:00.000-08:00

The National Institute for Health and Clinical Excellence (NICE) is believed to be considering reversing its decision not to recommend four kidney cancer drugs for use on the NHS.
Although NICE has not commented on whether their final guidance will be different to that published in August, reports in several newspapers from unnamed sources suggest that it may recommend at least two of the medicines which were previously ruled cost-ineffective, early next year.
The health watchdog's preliminary guidance suggested that, as the advanced kidney cancer drugs Sutent, Nexavar, Avastin and Torisel were massively over their cost-effectiveness threshold, these should not be provided by the NHS.
However, the public uproar and media debate that followed the decision, and the subsequent publication of a review by Professor Mike Richards, the government 'cancer tsar', of how drugs are funded, is thought to have helped persuade the institute to reconsider - a move that experts estimate could extend the lives of up to 3,600 patients.
NICE has said that it is looking at the drugs again in light of new evidence about their effectiveness. The institute plans to hold a meeting in January with a view to publishing new guidance on all four treatments within four weeks of the meeting, with final guidance published in March 2009.
According to reports in the Daily Mail, the new evidence being considered is a US study which found that Sutent was more effective than first thought.
In addition, the Department of Health is revealed to have been in discussion with Pfizer and Roche, which manufacture Sutent and Avastin, about the cost of the drugs.
Hilary Jackson, Cancer Research UK policy manager, said: "We were very disappointed with NICE's initial recommendation that none of these drugs would be available for patients on the NHS. We hope that the extra time taken by NICE to review new data provided by the pharmaceutical company, and the negotiations being led by the Department of Health to find a more appropriate price for these drugs, will mean that they are able to change this decision.
"We are also pleased that NICE has responded to our concerns and is drafting additional advice for its appraisal committees on how they are reviewing drugs for patients with rarer cancers. This should mean that more of these drugs will be available to patients on the NHS in future

Melanoma appears to defy cancer stem cell theory

2008-12-05T06:30:00.000-08:00

US scientists have found evidence suggesting that the 'cancer stem cell' theory may not apply to melanoma - the most deadly form of skin cancer.
The theory that cancers develop from 'rogue' stem cells was put forward in 1997, when evidence for such 'cancer stem cells' was published in Nature Medicine. Scientists found that only a tiny proportion of cells taken from a given tumour had the ability to grow into new tumours when transplanted into laboratory animals.
Since then, stem-like cells have been found in many types of cancer, including breast, bowel and prostate cancer.
This study shows how important it is that we continue to fund research into how cancers develop at a fundamental level. - Ed Yong, science information manager, Cancer Research UK
Further work on melanoma previously estimated that only about one in one million melanoma cells were able to grow into new tumours.
However, a new study by researchers at the University of Michigan, which appears as the cover article in Nature, has found that at least one quarter of melanoma cells have the ability to form new tumours.
When scientists updated and improved the laboratory tests used to detect cancer stem cells and applied them to human melanoma cells transplanted into mice, they found the cells to be quite common.
According to the researchers, the findings suggest that the stem cell model needs to be reassessed as it appears not to hold true in melanoma.
Ed Yong, Cancer Research UK's science information manager, said: "The idea that most types of tumour grow from a tiny population of 'cancer stem cells' is one of the most interesting ideas in current cancer research. But this study suggests that it may not be true for every type of cancer - in melanoma, a much larger proportion of cancer cells are able to give rise to a new tumour.
"This study shows how important it is that we continue to fund research into how cancers develop at a fundamental level."
Sean Morrison, director of the University Of Michigan's Centre for Stem Cell Biology, said that the test usually used to detect cancer stem cells "misses" most of them.
He commented: "I think the cancer stem cell model will, in the end, hold up for some cancers.
"But other cancers, like melanoma, probably won't follow a cancer stem cell model at all. The field will have to be reassessed after more time is spent to optimise the methods used to detect cancer stem cells."
Study co-author Dr Timothy Johnson, director of the university's Multidisciplinary Melanoma Programme, noted that the cancer stem cell model has been regarded by some people as an "exciting new source for the development of life-saving cures for advanced melanoma".
"Unfortunately, our results show that melanoma does not strictly follow this model," he revealed.
"So we'll need to redirect our scientific efforts and remain focussed on the fundamental biological processes underlying the growth of melanomas in humans. And as we pursue new treatments for advanced melanoma, we'll have to consider that a high proportion of cancer cells may need to be killed

UK scientists identify gene that protects against lung cancer

2008-12-05T06:23:00.000-08:00

Scientists at the University of Nottingham have identified a gene that helps to protect the body against lung cancer.
The researchers analysed tumour samples from patients with lung cancer and compared them with healthy lung tissue.
They found that a tumour suppressor gene called LIMD1 was missing in the majority of lung cancer samples, suggesting that this gene plays a role in protecting the body against the disease.
This study fills in another piece of the lung cancer puzzle. - Ed Yong, science information manager, Cancer Research UK
Meanwhile, a collaborating team in the US, led by Dr Greg Longmore, carried out tests on mice which lacked the LIMD1 gene and confirmed that loss of the gene was associated with the development of lung cancer.
Dr Tyson Sharp, lead researcher at the University of Nottingham, revealed that LIMD1 is located on a region of chromosome 3 called 3p21.
"Chromosome 3p21 is often deleted very early on in the development of lung cancer due to the toxic chemicals in cigarettes, which implies that inactivation of LIMD1 could be a particularly important event in early stages of lung cancer development," he said.
The findings are published in the Proceedings of the National Academy of Sciences and could pave the way for new treatments and screening techniques to improve the diagnosis of lung cancer.
Dr Sharp added: "We are now going to extend these finding by developing LIMD1 as a novel prognostic tool for detection of early stage lung cancer."
Ed Yong, Cancer Research UK's science information manager, commented: "This study fills in another piece of the lung cancer puzzle.
"Now we know that LIMD1 is one of an elite group of genes that defend our cells against changes that could lead to cancer.
"Without its protection, cells become more vulnerable to cancer-causing chemicals, such as those found in cigarette smoke."

Children with cancer 'failed' by system

2008-12-05T06:21:00.000-08:00

Children and young people with cancer are spending longer than necessary in hospital because there are not enough children's community nurses and social workers, the charity CLIC Sargent has said.
The charity, which cares for young children with cancer, surveyed children with cancer and their families to mark the start of Childhood Cancer Awareness Month.
Researchers found that nearly half of families felt they did not get the support they needed at home.
Going home in-between treatments and when treatment has finished can be an anxious time for children with cancer. - Helen Thompson, senior information nurse, Cancer Research UK
Parents reported feeling isolated and unable to look after their child properly at home and many revealed that their child had spent longer than necessary in hospital as a result.
Meanwhile, 50 per cent of children and young people with cancer said that they needed help keeping up with their education, but only one out of three received the support they required.
One young cancer survivor, 19-year-old Manvir Randhawa, described what it is like to return home after undergoing cancer treatment.
"Being sick is the easy bit," Manvir said. "It is the other things - school, confidence, getting back to having friends, your emotions - that are really difficult. And yet children and young people are being left to cope with all of this on their own."
CLIC Sargent's chief executive, Dr Carole Easton, commented: "Each day spent in hospital is an extra day a child is losing out on his or her childhood.
"Being cared for safely at home so that they can be with family and friends or go back to school not only helps children and young people with cancer lead as normal a life as possible, but also helps them cope better with the challenges of cancer treatment."
The charity is campaigning for equal provision of services throughout the UK and a more coordinated approach to community-based care and support for children with cancer to ease their return home from hospital, involving children's cancer nurses, social workers, GPs, children's community nurses and teachers.
Helen Thompson, senior information nurse at Cancer Research UK, commented: "Going home in-between treatments and when treatment has finished can be an anxious time for children with cancer and their families.
"We welcome any measures that ensure the care and support provided for children and teenagers at home is of a high standard and consistent throughout the country."

Advanced-Stage Ovarian Cancer Patients with BRCA Live Longer with Standard Treatment

2008-12-05T06:03:00.000-08:00

Advanced-Stage Ovarian Cancer Patients with BRCA Live Longer, May Respond Better to Standard Treatment
Majority of Women with Ovarian Cancer Unaware BRCA Testing is AvailableTwo abstracts underscoring the importance of testing for BRCA1/2 mutations in women with ovarian cancer were presented at this week's Society of Gynecologic Oncologists 39th Annual Meeting on Women's Cancers, by researchers from The University of Texas M. D. Anderson Cancer Center. In the first study, a multicenter research team led by M. D. Anderson found advanced- stage ovarian cancer patients with non-Ashkenazi Jewish BRCA (non-AJ BRCA) mutations experience longer progression-free and overall survival rates compared to those with sporadic ovarian cancer. The data confirms previous research which reported that among ovarian cancer patients of Ashkenazi-Jewish heritage, BRCA1/2 mutations (AJ BRCA) are associated improved long-term survival. For this study, researchers examined 85 advanced-stage ovarian cancer patients with non-AJ BRCA mutations and 116 patients who did not express any type of BRCA mutation. Compared to patients without BRCA mutations, non-AJ BRCA carriers had longer progression-free survival of 19.0 vs. 27.8 months and improved overall survival of 65.6 vs. 101.4 months. Non-AJ BRCA patients had a 2.15 times greater odds of complete response to initial chemotherapy response over sporadic, non-carrier patients. Karen Lu, M.D., associate professor in the Department of Gynecologic Oncology at M. D. Anderson and senior author on the study said the difference in survival rates indicate that individuals with BRCA mutations might respond better to standard chemotherapy for ovarian cancer. "Thus, it becomes increasingly valuable to know a patient's BRCA status to guide and personalize treatment decisions," Lu said. Majority of Patients Unaware BRCA Testing Available A second study conducted at M. D. Anderson concluded that, despite being available for more than 10 years, a majority of women with ovarian cancer were unaware genetic counseling and testing for BRCA1/2 mutations was an option. Of the 225 ovarian cancer patients surveyed, 56 percent had not heard of BRCA testing. This lack of awareness was more profound in minorities - 69 percent of Hispanic and 88 percent of African American respondents were unaware of BRCA testing compared to 52 percent of white women. "Patients typically associate genetic testing with benefiting family members and offspring," Lu said. "Both of these studies illustrate that it is equally important for the cancer patient to get information from their doctors about genetic testing because it not only has implications for their family, but their own treatment and prognosis." She said that more than 85 percent of ovarian cancer patients surveyed would be willing to undergo BRCA testing if it would affect their care, but the cost of testing may be a barrier. "Currently, oncologists are inconsistent in their testing for BRCA mutations. Based on the treatment implications of our findings and the surprisingly low knowledge that such testing is available, we recommend developing ways to systematically evaluate every ovarian cancer patient for BRCA," Lu said. A family history of breast and/or ovarian cancer is reported in approximately five percent to 15 percent of ovarian cancer cases, with BRCA1/2 mutations expressed in a significant proportion of these cases. In addition to Lu, researchers contributing to the abstract on BRCA survival advantage include lead author Robin Lacour, M.D., Molly Daniels, M.S., Shannon Westin, M.D., Larissa Meyer, M.D., Charlotte Sun, Dr.P.H., Diana Urbauer, M.S., Pedro Ramirez, M.D., Diane Bodurka, M.D., David Gershenson, M.D., all of M. D. Anderson. Others include Veena Choubey and Stephanie Blank, M.D., New York University Medical Center; Heather MacDonald, M.D. and Lynda Roman, M.D., University of Southern California Medical Center; Jacob Estes, M.D. and Mack Barnes, M.D., University of Alabama Birmingham; Deanna Teoh, M.D. and Beth Ann Powell, M.D., University of California at San Francisco Medical Center; Rebecca Brooks, M.D., David Mutch, M.D. and Sherri Babb, M.S., Washington University (St. Louis) Medical Center; Shana Wingo, M.D. and John Schorge, M.D., The University of Texas Southwestern Medical Center at Dallas. On the BRCA genetic testing abstract, with Lu other authors include: Lacour, Kristin White, Molly Daniels, Shannon Westin, Larissa Meyer, Catherine Burke, W.H.N.P., Kimberly Burns, W.H.N.P., Shiney Kurian, W.H.N.P., Nicki.Webb, W.H.N.P., Terri Pustilnik, M.D., Diana Urbauer, Charlotte Sun, Diane Bodurka, David Gershenson of M. D. Anderson.

The Role of Radiotherapy in the Management of Ovarian Cancer

2008-12-05T06:01:00.000-08:00

The Role of Radiotherapy in the Management of Ovarian CancerArticle by: Nagendra Sai Koneru, M.D., Anthony Fyles, M.D., William Small Jr., M.D.What is Radiation Therapy?Radiation oncology is a branch of medicine that manipulates ionizing radiation to treat cancer and other benign diseases. The goal of radiation therapy is to eradicate cancer cells through the delivery of a measured dose of radiation to a precisely defined tissue volume, while attempting to minimize damage to any healthy surrounding tissue. In ovarian cancer radiation oncologists work closely with gynecologic oncologists, who are the primary surgical oncologists that treat ovarian cancer, and medical oncologists. Both medical and gynecologic oncologists deliver chemotherapy.Radiation kills cancer cells by damaging the DNA. Tumor cells often have impaired repair mechanisms that are normally found in healthy cells. Thus, tumor cells can be inherently sensitive to radiation effects. Damage to DNA can occur by direct interaction of radiation with a cell’s DNA or indirectly by the creation of free radicals that are produced by the interaction of radiation and water within the cell.Radiation oncologists use linear accelerators to deliver radiation to a patient. Linear accelerators are treatment machines that selectively create high-energy radiation beams which are then directed at a specific target. Epidemiology of Ovarian CancerThere are three primary types of ovarian cancer. Epithelial ovarian cancer comprises approximately 80%-90% of ovarian cancer and will be the subject of this review. Germ and stromal tumors represent the remaining 10-20%. There are numerous risk factors for ovarian cancer and can include lower number of pregnancies, nulliparity and infertility [3]. Oral contraceptive use has been shown to reduce the risk of ovarian cancer [4]. Women who have a family history of breast cancer or ovarian cancer are at increased risk. Gene mutations in BRCA1 and BRCA2 have been observed in many of these families. Hereditary non-polyposis colon cancer (HNPCC) is a genetic syndrome that has been associated with colon, endometrial and ovarian cancer.Detection/ScreeningRoutine screening for ovarian cancer has not been recommended because there have been no reliable markers for detecting early epithelial ovarian cancer [1,5] although routine gynecologic care should still be recommended. The tumor marker CA-125 has been found to be helpful in ovarian cancer screening. The combination of a pelvic exam, transvaginal ultrasound and a blood test for CA-125 can be offered for women who are symptomatic or at high risk [1,5].Clinical PresentationEpithelial ovarian cancer does not present with specific signs or symptoms. Patients most commonly present with abdominal distention, however, heartburn, nausea, and lower abdominal pain can also manifest [5].Ovarian cancer is often metastatic or spread beyond the ovaries at presentation and confined to the ovary in only 23% of cases [6]. The peritoneum is a multilayered membrane which lines the abdominal cavity, and supports and covers the organs within it. The most common route of spread is through the peritoneum (transperitoneal) and the disease is confined to the abdominal cavity in 85% of patients [6]. However, ovarian cancer may also spread through the blood or lymphatics.The Federation of International Gynecologists and Obstetrics (FIGO) has grouped ovarian cancer into four primary stages. Stage I disease is limited to the ovaries. Stage II involves tumor spread in the pelvis beyond the ovaries. Stage III involves spread outside the pelvis but confined within the abdominal cavity or inguinal nodes. Stage IV disease involves tumor in one or both ovaries with distant metastasis, such as the liver parenchyma or lungs. Microscopically the aggressiveness of the tumor is classified according to its grade, ranging from 1 to 3. Grade 1 shows the least aggressiveness, while grade 3 shows the most.Overall 5 year survival, including all stages for ovarian cancer, is 53% [1]. For early stage disease, the 5 year survival is 94.7%. For intermediate stage disease, the 5 year survival is 72% [1]. For late stage, the 5 year survival is 30.7% [1].TreatmentSurgery is the standard initial management of ovarian cancer [6]. Because of transperitoneal spread and the frequent appearance of upper abdominal disease, pre-treatment surgical staging is performed. Surgical staging involves partial omentectomy, visualization or the entire peritoneum, biopsy of any suspicious or palpable lesions, and cytologic examination of ascites or peritoneal washings from pelvis, paracolic gutters, and diaphragm [6].Studies have revealed that the amount of residual tumor volume after surgery may impact survival. As residual tumor volume increases, median survival decreases [6]. Cytoreductive surgery is thus recommended for maximum tumor removal [6]. For stage I, grade 1 disease, surgery alone has a 5% relapse rate and is often the only treatment modality used [6]. Patients with stage I disease with unfavorable prognostic factors, such as grade 2 or 3, and patients with stage II and III disease are often recommended to have surgery followed by intravenous (IV) carboplatin and paclitaxel chemotherapy, since there is often at least a 30% risk of recurrence [2]. Recent trials have shown that platinum-based adjuvant chemotherapy improved survival and recurrence-free survival in early-stage ovarian cancer [7]. Alternatively, intraperitoneal (IP) chemotherapy, which involves injecting chemotherapy directly into the abdomen, has gained recent attention and may be considered an alternative to IV chemotherapy in certain clinical situations [8]. Adjuvant abdominopelvic radiotherapy can also be used in selected patients [9].Rationale for Radiation TherapyEvidence that radiation therapy is an effective adjuvant therapy in certain stages and extents of ovarian cancer has been proven in several trials [6]. For early and intermediate stage disease, trials have shown that radiotherapy to the whole abdomen following surgery to be more effective than certain chemotherapy and pelvic radiation. Although there have been no randomized trials comparing platinum based chemotherapy to whole abdominal therapy, platinum based chemotherapy has largely supplanted the use of radiotherapy in the United States. However, radiotherapy does have a role in both cure and symptom control in patients with ovarian cancer.A Princess Margaret Hospital randomized trial of 147 patients compared pelvic radiotherapy alone or with chlorambucil chemotherapy to whole abdomen radiotherapy, in patients with stages I-III disease. After a 7 year follow-up, the 10-year difference in survival was significantly higher in the 76 patients treated with pelvis plus whole abdomen radiotherapy compared to the 71 patients treated with pelvic irradiation and chlorambucil (46% vs 31%, p=0.05) [10]. The survival benefit was only seen in patients with small macroscopic residual tumor

Ovarian Cancer: Researches Identify Unique Biomarkers for this Disease

2008-12-05T05:58:00.000-08:00

Researchers identify ovarian cancer biomarkersFinding could be first step toward new screening tool, treatmenttargetAnn Arbor - Researchers have identified markers unique to the cells of blood vessels running through ovarian tumors. The finding, while preliminary, could one day improve screening, diagnosis and treatment for this disease. The team of researchers from the University of Michigan, University of Pennsylvania, and universities in Greece and Italy used a laser technique to isolate blood vessel cells from 21 ovarian tumors and four normal ovarian tissue samples. From there, they were able to determine which genes the vascular cells expressed.The results identified more than 70 markers that were present in large amounts in the blood vessels of cancer tissue but not in the vessels of normal tissues. The researchers went on to study in detail 12 markers that had not previously been linked to tumor blood vessels. The study appears in the March 1 issue of the Journal of Clinical Oncology."Some of these genes, depending on how highly expressed they were in the tumor vasculature, were also prognostic of a patient's survival. We suspect when these genes are highly expressed it may be a sign of a tumor that's able to grow blood vessels more efficiently, and therefore is more aggressive. This may help us down the road in treatment decisions," says lead study author Ronald Buckanovich, M.D., Ph.D., assistant professor of internal medicine and obstetrics and gynecology at the University of Michigan Medical School. Buckanovich was at the University of Pennsylvania when he conducted this research.The study analyzed the largest number of samples to date in tumor vasculature, or blood vessel, profiling. While many of the genes identified in this analysis have been shown previously to be involved in tumor vasculatures for other cancer types, several of the markers appear to be new.In addition, the researchers were able to determine that some of the markers present in large amounts in ovarian tumors were not expressed by normal ovaries or other healthy organs. The researchers also found these markers were not present in normal reproductive tissues that experience blood vessel growth, such as the placenta or endometrium. This suggests that the markers are specific to tumors and would not be mistaken for normal blood vessel growth in women of reproductive age.If the markers do prove to be specific to ovarian tumors, researchers believe that could be a new avenue to develop drugs that would target the blood vessels and strangle the tumor.Biomarkers are also seen in other cancer types as a potential screening tool. A new way of detecting ovarian cancer could make a significant dent in this disease, where 70 percent of patients are diagnosed after the tumor has grown large or spread. There are few or no symptoms early in the disease and no effective screening tests. Early diagnosis is crucial, marking the difference between a 95 percent survival rate for cancers found at the earliest stage and 20 percent survival among patients diagnosed with advanced disease."All the things we could hope for are present with this approach: It has potential for diagnosis, imaging, treatment and prognosis. It needs more work and much more confirmation, but our early results are promising," Buckanovich says.Continued research will look at developing antibodies and methods to detect these novel proteins. "In some cases, these are genes that many people have never worked on before," Buckanovich says.The American Cancer Society estimates 22,430 women will be diagnosed with ovarian cancer this year and 15,280 women will die from it.The research is very preliminary at this point. Any potential screening or treatment benefit would be many years in the future. For information about currently available therapies, call the Cancer AnswerLine at 800-865-1125 or visit their web page.In addition to Buckanovich, study authors were Dimitra Sasaroli, Anne O'Brien-Jenkins, Jeffrey Botbyl, Rachel Hammond, Lance A. Liotta, Phyllis A. Gimotty and George Coukos, all from the University of Pennsylvania; Dionysios Katsaros of the University of Turin in Italy; and Raphael Sandaltzopoulos of the Democritus University of Thrace in Greece.Funding for the study was from the National Institutes of Health, a National Cancer Institute Specialized Program of Research Excellence (SPORE) grant, the U.S. Army Medical Research and Materiel Command Grant, the Marcia and Philip Rothblum Foundation and the Ovarian Cancer Research Fund. The laser-capture microdissection facility was supported by the Fannie Rippel Foundation.

Ovarian Cancer Treatment Found to Significantly Improve Survival

2008-12-05T05:54:00.000-08:00

Source: Memorial Sloan Kettering Cancer CenterUnderutilized Treatment for Advanced Ovarian Cancer Found to Significantly Improve SurvivalNEW YORK, January 4, 2006 - According to a study published in the January 5 issue of the New England Journal of Medicine, women with Stage III ovarian cancer given a combination of intravenous (IV) and intra-abdominal chemotherapy, following the successful surgical removal of tumors, experienced a median survival time 16 months longer than women who received IV chemotherapy alone. Intra-abdominal chemotherapy, also known as intraperitoneal (IP) chemotherapy, involves the delivery of anticancer drugs directly into the abdomen. This type of chemotherapy administration is underutilized, but significant evidence from this new study confirms the survival benefit of IP chemotherapy for most women with advanced ovarian cancer.The study, conducted by Deborah K. Armstrong, MD, an assistant professor at the Johns Hopkins Kimmel Cancer Center in Baltimore, Maryland, and her colleagues, builds upon evidence from eight other clinical trials -- including those conducted at Memorial Sloan-Kettering Cancer Center (MSKCC) -- showing an overall survival period of approximately one year for women treated with IP chemotherapy after "optimal debulking" -- surgery to remove most, if not all, of the cancer in the abdomen. Based on this overwhelming evidence, the National Cancer Institute (NCI) will issue a clinical announcement on January 5 encouraging the administration of a combination of IV and IP chemotherapy to treat women with advanced ovarian cancer, who have undergone optimal surgical debulking. After pioneering the first clinical trials of IP chemotherapy in the late 1980s, MSKCC is one of the most experienced centers with the largest volume of patients who have undergone the procedure. The Center has been using IP chemotherapy as a standard of care based on Dr. Armstrong's presentation at the American Society of Clinical Oncology's annual meeting in May 2005 and research conducted at MSKCC.

Endometrial Cancer: Researchers have developed a customized fitness program to help survivors

2008-12-05T05:50:00.000-08:00

The Shape of Health to Come M. D. Anderson to help endometrial cancer survivors take "Steps to Health"While millions of Americans place fitness as one of their top New Year's resolutions to improve shape, muscle tone and overall appearance, cancer survivors have another priority - life.Researchers at The University of Texas M. D. Anderson Cancer Center have developed a customized fitness program to help survivors of endometrial cancer - or cancer of the uterus - shed pounds and keep cancer at bay. Karen Basen-Engquist, Ph.D., principal investigator of the five-year "Steps to Health" study and associate professor in the Department of Behavioral Science, aims to determine how well participants adhere to a personalized fitness plan, motivation both for beginning and sustaining regular workouts and the role of a support system in encouraging determination.All endometrial cancer survivors who are six months post treatment - from M. D. Anderson or elsewhere - are eligible to participate in the Steps to Health study, funded by the National Cancer Institute.Following an initial 30-minute orientation, including an electrocardiogram, researchers will assess participants at baseline and again every two months using a series of health and quality-of-life questionnaires, as well as fitness tests on an exercise bike. Depending on a participant's current physical ability, exercise physiologists and fitness specialists then will create a customized plan for each survivor.According to Basen-Engquist, cancer survivors' confidence following a stressful course of treatment often can be diminished."I'm most interested in learning which factors encourage survivors to persist with exercise and take charge of their cancer prevention for the future," said Basen-Engquist. "As the risk for endometrial cancer is two-to four-fold greater in obese women than the general population, we hope that providing a personalized exercise plan for this population will be an incentive to achieve improved physical and psychological well-being.Basen-Engquist and her team intend to enroll 270 participants into the study, each of whom will personally record her physical activity for six months using a portable personal computer. Researchers will build on the body of evidence gleaned from a five-week pilot study conducted before the official launch of the Steps to Health study."Our team is interested in assisting participants with the actual process of initiating and incorporating physical activity into daily life," said Basen-Engquist. "We hope to discover individual traits and tools that enable certain people to stay with an exercise plan better than others."In addition to bimonthly assessments, M. D. Anderson researchers will mail information regarding goal setting and fitness tools to all participants and provide weekly telephone counseling. Study leaders will use social cognitive theory, which measures how individuals adopt and maintain behavioral patterns, in developing intervention strategies for participants."By participating in the Steps to Health pilot study, I developed an increased awareness of how essential exercise really is to maintain health," said Maureen Hughes, endometrial cancer survivor. "It is easy to keep putting exercise off, but when I was presented with all the information, I couldn't deny its importance for my well-being."While researchers will measure physical and biological changes in participants, they also will evaluate self-efficacy, or survivors' confidence that they can succeed. Researchers also plan to determine the level of support participants need to exercise and feel successful.According to the American Cancer Society, approximately 41,200 women in the United States will be diagnosed with endometrial cancer in 2006 and approximately 7,350 of these women will die from the disease, making it the most commonly diagnosed cancer of the female reproductive organs.

Cervical Cancer: 15 common myths

2008-12-05T05:44:00.000-08:00

Source: University of Michigan Comprehensive Cancer Center (January 10, 2007) 15 common myths about cervical cancerU-M experts explain common misconceptions, fears about this largely preventable diseaseAnn Arbor - About 9,700 women in the United States will be diagnosed with cervical cancer this year. It may seem like a small number, until you consider that another 1.2 million women will develop a pre-cancerous condition called dysplasia. And if left untreated, dysplasia will become cervical cancer.Because of Pap smears, a huge number of women are no longer dying of cervical cancer in this country, but this is a disease that can be almost entirely prevented," says Carolyn Johnston, M.D., clinical associate professor of obstetrics and gynecology at the University of Michigan Medical School and a gynecologic oncologist at the U-M Comprehensive Cancer Center.In addition to early detection through screening, a new vaccine now available could help prevent cervical cancer. In honor of Cervical Cancer Awareness Month, which is January, U-M experts respond to common myths and misconceptions about this disease.Myth 1: Cervical cancer cannot be prevented.Truth: Infection with the human papillomavirus, or HPV, is an absolute requirement for cervical cancer to develop. This virus is transmitted sexually, but the majority of the most worrisome types of infection can be prevented with a newly available vaccine. Preventing HPV infection dramatically reduces a woman's risk of cervical cancer. In addition, cervical cancer usually develops slowly after persistent infection with HPV and will first appear as a precancerous condition called dysplasia. If detected at this stage, it can be effectively treated to prevent cervical cancer from developing. Screening with Pap smears and tests for HPV detect these pre-cancerous conditions so patients are treated early.Behavioral issues can also influence cervical cancer. "A woman can reduce her risk of these problems by limiting the number of sexual partners over a lifetime, by not smoking cigarettes and by following accepted screening guidelines. Each of these behaviors relates to known risk factors for this disease," says Anthony Opipari, M.D., Ph.D., associate professor of obstetrics and gynecology at the U-M Medical School. Myth 2: I'm too young to worry about cervical cancer.Truth: The average age of cervical cancer patients is 48. While it's not common, women can be diagnosed in their 20s. HPV infection and the precancerous condition dysplasia are common in younger women.Myth 3: I don't have intercourse, so I don't need the HPV vaccine.Truth: HPV can be passed from one partner to another through intercourse, as well as orally and through touching. In 2006, the Food and Drug Administration approved a vaccine, Gardasil, to protect against four types of HPV, two of which are commonly linked to cervical cancer and two linked to genital warts. A CDC advisory committee recommended that Gardasil be given routinely to girls age 11-13. Until everyone is vaccinated, girls and women ages 13-26 are also candidates for the vaccine. Experts believe the vaccine should be given at a young age before a woman becomes sexually active. Myth 4: I had the HPV vaccine, so I don't need to use condoms during sex.Truth: The HPV vaccine will protect you from infection with four types of HPV - but there are other strains of this virus and many other sexually transmitted diseases that it does not protect against. Continue using condoms to protect against STDs.Myth 5: I don't need a Pap test.Truth: A woman's first Pap test should be given when she turns 21 or three years after she begins having intercourse, whichever comes first. Recommendations differ for how often a woman should receive a Pap test. Ask your doctor how often you should be screened. Even if you have the HPV vaccine, you still need a regular Pap test. The vaccine targets four types of HPV but it will not protect against all the types of HPV that can cause cervical cancer, so it's still important to continue regular screenings.Myth 6: I'm too old to need a Pap test any longer.Truth: "We have seen an increase in cervical cancer and HIV in older populations," says Lauren Zoschnick, M.D., clinical assistant professor of obstetrics and gynecology at the U-M Medical School. "Women can have new sexual partners, which puts them at risk of cervical cancer and other STDs." Talk to your health care provider about the need to have Pap smears even if you have gone through menopause, have had a hysterectomy, or are over the age of 65.Myth 7: My doctor gave me a pelvic exam, which is the same as a Pap test.Truth: The Pap test collects cells from the cervix, which are sent to a lab to be evaluated. In a pelvic exam, your doctor physically examines the cervix and other parts of a woman's anatomy. Both are important to detect problems early.Myth 8: My Pap test was abnormal, which means I must have cancer.Truth: Not necessarily. You'll likely need follow-up tests, possibly a test for HPV, colposcopy or a biopsy to test for cancerous cells. An abnormal Pap test could indicate a precancerous condition that can be treated. Conversely, a negative Pap test does not always mean a woman is cancer-free. About 10 percent of all Pap tests return a false negative result, meaning the test did not identify a problem that is there. If you have problems such as bleeding or pain, seek further care even if your last Pap test was normal.Myth 9: Cervical cancer has no symptoms.Truth: Bleeding after intercourse, bleeding between menstrual periods or bleeding after menopause may indicate cervical cancer. Other symptoms include an abnormal discharge or pain in the pelvic region.Myth 10: If I am diagnosed with cervical cancer, I am going to die.Truth: Survival after cervical cancer caught in its earliest stage is 92 percent. The later it is diagnosed, the lower the chance of survival. Survival is lower in developing countries because of inadequate screening. Regular screening will help ensure cervical cancer is caught at an early, treatable stage.Myth 11: After I finish treatment, I will live the rest of my life worried about cancer returning.Truth: If cervical cancer is going to recur, it is most likely to happen in the first two years after treatment. Most patients are followed for five years, after which the risk of recurrence is extremely low.Myth 12: I must have a hysterectomy to treat cervical cancer.Truth: Early cervical cancer is typically treated with a hysterectomy, surgery that removes the cervix and uterus. But it's not the only option. Radiation and chemotherapy are used to treat more advanced disease and may also be options for women with early stage disease who cannot have surgery. Some women with early cervical cancer can also avoid hysterectomy with procedures such as a cone biopsy that removes only the cancerous tissue and a small margin of surrounding healthy tissue, or a procedure called radical trachelectomy, which removes the cervix but not the uterus.Myth 13: I won't be able to conceive a child after cervical cancer treatment.Truth: If you have a hysterectomy or radiation to treat cervical cancer, you will not be able to conceive. But newer surgical procedures help preserve a woman's fertility without compromising survival. A radical trachelectomy removes the cervix but not the uterus so that a woman can still conceive. For small, early cancers, a cone biopsy may be appropriate and will also preserve fertility.Myth 14: A hysterectomy to treat cervical cancer will put me in menopause afterward.Truth: Hysterectomy to treat cervical cancer does not remove the ovaries, which are what determines whether a person is menopausal. Cervical cancer very rarely spreads to the ovaries. Women who receive pelvic radiation to treat cervical cancer will likely experience menopause because the radiation will affect the ovaries.Myth 15: Taking hormone replacement therapy will increase my risk of cervical cancer.Truth: Cervical cancer does not respond to hormones like breast or ovarian cancers. Low doses of hormone replacement therapy can treat menopausal symptoms without increasing the risk of cervical cancer.For more information about cervical cancer and the HPV vaccine, visit the following resources: U-M Cancer Center Cervical Cancer information page U-M Cancer AnswerLine: 800-865-1125

Esophageal cancer rates climb with obesity; U-M study finds esophagectomy safe in obese patients

2008-12-05T05:36:00.000-08:00

ANN ARBOR, Mich - The rapidly climbing obesity rates in the United States have created a higher risk of esophageal cancer linked to reflux disease. And this has some surgeons wondering if a currently popular procedure to remove the esophagus is as safe in obese patients.According to a new study at the University of Michigan Health System, obese patients who underwent a procedure called transhiatal esophagectomy primarily for esophageal cancer had outcomes similar to their lean counterparts. "The type of patient who currently develops esophageal cancer has changed dramatically in the last 20 years. Esophageal cancer used to be primarily squamous cell carcinoma found in people who drank alcohol and smoked excessively. In association with the horrendous epidemic of obesity in this country, we have seen a 350 percent increase of adenocarcinoma over the last 30 years. This is related to more gastroesophageal reflux and Barrett’s esophagus in these patients," says Mark Orringer, M.D., John Alexander Distinguished Professor of Surgery at the U-M Medical School.Orringer and lead study author Christopher Scipione, a U-M medical student, will present the study results Tuesday, Jan. 30, at the Society of Thoracic Surgeons 43rd annual meeting in San Diego.Adenocarcinoma of the esophagus is often the result of chronic reflux disease. When acid continuously backs up into the esophagus, it wears down the natural lining. This can cause a condition called Barrett’s esophagus in which the body replaces the normal esophageal lining with one similar to that found in the intestines. People who develop Barrett’s are at a higher risk of developing adenocarcinoma.Transhiatal esophagectomy, or THE, is an operation in which most of the esophagus is removed without the need to open the chest, and swallowing is restored by pulling the stomach to the neck and connecting it there to the remaining esophagus. THE is used to treat esophageal cancer and Barrettآ’s esophagus with severe precancerous changes. It was originally developed at the University of Michigan as a surgical alternative to removing the esophagus by going through the chest, a much more difficult operation for the patient. The researchers sought to determine if THE is a safe procedure for the growing number of obese patients requiring esophageal surgery. They pulled the records of 133 profoundly obese patients who had this surgery at U-M between 1977 and 2006. Profound obesity was defined as a body mass index of 35 or more. Those 133 patients were matched to a randomly selected control group of non-obese patients undergoing the same procedure. Both groups were matched for factors including gender, age, year of operation and pre-existing medical conditions.After comparing measures such as hospital length of stay, infection and mortality, the researchers found both groups had comparable outcomes. This suggests the THE procedure is safe to perform in obese patients. The study authors stress, however, that the results may be influenced by the high volume of patients U-M surgeons see for this procedure. U-M surgeons perform 120 to 150 transhiatal esophagectomies each year and have completed more than 2,000 of these procedures in total. Because the procedure in obese patients is more demanding on surgeons, the results may not be the same in hospitals that see relatively few patients in need of an esophagectomy."Profoundly obese patients undergoing a THE at a high-volume center can have surprisingly and acceptably low morbidity and mortality rates, similar to those of non-obese individuals matched for co-morbidities," says Orringer, head of the U-M Section of Thoracic Surgery and co-director of the Thoracic Oncology Program at the U-M Comprehensive Cancer Center.Currently about 85 percent of esophageal cancers removed in this country are adenocarcinomas, most related to obesity and reflux disease, and 15 percent are squamous cell carcinomas, typically due to smoking or alcohol consumption. Two decades ago, those numbers were reversed."Reflux is an extraordinarily common problem now, and it’s because we’re a fat society. If heartburn is persistent or chronic, patients should have a thorough exam and endoscopy to see if they have developed Barrett’s esophagus, which carries an increased risk of cancer and signals the need for close surveillance with periodic endoscopies and biopsies," Orringer says.About 14,500 people will develop esophageal cancer this year. For more information on this disease, contact Cancer AnswerLine at 800-865-1125 or visit

Breast Cancer Incidence Higher Among Young African-American Women than Young White Women

2008-12-04T06:25:00.000-08:00

Breast Cancer Incidence Higher Among Young African-American Women than Young White Women

The incidence of breast cancer among African-American women under 40 is higher than that of White women under 40, according to the results of an analysis published in the Journal of the National Cancer InstituteBreast cancer is the second leading cause of cancer death in women in the United States, with approximately 180,000 cases diagnosed each year. Progress in the areas of screening and treatment has allowed for earlier detection and higher cure rates. Researchers continue to study the incidence rates and patterns of this disease with the hopes of further improving screening, prevention, and treatment.
The incidence of postmenopausal breast cancer has been on the rise, which may be largely attributable to more successful screening for the disease, as well as the use of menopausal hormones. However, the incidence rates of breast cancer in younger women have received less attention. Researchers at the National Cancer Institute recently used the Institute’s Surveillance, Epidemiology, End Results (SEER) Database to analyze trends in breast cancer incidence during the period of 1992-2004.
The researchers analyzed over 300,000 cases of breast cancer based on age at diagnosis, year of diagnosis, racial and ethnic categories, and pathologic features of the cancer. They found that although white women had higher incidence rates than black women after age 40, the reverse was true for younger women. In women under 40, the incidence rate per 100,000 woman-years was approximately 17 for black women, compared with approximately 15 for white women. The discrepancy was even higher for women under age 30.
Furthermore, they found that younger women were more likely than older women to have tumors with poor prognostic features (larger than 2 cm, positive lymph node status, and higher stage). Younger women also had higher incidence rates for inflammatory breast cancers and estrogen-receptor positive tumors.
The researchers concluded that based on this data, it is important to continue to monitor the trends in breast cancer incidence among younger women. Mammography is not recommended in younger women because high breast tissue density makes it less sensitive. However, if the incidence of breast cancer in younger women continues to trend upward, it will be important to identify preventive approaches, including the identification of early risk factors and biomarkers.

Reference:
Brinton LA, Sherman ME, Carreon JD, et al. Recent trends in breast cancer among younger women in the United States. Journal of the National Cancer Institute

Moh’s Micrographic Surgery More Effective than Excision for Recurrent Basal Cell Carcinoma of the Face

2008-12-04T06:21:00.000-08:00

Moh’s Micrographic Surgery More Effective than Excision for Recurrent Basal Cell Carcinoma of the Face

Moh’s micrographic surgery (MMS) for the treatment of recurrent basal cell carcinoma (rBCC) of the face results in fewer recurrences than surgical excision, according to the results of a study published in the December 2008 issue of the Lancet Oncology.[1]
Skin cancer is often divided into two broad categories: melanoma and nonmelanoma. Nonmelanoma skin cancer refers to several different types of skin cancer, but the most common types are basal cell carcinoma and squamous cell carcinoma. Each year in the U.S., more than one million people are diagnosed with basal cell or squamous cell skin cancers. Unlike melanoma, these types of skin cancer are rarely deadly.
Basal cell carcinoma accounts for roughly 80% of all cases of nonmelanoma skin cancer. It most commonly develops on sun-exposed skin, with the head (particularly the nose) and neck being the most common sites. This type of skin cancer very rarely metastasizes (spreads beyond the skin), but it can cause extensive local damage to the skin and surrounding tissues.
Basal cell carcinoma is typically treated with either surgical excision or Moh’s micrographic surgery (MMS). Surgical excision involves the use of a scalpel to remove the cancer and some surrounding normal tissue, which is then sent to the lab where the margins are checked for cancer. If the margins are clear, it’s likely that the cancer was completely removed. Moh’s micrographic surgery is a more complicated procedure, during which a doctor removes thin layers of skin one at a time and evaluates them for cancer while the patient waits. The doctor keeps removing layers of skin until he or she reaches a layer that is cancer-free. This procedure removes the least amount of normal tissue, and also has the highest cure rates for both primary and recurrent cancers. The procedure generally requires less than four hours to complete but can take longer if the cancer is extensive.
In a study performed in the Netherlands, 408 primary BCCs (pBCC) and 204 recurrent BCCs (rBCC) were randomly assigned to surgical excision or MMS. After five years of follow-up, the researchers found that MMS produced significantly lower recurrence rates than surgical excision in the rBCC group. (Two patients in the rBCC group treated with MMS experienced a recurrence of cancer, versus ten patients treated with surgical excision.) However, in the group of patients with pBCC, there was not a significant difference between the two surgical modalities.
The researchers concluded that MMS is preferred over surgical excision for the treatment of facial rBCC because it produces significantly fewer recurrences.
Reference:
[1] Mosterd K, Krekels GAM, Nieman FHM, et al. Surgical excision of Moh’s micrographic surgery for primary and recurrent basal-cell carcinoma of the face: a prospective randomised controlled trial with 5-years’ follow-up. Lancet Oncology

Pulmonary Scarring on Chest X-Ray Associated with Lung Cancer

2008-12-04T06:17:00.000-08:00

Pulmonary Scarring on Chest X-Ray Associated with Lung Cancer

Individuals who have evidence of pulmonary scarring on a chest X-ray are at an increased risk for developing lung cancer, according to the results of a study published in the November 24, 2008 issue of the Archives of Internal Medicine.[1]
Lung cancer is the most common cancer in the world and is the leading cause of cancer death, with 160,000 deaths in the United States annually. Each year lung cancer kills more people than breast cancer, colon cancer, and prostate cancer combined. Lung cancer is primarily associated with environmental factors such as smoking and other carcinogens. There has been much debate regarding screening for lung cancer because no screening procedure has proven to decrease the number of lung cancer deaths. Historically, chest X-rays have been used as a preliminary method to detect lung cancer.
Because fibrotic scars are often found in proximity to lung cancer when it is diagnosed, researchers have speculated that there might be a relationship between scarring and the subsequent development of lung cancer. In order to examine this, researchers evaluated data from 66,863 patients involved in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. The patients were aged 55-74 and were cancer-free upon initiation of the trial. Patients underwent a baseline screening chest X-ray and were then followed for up to 12 years.
Scarring was present in 5,041 patients, or 7.5% of all baseline X-rays. Individuals with scarring had a 50% increased incidence of lung cancer in the same lung compared with individuals with no scarring. However, there was no increased risk in the opposite lung. This elevated risk persisted throughout the entire follow-up period.
The researchers concluded that pulmonary scarring is associated with an increased risk of lung cancer and even speculated that “localized inflammatory processes associated with scarring promote the subsequent development of lung cancer.” Research will likely be ongoing to examine the relationship between pulmonary scarring and lung cancer. In addition, the results of this study may help to validate the use of screening chest X-rays in certain high-risk individuals.

Reference:
[1] Yu YY, Pinsky PF, Caporaso NE, et al. Lung cancer risk following detection of pulmonary scarring by chest radiography in the prostate, lung, colorectal and ovarian cancer screening trial. Archives of Internal Medicine.

Motesanib Diphosphate Provides Anticancer Activity Among Patients with Progressive Thyroid Cancer

2008-12-04T06:15:00.000-08:00

Motesanib Diphosphate Provides Anticancer Activity Among Patients with Progressive Thyroid Cancer

The investigative agent motesanib diphosphate (AMG 706) produces a regression of cancer among patients with thyroid cancer that is progressing despite standard therapies. These results were recently published in the New England Journal of Medicine.
The thyroid is a gland in the throat that produces hormones mostly related to metabolic processes in the body. According to the American Cancer Society, approximately 37,340 new cases of thyroid cancer will be diagnosed in 2008 in the United States. Nearly two-thirds of all thyroid cancers occur in people between the ages of 20 and 55. Overall, thyroid cancer is considered to be a highly curable cancer, with 97% of individuals alive at least five years following diagnosis. Nearly 95% of all thyroid cancers are classified as differentiated thyroid cancers, which refers to the type and characteristics of the cancer cells.
Standard therapy for thyroid cancer includes the removal of the thyroid, which is followed by drugs to suppress certain hormone levels related to the thyroid and radiation plus iodine (radioiodine) therapy, which is targeted to eliminate any remaining thyroid cancer cells. Patients whose thyroid cancer progresses or fails following standard therapy have a 10-year survival rate of less than 15%. Thus, novel agents targeting progressive thyroid cancers are needed.
The vascular endothelial growth factor (VEGF) is a protein that is an important component to cellular growth and replication. Often, cancer cells will have an overexpression or mutation of VEGF. Targeted therapies, including those targeted against VEGF, have recently demonstrated anticancer activity in certain types of cancers. Research into blocking VEGF continues in clinical trials.
Researchers from the M.D. Anderson Cancer Center recently conducted a clinical trial to evaluate motesanib diphosphate, a VEGF inhibitor, for the treatment of differentiated thyroid cancers that progress following standard therapies. This trial included 93 patients whose cancer had progressed following standard radioiodine therapy.
Anticancer responses were achieved in 14% of patients.
Disease stabilization was achieved in 67% of patients.
35% of patients achieved disease stabilization for at least six months.
The median duration of anticancer responses was 32 weeks.
Median progression-free survival was 40 weeks.
The most common side effects of therapy were diarrhea, increased blood pressure, fatigue, and weight loss.
The researchers concluded that motesanib diphosphate appears to provide significant anticancer activity, as well as long-lasting disease stabilization, in advanced thyroid cancer that progresses following standard therapies. Patients with progressive thyroid cancers may wish to speak with their physician regarding their individual risks and benefits of participating in a clinical trial further evaluating therapies such as motesanib diphosphate or other novel therapeutic approaches. Two sources of information regarding ongoing clinical trials include the National Cancer Institute (www.cancer.gov) and www.eCancerTrials.com.
Reference: Sherman S, Wirth L, Droz J-P, et al. Motesanib diphosphate in progressive differentiated thyroid cancer. New England Journal of Medicine.

Nexavar® Provides Anticancer Activity in Advanced Thyroid Cancer

2008-12-04T06:07:00.000-08:00

Nexavar® Provides Anticancer Activity in Advanced Thyroid Cancer

Nexavar® (sorafenib) provides cancer control among patients with thyroid cancer that has progressed following standard therapy. These results were recently published in the Journal of Clinical Oncology.
The thyroid is a gland in the throat that produces hormones mostly related to metabolic processes in the body. According to the American Cancer Society, approximately 37,340 new cases of thyroid cancer will be diagnosed in 2008 in the United States. Nearly two-thirds of all thyroid cancers occur in people between the ages of 20 and 55. Overall, thyroid cancer is considered to be a highly curable cancer, with 97% of individuals alive at least five years following diagnosis. Nearly 95% of all thyroid cancers are classified as differentiated thyroid cancers; the distinction refers to the type and characteristics of the cancer cells.
Standard therapy for thyroid cancer includes the removal of the thyroid, which is followed by drugs to suppress certain hormone levels related to the thyroid, and radiation plus iodine (radioiodine) therapy, which is targeted to eliminate any remaining thyroid cancer cells. Patients whose thyroid cancer progresses or fails following standard therapy have a 10-year survival rate of less than 15%. Thus, novel agents targeting progressive thyroid cancers are needed.
Researchers from the University of Pennsylvania recently conducted a clinical trial to evaluate Nexavar in the treatment of patients with advanced thyroid cancer who had stopped responding to iodine-based therapy. This trial included 30 patients who were treated with Nexavar for at least 16 weeks.
Partial anticancer responses occurred in 23% of patients.
Stabilization of cancer occurred in 53% of patients.
Total disease control (partial anticancer responses plus disease stabilization) occurred in 76% of patients.
Median progression-free survival was 79 weeks.
The researchers concluded that Nexavar provides significant anticancer activity among patients with thyroid cancer who have progressed following standard therapy, and that the results appeared to be improved compared with that of chemotherapy for patients with this disease. Patients with advanced thyroid cancer may wish to speak with their physician regarding their individual risks and benefits of participation in a clinical trial further evaluating Nexavar or other promising therapeutic agents. Two sources of information regarding ongoing clinical trials include the National Cancer Institute (www.cancer.gov) and www.eCancerTrials.com.
Reference: Gupta-Abramson V, Troxel AB, Nellore A, et al. Phase II trial of sorafenib in advaced thyroid cancer. Journal of Clinical Oncology [early online publication]. June 9, 2008.

New drug therapy may halt the spread of metastatic kidney cancer

2008-12-04T06:00:00.000-08:00

New drug therapy may halt the spread of metastatic kidney cancer

NEW YORK, NY - New data from an international, multicenter Phase III clinical trial has found that the experimental targeted therapy everolimus (RAD001) significantly delays cancer progression in patients with metastatic kidney cancer whose disease had worsened on other treatments. The study was led by Robert Motzer, MD, an attending physician at Memorial Sloan-Kettering Cancer Center (MSKCC), who will present the findings on May 31 at the annual meeting of the American Society for Clinical Oncology."This study has given us a new and clearly useful tool for treating renal cell tumors, and everolimus is an important step forward in terms of disease management and quality of life for patients living with this disease," said Dr. Motzer.Kidney cancer is among the ten most common cancers in both men and women. The American Cancer Society estimates that there will be about 54,390 new cases of kidney cancer diagnosed in the US in 2008, and that about 13,010 people will die from the disease.Everolimus, a once-daily oral therapy, targets the mTOR protein, which acts as a central regulator of tumor cell division, cell metabolism, and blood vessel growth. It is currently being evaluated for the treatment of several other cancers including lymphoma and neuroendocrine tumors.
“This study has given us a new and clearly useful tool for treating renal cell tumors, and everolimus is an important step forward in terms of disease management and quality of life for patients living with this disease. -- Robert J. Motzer, MD”More than 400 patients participated in this study, all of whom had disease that had progressed with currently available targeted therapies sunitinib and/or sorafenib. Patients were randomized to receive everolimus or placebo. After six months, 26 percent of patients in the everolimus group had disease that had not progressed, compared to only 2 percent of the placebo group. The average difference in progression free survival was four months for everolimus, compared to 1.9 months for the placebo group. In February, 2008, an independent monitoring committee stopped the Phase III trial after interim results were positive and allowed researchers to offer everolimus to the patients receiving placebo."For almost 20 years, we made no headway in the management of advanced kidney cancer," notes Dr. Motzer. "Recently, the identification of several new angiogenesis- targeted agents has provided us with new treatment options and an improved outlook for patients with advanced kidney cancer. Based on the results of this trial, everolimus could become another tool in our armamentarium and, in the future, kidney cancer is likely to be managed as a chronic disease with these types of treatment advances."Everolimus was well tolerated by patients and the most common side effects were mouth ulcers, anemia, skin rash and weakness.In addition to Dr. Motzer, contributors to the study included researchers from Institut Gustave Roussy in Villejuif, France; Georges Pompidou European Hospital in Paris, France; San Matteo University Hospital in Pavia, Italy; US Oncology, Baylor-Sammons Cancer Center/TOPA in Dallas, Texas; Azienda Ospedaliera in Perugia, Italy; Novartis Pharmaceuticals in Florham Park, New Jersey; and Hôpital Saint André CHU in Bordeaux, France. The study was funded by grants from Novartis Pharmaceuticals.

Kidney Cancer: New Drug Combination Shrinks Kidney Cancers

2008-12-04T05:53:00.000-08:00

Kidney Cancer: New Drug Combination Shrinks Kidney Cancers

Information courtesy of Duke University Medical Center News Office New Drug Combination Shrinks Kidney Cancers DURHAM, N.C. -- By using a new combination of two anticancer drugs, researchers at Duke University Medical Center have dramatically improved response rates of patients with metastatic kidney cancer, which is now generally considered incurable.The results suggest that combining the two drugs may slow the disease's progression in significant numbers of patients, although the drug combination is not a cure, said the researchers.In the study, 40 percent of patients who received the newly approved drug sorafenib together with the established drug interferon-alpha experienced "major shrinkage" of their kidney tumors and tumors that had metastasized, or spread elsewhere. A "major" response is generally is defined as 30 percent or greater shrinkage of all tumors in the body.In comparison, only 5 percent of patients who receive sorafenib alone show a major response, recent studies have shown. Similarly, just 10 percent to 15 percent of patients who receive only interferon alpha, considered the standard treatment for kidney cancer, show a major response."By combining the drugs, we are seeing more major responses in greater numbers of patients, but we don't yet know how long the responses will last," said Jared Gollob, M.D., associate professor of medicine and immunology at Duke. "There are great new drugs on the market with relatively low toxicity, but the question physicians now face is how to make them work better for patients."Gollob will present the findings, funded by the National Cancer Institute, June 3, 2006, at the American Society of Clinical Oncology annual meeting in Atlanta.Kidney cancer, also known as renal cell carcinoma, strikes an estimated 40,000 patients in the United States each year, representing 2 percent to 3 percent of all cancers diagnosed annually. Most cases of kidney cancer arise from unknown causes, but smoking and high blood pressure are known risk factors of the disease.According to Gollob, cancer therapy has two main goals: shrinking tumors and delaying the disease's progression, with as few side effects as possible. Although the goals are seemingly congruent, they often are not attainable with the same drug, Gollob said."Sorafenib alone has been shown to delay progression of kidney cancer, but it induces major responses in only a small percentage of patients," he said. "Interferon alpha has a higher major response rate in kidney cancer, but it does not necessarily slow disease progression. By combining the two therapies, we will hopefully accomplish both goals."In the current study, Gollob and colleagues at the University of North Carolina, Chapel Hill, used the new combination therapy on 31 patients with metastatic kidney cancer. Among patients who responded, the drug combination shrank both kidney tumors and tumors that had spread to the lungs, liver, pancreas and lymph nodes. The drug also shrank tumors in some patients who had failed to respond to interleukin-2, another drug commonly used for metastatic kidney cancer, the study showed.Conventional chemotherapy has proved to be a weak weapon against kidney cancer, because the very cells that the drugs attack are programmed to handle toxic substances, Gollob said. The job of renal "tubule" cells is to pump toxic substances from the body into the urine, so these cells are well-equipped to pump out chemotherapy before it can perform its task. Likewise, it is believed that the necessarily hearty constitution of renal cells – tough by nature, given their job -- also makes them resistant to anticancer drugs.Combined therapies have an advantage over individual therapies because the two drugs typically attack cancer from two angles at once, by targeting different cellular mechanisms, Gollob said. Sorafenib acts by inhibiting two proteins, one that boosts the growth of the cancer cells themselves and one that sustains blood vessels which nourish the tumors. The Food and Drug Administration approved sorafenib in December, 2005 for use in kidney cancer, and it is sold under the trade name Nexavar.Interferon alpha also acts in two ways -- by directly attacking cancer cells, and by stimulating the immune system to battle cancer. On the market for 20 years, the drug is used to treat a variety of cancers, including melanoma.The Duke study showed the combination of drugs can be given safely and on an outpatient basis, meaning patients receive treatment in the doctor's office without a hospital stay, he said. Sorafenib is a pill, while interferon alpha is an injection given under the skin three times a week.Patients in the Duke study experienced the same type and degree of side effects as would be expected among patients receiving either drug by itself, Gollob said. Sorafenib can cause fatigue, hair loss, diarrhea and skin rash. Interferon alpha can cause fatigue, weight loss, and periodic flu-like symptoms. Patients experienced varying degrees of these symptoms in the study.Gollob said the next step is to conduct a randomized clinical trial to determine if the drug combination extends progression-free survival, over and above the survival currently seen with sorafenib alone

Colon Cancer: Experts Debunk the Myths

2008-12-04T05:49:00.000-08:00

Colon Cancer: Experts Debunk the Myths

12 myths about colon cancerU-M experts debunk fears, misconceptions about this diseaseANN ARBOR, Mich-Colon cancer is the second leading cause of cancer death in the United States, and the No. 1 cause of cancer death among non-smokers. More than 150,000 Americans will be diagnosed with colon cancer this year, and 52,000 will die from the disease. It doesn't have to be that way."Most colorectal cancers are predictable by early diagnosis and screening. If colonoscopy can identify a problem early, we could completely prevent colorectal cancer," says D. Kim Turgeon, M.D., clinical associate professor of gastroenterology at the University of Michigan Medical School.In fact, colorectal cancer screening prevents more deaths due to early detection than breast or prostate cancer screening. Here, experts from the University of Michigan Comprehensive Cancer Center address some of the common myths and misconceptions about colorectal cancer.Myth 1: Colon cancer is a white man's disease. Truth: Colon cancer affects both men and women equally, and it affects people of all races. In 2007, the American Cancer Society estimates, 55,290 men and 57,050 women will be diagnosed with colon cancer. About equal numbers will die from the disease: 52,000 Americans altogether. The No. 1 risk factor for colon cancer is age.Myth 2: I don't have any symptoms, so I must not have colon cancer. Truth: "One of the most common misconceptions is that symptoms will be evident if a person has colorectal cancer. In fact, the most common symptom is no symptoms at all," says Emina Huang, M.D., assistant professor of surgery at the U-M Medical School. More than half of people diagnosed with colon cancer have no symptoms. Symptoms such as a change in stool, rectal bleeding, abdominal pain and unexplained weight loss can all signal colon cancer. But once these symptoms begin to develop, it may be a sign of more advanced disease. Half of people diagnosed after symptoms develop will die from colon cancer. Myth 3: Colonoscopy is difficult to prepare for.Truth: Preparing for a colonoscopy involves cleaning the colon with the help of prescription and over-the-counter medications. Typically these are liquid drinks that must be consumed a day or two before the procedure. "People shouldn*t be afraid of it because they don't want to drink the laxative. There are many more options so you can find something that is tolerable," Turgeon says. Ask your doctor or pharmacist about your options.Myth 4: Colonoscopy is unpleasant and uncomfortable.Truth: It's not as bad as you think. Most people agree the prep is the worst part (see Myth 3). During the actual procedure, patients are sedated to eliminate discomfort. The procedure itself takes 15-30 minutes and you can resume normal activities the next day.Myth 5: I saw Katie Couric get a colonoscopy on the Today Show, so I should get one too.Truth: Colonoscopy screening is recommended for men and women beginning at age 50, unless other risk factors exist. If you're 50 or older, talk to your doctor about screening. If you are younger than 50 but have other risk factors * such as family history, obesity, smoking, ulcerative colitis or Crohn's disease * talk to your doctor about your screening needs. But remember, age is the most significant risk factor for colon cancer.Myth 6: Colonoscopy is the only way to screen for colon cancer.Truth: There are several screening options for colorectal cancer, including flexible sigmoidoscopy, fecal occult blood test and double-contrast barium enema. But colonoscopy is considered the gold standard. It detects more cancers, examines the entire colon, and can be used for screening, diagnosis and removing polyps in one visit.Myth 7: A polyp means I have cancer.Truth: Polyps are benign growths that, if left unchecked, have the potential to develop into cancer. Polyps can be easily removed during colonoscopy. Not all polyps are pre-cancerous.Myth 8: Colonoscopy is just a screening technique. Truth: Colonoscopy is an all-in-one tool. It can find and remove polyps and small cancers all during one procedure. If your colonoscopy reveals a polyp, your doctor will remove it immediately. By removing the polyp at this stage, it prevents it from becoming cancerous. If colonoscopy reveals cancerous lesions, further treatments may be necessary.Myth 9: If I have colon cancer, it means I am dying.Truth: When colon cancer is caught early, it has a 95 percent survival rate. That's why screening is so important. Once colon cancer has spread to the liver, it's usually deadly, with only a 9 percent survival rate. But even then, treatments are improving. Radiation oncologists at U-Mhave developed a method to shrink tumors that spread to the liver, in some cases allowing them to be removed with surgery. This has led to higher survival rates even in the most advanced cases.Myth 10: Surgery will be disfiguring and recovery painful.Truth: New surgical advances allow for minimally invasive procedures that leave only a small scar. Patients undergoing laparoscopic surgery may have an easier recovery than patients who have open surgery. Some evidence suggests cancer control is better with a minimally invasiveapproach. Myth 11: If I have colon surgery, I'll need a colostomy bag.Truth: A colostomy, in which surgeons create an artificial, external method to collect excrement, is rarely done anymore. Surgical techniques have improved so that the cancer can be effectively removed while sparing the rectum. In the past, cancers within 4 inches of the anus routinely required removing the anus for effective surgical control. Now, 80 percent of these cancers may be effectively removed whilesparing the anus.Myth 12: Few research advances focus on colon cancer.Truth: Much exciting research is occurring in colon cancer. At U-M, research has focused on improving radiation techniques, including using radiation to shrink tumors that have spread to the liver. Researchers are also working with colon cancer stem cells, the small number of cellswithin a tumor that fuel its growth. It's believed that identifying the cancer stem cells will allow more effective drugs to be developed. Other research is looking at multiple genes involved in colon cancer and at improving screening techniques so more cancers can be detected early.This includes searching for markers in blood, stool or urine that might provide an easier screening tool to early signs of colon cancer. In the area of prevention, researchers are looking at the effects of curcumin (found in curry), resveratrol (found in red wine), ginger and the Mediterranean diet on the growth and development of colon cancer.

Colon Cancer: Research Investigates the Role of Combined Surgery for Colon and Liver Involvement

2008-12-04T05:44:00.000-08:00

Colon Cancer: Research Investigates the Role of Combined Surgery for Colon and Liver Involvement

WASHINGTON, D.C. – A single surgery to remove cancer from both the colon and the liver to which it has spread may be better in some cases than the current standard treatment of two separate surgeries with chemotherapy in between, according to a study led by Duke University Medical Center researchers. Simultaneous surgeries on the colon and liver may reduce the length of a patient's stay in the hospital and potentially lessen the risk of surgical complications without compromising long-term survival, according to the study. "In about a third of patients who are newly diagnosed with colorectal cancer, the cancer has already spread to the liver," said Bryan Clary, M.D., a surgical oncologist at Duke and senior investigator on the study. "The standard approach for these patients has been to remove the colorectal cancer and give them chemotherapy afterwards, waiting to remove liver tumors later if patients do not appear to be developing disease elsewhere in the body. These findings suggest there might be an alternative that is as safe and may even lead to better outcomes." Colorectal cancer is the third most common cancer in both men and women in the United States, and it is the second-leading cause of cancer-related deaths in this country. The researchers presented their findings on Saturday, March 17, in a plenary session at the annual meeting of the Society of Surgical Oncology in Washington, D.C. The study was funded by the National Institutes of Health and Duke's Department of Surgery. The researchers looked at outcomes for 610 patients who had undergone either simultaneous or separate surgeries for removal of colorectal cancer from the colon or rectum and from the liver, where it had spread. The patients were treated at three academic medical centers -- Duke, the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University and the University of Texas M.D. Anderson Cancer Center -- between 1985 and 2006. "We looked at factors including surgical complications and survival data among the groups and found that in certain patient groups, simultaneous surgery was as safe as separate surgeries, could shorten the length of hospital stay and might lead to fewer surgery-related complications," said Srinevas Reddy, M.D., a general surgery resident at Duke and the study's lead author. Chemotherapy is used in addition to cancer surgery to kill cancer cells that may reside undetected in other parts of the body. Patients having separate surgeries commonly receive chemotherapy both after their initial colon surgery and then again after their liver surgery, Clary said. But the powerful drugs used in chemotherapy can have a toxic effect on other organs, including the liver, that may increase the risk of liver surgery, he said. The researchers also discovered that chemotherapy administered after surgical removal of cancerous liver segments favorably affected survival rates, whether or not that surgery was done alone or in conjunction with colorectal surgery. Chemotherapy administered before liver surgery showed no benefits, Clary said. The researchers found that simultaneous surgery was only as safe as standard treatment among patients who required a minimal amount of liver to be removed. But for those whose cancer was more extensive requiring larger amounts of liver to be removed, separate surgeries remain the better treatment choice. "For patients who require a great deal of liver to be removed, the complication risks associated with such extensive surgery outweigh the benefits of doing it all at once," Clary said. About half of patients with colorectal and liver tumors could be eligible for the simultaneous surgery, which could translate to about 25,000 patients per year, he said. "This study is important because it shows that patients with liver metastases at the time of their original colorectal cancer diagnosis might benefit from evaluation at a multidisciplinary center that includes not only medical oncologists and surgical oncologists skilled in colorectal surgery, but also surgeons capable of performing liver surgery," Clary said. Other Duke researchers involved in this study include Andrew Barbas, Kirk Ludwig, Michael Morse and Christopher Mantyh. Timothy Pawlik, Ana Gleisner, Lia Assumpcao and Michael Choti of Johns Hopkins and Dario Ribero, Daria Zorzi, Eddie Abdalla and Jean-Nicolas Vauthey of M.D. Anderson also participated in the research.

Blood Vessel Inhibitor Shows Promise Against Metastatic Thyroid Cancer

2008-12-04T05:41:00.000-08:00

Blood Vessel Inhibitor Shows Promise Against Metastatic Thyroid Cancer

Blood Vessel Inhibitor Shows Promise Against Metastatic Thyroid CancerResearchers also find evidence tying a genetic mutation to clinical outcomeThyroid cancer that has spread to distant sites has a poor prognosis, but an experimental drug that inhibits tumor blood vessel formation can slow disease progression in some patients, a research team led by investigators from The University of Texas M. D. Anderson Cancer Center reports in the July 3rd edition of The New England Journal of Medicine.The investigational drug, motesanib diphosphate, is a VEGF inhibitor, a biologic agent that targets receptors on a protein known as vascular endothelial growth factor (VEGF). VEGF is instrumental in angiogenesis (formation of new blood vessels), a process that allows tumors to grow and spread. Study lead author Steve Sherman, M.D., chair and professor of M. D. Anderson's Department of Endocrine Neoplasia and Hormonal Disorders, noted strong evidence that VEGF receptors play an important role in metastatic thyroid cancer, a disease with few treatment options."There is no standard accepted chemotherapy for advanced metastatic differentiated thyroid cancer, and response rates have typically been 25 percent or less," Sherman said. "Most patients are not treated with systemic chemotherapy because the limited benefit rarely justifies the side effects. Treatment of thyroid cancer has been a completely unmet need."Sherman, colleagues in 10 countries, and scientists from Amgen, which is developing motesanib diphosphate (AMG 706), planned and conducted one of the largest clinical trials ever done for metastatic thyroid cancer. Of the 93 patients with rapidly progressing cancer who were enrolled in the study, 49 percent had a positive response. From that group 14 percent had their tumors shrink and 35 percent had their tumors stabilize for more than 24 weeks. Median progression-free survival was estimated to be 40 weeks.Genetic analyses of 25 patients indicated that those with a specific mutation known as BRAF V600E in their tumors had a better response to motesanib diphosphate than did those without the mutation. Additional research is needed on this genetic connection, but the early results are a good start, Sherman said."Finding that patients whose tumors bear a particular mutation were more likely to respond to the drug is an example of where we would like to head in our research," Sherman said. "This is the first of the various thyroid cancer trials to identify specific mutations that might allow us to individualize or personalize therapy."Only 15 percent survive for 10 yearsFor most patients, papillary or follicular thyroid carcinomas are not lethal. Surgical removal of the thyroid-often followed by treatment with radioactive iodine-and lifelong thyroid hormone therapy are usually sufficient. But about 15 percent of patients will develop distant metastases, typically to the lungs. A small percentage of these patients will respond well to radioactive iodine treatment and survive for many years. But for others, the estimated median survival duration is two to four years, with a 10-year survival rate of less than 15 percent.Multinational trialForty-two institutions internationally participated in the clinical trial, including an important collaboration with the Institut Gustave Roussy, M. D. Anderson's sister institution in Villejuif, France. The study enrolled patients with progressive, locally advanced or metastatic, radioiodine-resistant thyroid cancer. Study participants took 125 milligrams of oral motesanib diphosphate once a day for 48 weeks or until they experienced unacceptable side effects or disease progression. The primary treatment outcome was radiographic evidence of tumor shrinkage as determined by an independent review. The researchers also analyzed the duration of tumor response, progression-free survival, and drug safety.Stable Disease in 67 percent of patientsThe researchers monitored tumor response with computed tomography (CT) or magnetic resonance imaging (MRI) scans of the neck, chest, and abdomen every eight weeks or in response to signs of disease progression. Partial or complete responses to the drug were evaluated by independent review and confirmed with repeat scans four or more weeks later.Thirty-two patients completed the full 48 weeks of treatment. Motesanib diphosphate was discontinued in 35 patients because of disease progression and in 12 patients because of drug-related adverse events. Five patients died, and nine withdrew for various administrative or personal reasons.Thirteen patients (14 percent) achieved an objective partial response to the drug. Sixty-two patients (67 percent) experienced stable disease during the study; 33 of these (35 percent) achieved durable stable disease for at least 24 weeks. Nine patients (10 percent) had unconfirmed partial responses, which were classified as stable disease. Seven patients (8 percent) experienced only disease progression, and no response information was available for 11 patients (12 percent) because of incomplete or uninterpretable radiographic scans.Eighty-seven patients (94 percent) experienced at least one treatment-related adverse event. The most common events were diarrhea, hypertension, fatigue, and weight loss. In 51 patients, the adverse events were classified as severe (grade 3). Five patients had grade 4 (life-threatening) adverse events, including low calcium levels, high levels of uric acid, low potassium levels, cerebral hemorrhage, mental confusion, agitation, or decreased urine production. Two patients whose disease had progressed died of pulmonary hemorrhage.Phase I Program Revealed Drug's PotentialThe drug's potential benefit for advanced thyroid cancer was identified by researchers in M. D. Anderson's innovative Phase I Clinical Trials Program, led by Razelle Kurzrock, M.D., chair and professor of M. D. Anderson's Department of Investigational Cancer Therapeutics.The program typically has about 80 Phase I clinical trials under way, testing new targeted therapies for the first time in cancer patients. In addition to closely monitoring a new drug for safety, the program tests it against many different types of cancer."The molecular targets of new potential drugs are important for cancer in general, but at this stage the drugs aren't specific for any one type of cancer, so we include patients with different types on these early studies," Kurzrock said. "This gives us a unique opportunity to see response signals for the first time in specific cancers, flagging a drug for more extensive study in phase II or phase III clinical trials."In the Phase I trial led by Roy Herbst, M.D., Ph.D., professor in M. D. Anderson's Department of Thoracic/Head and Neck Medical Oncology, two out of five study patients with metastatic differentiated thyroid cancer responded to the drug, which was then taken directly to Sherman's phase II study. Other therapies are being rapidly transitioned from Kurzrock's program to Sherman's or other groups to establish efficacy as soon as evidence of response is seen in the phase I trial.The phase II trial was funded by Amgen, Inc. Co-authors with Sherman are Lori J. Wirth, M.D., of the Dana-Farber Cancer Institute in Boston; Jean-Pierre Droz, M.D., of the Centre Leon Berard in Lyon, France; Michael Hofmann, M.D., Ph.D., of the Medical School Bern in Bern, Switzerland; Lars Bastholt, M.D., of Odense University Hospital in Odense, Denmark; Renato G. Martins, M.D., of the University of Washington in Seattle; Lisa Licitra, M.D., of the Istituto Nazionale dei Tumori in Milan, Italy; Michael J. Eschenberg, Yu-Nien Sun, Ph.D., Todd Juan, Ph.D., and Daniel E. Stepan, M.D., all of Amgen, Inc. in Thousand Oaks, Calif.; and Martin J. Schlumberger, M.D., of the Institut Gustave Roussy, University Paris Sud in Villejuif, France, on behalf of the Motesanib Thyroid Study Group. 07/02/08

Melanoma Research: Interleukin-12 Indicates Survival Prospects for Melanoma Patients

2008-12-04T05:35:00.000-08:00

Melanoma Research: Interleukin-12 Indicates Survival Prospects for Melanoma Patients

Higher blood levels of an immune system protein predict poor survival prospects for melanoma patients with advanced disease, researchers at The University of Texas M. D. Anderson Cancer Center report today at the annual meeting of the American Association for Cancer Research.Their finding that elevated levels of interleukin-12 (IL-12) are a marker of poor prognosis also points to a molecular explanation for a long-known risk factor for melanoma patients - older age.Among 150 patients with Stage III melanoma, the study found that the highest levels of IL-12 are associated with a nearly 5-fold risk of death. Although older stage III patients also had an elevated risk of death, age was not a prognostic factor independent of IL-12."Melanoma in some cases can be vulnerable to attack by a patient's immune system," said senior researcher Jeffrey Lee, M.D., professor in M. D. Anderson's Department of Surgical Oncology. "What we've found could be evidence of a dysfunctional immune response that actually fuels the growth of melanoma."Blood-born IL-12 provides both an accessible prognostic marker and a key connection to other signaling proteins; IL-12 as well as these related proteins already have been targeted by antibody therapies in certain autoimmune disorders, Lee said.The research team examined age, stage of disease, and IL-12 levels in 658 melanoma patients - 445 with stage I or II disease, 150 with stage 3 and 63 at stage IV."First, we found that IL-12 levels increase with age," says first author and study presenter Yun Shin Chun, M.D. The mean levels of the protein increased at every age level above age 40. (See Chart) Age, disease stage and IL-12 levels were then analyzed separately as prognostic factors. Increases in all three were associated with poor overall survival."When we analyzed these three factors together, only stage of disease and IL-12 levels were independent predictors of overall survival," Chun said. Age dropped completely out of the picture. Stage of disease was the most powerful prognostic factor. Both IL-12 and IL-23 are cytokines, proteins that tell cells and other proteins what to do. Cytokines like IL-12 and IL-23 are particularly vital to immune system function. The general level of a person's immune function declines with age, Lee said, as do the levels of most cytokines. The rise of IL-12p40 with age is a relative anomaly.Chun, Lee and colleagues are investigating IL-12's connection to the tumor promoting IL-23 and about 30 other cytokines in high-risk melanoma patients. Some of the suspect cytokines, including IL-12 and IL-23, already are targeted by therapies used autoimmune disease, Lee noted.Funding for the research was provided by The Marit Peterson Fund for Melanoma Research, and the M.D. Anderson's SPORE grant in melanoma from the National Cancer Institute.

Mohs Surgery for Skin Cancer

2008-12-04T05:30:00.000-08:00

Mohs Surgery for Skin Cancer

Mohs surgery is named after its developer, Dr. Frederic E. Mohs. In the 1930’s, Dr. Mohs developed a method that “fixed” (preserved) and stained tissue directly on the patient. A chemical paste was applied to the tumor and was allowed to penetrate to a few millimeters depth. This required 6-24 hours, after which, the area was surgically removed and the entire peripheral and deep margin was examined for residual tumor. This process was repeated over days until all margins were found to be free of tumor. Defects resulting from Mohs surgery were generally allowed to granulate (fill-in) on their own and not sewn closed. This method had the disadvantages of being painful and time consuming (only one “stage” could be done per day) and the granulated wound often produced an ugly scar. Today, this technique has been modified; no chemicals are applied directly to the patient, multiple stages can be performed in hours, and the defect can be closed immediately if desired. The original concept of examining the entire peripheral and deep margin of the excised specimen remains.Background:When a routine excision is done, the specimen is processed by “breadloafing.” Like a loaf of bread is sliced, sections are taken vertically through the specimen at 3-4mm intervals and these sections are examined under the microscope. For practical reasons, only a few sections or “slices” are examined. Most skin cancers grow like the roots of a tree with extension of the tumor to the sides and downward. With breadloafing, tumor roots can be missed if they happen to grow in the 3-4mm gap between sections. In fact, less than 1% of the true peripheral and deep margin is examined by this method. This limitation is addressed by Mohs surgery.Technique:It is beyond the scope of this article to explain the Mohs procedure precisely step-by-step. However, the following are critical points that lead to the examination of theoretically 100% of the peripheral and deep surgical margin and conservation of surrounding normal tissue. After a pre-operative consultation has been completed and informed consent obtained:- The lesion is numbed with local anesthesia.- Tumor that can be seen or felt is removed with a curette or scalpel.- A thin, saucer-like layer of tissue is excised just a few millimeters around and underneath the resulting defect.- This layer is divided into pieces and inked. - A map is drawn that shows each piece in relation to the patient. - Each piece is frozen, mounted in a waxy substance and very thinly sectioned horizontally starting from the underside of the specimen. This is done by the Mohs histotechnician.- The slides are processed and examined by the Mohs surgeon. If tumor roots are seen on the slide, they extend beyond the underside of the tissue that was excised, and therefore, more tumor remains in the patient. The tumor site on the slide is matched to the previously drawn map and the precise location on the patient is identified. The process is then repeated and another saucer-like layer is removed, but only from the area that showed residual tumor. In this way, surrounding normal tissue is conserved.When no residual tumor is seen, the tumor is deemed completely removed and the defect can be repaired if desired. Often, the Mohs surgeon can repair the defect immediately. Alternatively, when the defect is more complex, closure can be coordinated with other physicians who specialize in reconstructive surgery such as plastic surgeons, facial plastic surgeons, otolaryngologists, or ophthalmologists. Cancers treatable by Mohs surgery:Mohs surgery has been used to excise many different types of skin cancer. However, BCCs and SCCs, the two most common forms of skin cancer, are the cancers most often treated by Mohs surgery. The treatment of melanoma by Mohs surgery is controversial at this time.Indications:Mohs surgery is a specialized technique that is not indicated for the treatment of every BCC or SCC and is most appropriately used under certain, well-defined circumstances. The majority of BCCs and SCCs can be treated with very high cure rates by standard methods including electrodessication and curettage (ED&C), local excision, cryosurgery (freezing) and irradiation. These are fairly quick and easy and can often be performed in the local physician’s office. Large or recurrent lesions or those that arise at sites where recurrence is more likely or where tissue conservation is important are most aptly treated with Mohs surgery. This includes many areas of the face. Training:The Mohs surgeon must be proficient in all aspects of the procedure including anesthesia, anatomy, surgery, pathology and reconstruction. Knowledge of these and other aspects of the procedure and most importantly, surgical judgement, are usually not acquired during the course of residency training and often require additional specialized fellowship training. Summary:Mohs surgery is a specialized surgical technique that results in high cure rates when used to remove skin cancers such as BCCs and SCCs. It is especially useful in lesions that, due to their size, location or other factors are at higher risk of recurrence if treated by standard methods or arise in areas where tissue conservation is important. It is not indicated for use in all cancers of the skin. Mohs surgery is labor intensive and requires a large support staff and specialized training in the technique.

Skin Cancer Research Suggests Novel way of Preventing Disease

2008-12-04T05:24:00.000-08:00

Skin Cancer Research Suggests Novel way of Preventing Disease

New insight into skin-tanning process suggests novel way of preventing skin cancerFindings from a study led by researchers at Dana-Farber Cancer Institute and Children's Hospital Boston have rewritten science's understanding of the process of skin tanning – an insight that has enabled them to develop a promising way of protecting fair-skinned people from skin cancer caused by exposure to sunlight. The study, to be published by the journal Nature in its Sept. 21 issue, involved giving tans to specially engineered mice, not by exposing them to ultraviolet rays in sunlight (the usual route to a tan), but by applying a cream that switched on the tanning machinery in their skin cells. Because people who tan easily, or have naturally dark skin, are far less likely to develop skin cancer than fair-skinned individuals – who tend to get sunburns rather than tan – the findings suggests that medicinally-induced tans can protect at-risk individuals from the disease. "The study involved using a small molecule to essentially mimic the process that occurs when skin cells are struck by ultraviolet light from the sun," says the study's senior author, David E. Fisher, MD, PhD, director of the Melanoma Program at Dana-Farber and a professor in pediatrics at Children's Hospital Boston. While the compound used in the study has not yet been tested in humans, the results "demonstrate the principle that actual tanning can be 'rescued' by recognizing the normal pathway and the precise step where it is blocked in people who do not tan well," he remarks. Melanoma is the fastest-increasing form of cancer in the world, accounting for 62,000 new cases in the United States every year and nearly 8,000 deaths, according to the American Cancer Society. It occurs when pigment-making skin cells called melanocytes begin dividing rampantly as a result of damage to their DNA. If melanoma tumors are detected and surgically removed before their cells spread to other parts of the body, patients have an almost 100 percent chance of surviving. The odds drop sharply, however, if treatment doesn't begin until the disease has spread, or metastasized. One trigger for melanoma development appears to be ultraviolet (UV) light from the sun, which can damage the skin's DNA. For most of human history, fair-skinned people, who tan poorly, occupied regions with low sun exposure, such as Nordic areas with winter months of darkness. As human populations have scattered throughout the globe, increasing numbers of fair-skinned people have come to live in sunny climes, and melanoma and other skin cancer rates have shot up. The new Dana-Farber report grew out of efforts by Fisher's laboratory to study melanoma in mice whose fair skin stemmed from the same genetic roots as fair-skinned people. The researchers succeeded in generating red-haired mice whose light skin contained melanocytes, but when the mice were subjected to low levels of UV radiation, they did not tan. Nor did they tan when the UV levels were raised slightly; but when they increased slightly more, the animals got skin sunburns. "These animals couldn't tan," Fisher remarks, who is also a professor of pediatrics at Harvard Medical School. "We'd proven in a rigorous genetic system what people have known for hundreds of years: Redheads don't tan well." This suggested that the mice were a good model for fair-skinned humans. It also led researchers to propose a new theory about how sun exposure triggers pigmentation in people who tan easily. If the researchers' theory was correct, it should be possible to induce dark pigmentation in fair-skinned mice with specific, targeted drugs. The most common origin of red hair and pale skin in humans is found in a tiny pouch-like receptor, called MC1R, on the surface of melanocytes. When the hormone MSH — for Melanocyte Stimulating Hormone — drops into the pouch, it causes a surge in the melanocyte's production of the chemical cAMP. cAMP then stimulates melanocytes to turn on a large number of genes, causing a pigment called melanin to be produced. If cAMP levels are low, the melanocytes make red/blond melanin. If cAMP levels are high, they make brown/black melanin. The melanin is eventually discharged from melanocytes and taken up by keratinocytes. MC1R is shaped differently in red-haired people, so that MSH cannot stimulate it strongly. The result is that cAMP production stays at low levels. Less cAMP means less red/blond pigment production, which results in fair skin. Many scientists have theorized that tanning occurs when ultraviolet radiation strikes the nuclei of melanocytes, causing DNA damage that prompts the melanocytes to produce pigment. This supposition, however, conflicted with the results of Fisher's experiments. "Our work suggested that a peculiarity in the MC1R receptor on melanocytes is responsible for a failure to tan," Fisher relates. "But that sort of change on the cell surface shouldn't impede UV radiation from reaching the melanocyte's DNA." If Fisher's results were correct, the traditional picture of the biology of tanning was wrong. In a series of experiments, Fisher's team found evidence to bolster their theory, leading to a new model of how tanning occurs. The experiments demonstrated that, rather than acting directly on the nuclei of melanocytes, UV radiation acts on keratinocytes (the most abundant as well as superficial cells in the skin), causing them to produce and secrete MSH, which attaches to adjacent melanocytes and starts the pigment-making process. While Fisher's model adequately explains why redheads don't tan, it isn't the only possibility. "Suppose that during the embryonic or fetal period MC1R never activated cAMP production in developing melanocytes," Fisher proposes. "Would mature melanocytes then be permanently 'crippled,' unable to respond to UV, regardless of how its signals were transmitted?" One way to disprove that 'permanently crippled' scenario would be to see if melanocytes with abnormal MC1R receptors can be coaxed into producing pigment in adult mice. To attempt this, Fisher and his associates treated the skin of red-haired, fair-skinned mice with a compound known to increase cAMP levels. The compound, called forskolin, is derived from the root of the forskohlii plant found in India. The mice involved in the experiment turned dark, proving that melanocytes in redheads aren't inherently unable to make pigment if appropriately stimulated. Further experiments showed that not only can red-haired mice be given tans without exposing them to UV light, but this sunless tanning process is virtually indistinguishable from that in dark-haired mice that tan naturally."When keratinocytes absorb melanin pigment, the pigment isn't randomly distributed within them," Fisher explains. "It forms arcs that look like tiny umbrellas over the keratinocyte's nucleus. When we artificially caused our red-haired mice to tan, the pigment in their keratinocytes made the exact same umbrella-like pattern."The Dana-Farber researchers also showed that tans acquired through forskolin conferred significant protection against skin cancer caused by exposure to UV light. Fisher notes that while it is unknown whether forskolin will penetrate deeply enough in human skin to activate melanocytes, these results suggest that the search for other substances that do reach deep into the skin may well have the same pigmentation effects in people."These studies suggest that a drug-induced 'rescue' of the tanning mechanism may correspondingly rescue at least some aspect of skin cancer protection," Fisher observes. "Such sunless tanning may also dissuade sun-seeking behaviors, which undoubtedly contribute significantly to high skin cancer incidence."

Cancer Genetics: Massive cancer gene search finds potential new targets in brain tumors

2008-12-04T05:21:00.000-08:00

Cancer Genetics: Massive cancer gene search finds potential new targets in brain tumors

Results validate ambitious NIH-funded project to uncover cancer mutationsBOSTON--An array of broken, missing, and overactive genes -- some implicated for the first time -- have been identified in a genetic survey of glioblastoma, the most common and deadly form of adult brain cancer, report scientists from Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard, together with their collaborating investigators at 18 institutions and organizations.The large-scale combing of the brain cancer genome confirms the key roles of some previously known mutated genes and implicates a variety of other genetic changes that may be targets for future therapies.The findings, posted online by Nature on Thursday, Sept. 4, help solidify and expand the "parts list" of genetic flaws linked to glioblastoma multiforme (GBM), the incurable brain tumor that Sen. Edward M. Kennedy is battling. Lynda Chin, MD, at Dana-Farber and Harvard Medical School (HMS) and Matthew Meyerson, MD, PhD, at Dana-Farber, HMS, and Broad, co-led the writing effort for the first summary of data from the $100 million pilot project of The Cancer Genome Atlas (TCGA), funded by the National Institutes of Health (NIH). The data are released to the public at TCGA's website as they are generated.Systematic multi-dimensional genomic studies of patient samples of glioblastoma began in 2006 as the first TCGA program. The pilot is designed to determine the feasibility of a full-scale effort to systematically explore the universe of genomic changes involved in all types of human cancer and to demonstrate the values of such efforts in advancing cancer research and improving patient care.The current report in Nature summarizes the interim analyses of data gathered in the GBM pilot study. "The findings of significant mutations in genes that have implications for therapeutic development illustrate precisely how unbiased and systematic cancer genome analyses can lead to paradigm-shifting discoveries," said Chin, who chairs the GBM disease working group within TCGA.An exciting example, Chin said, is an unanticipated observation of a link between DNA methylation of specific genes and DNA repair defects, leading to a hypothesis about a potential mechanism of resistance to a common chemotherapy drug used for brain cancer.The Nature paper complements a parallel study by Johns Hopkins researchers of 22 GBM tumors, which was also published on Sept. 4 in the journal Science."These data show that this approach, of looking at large numbers of tumors and a large number of genetic factors, can be done and the results are really valuable," said Meyerson. "We have made significant novel findings, and the reproducibility of the data is high."Collaborating teams analyzed 206 specimens of glioblastoma tissue donated by patients at four medical centers. Their approach was "multidimensional" -- looking for several categories of flaws simultaneously. These included mutations -- "typos" in the DNA code of a gene that alters its function; too many or too few copies of a given gene; damage to chromosomes causing loss or dislocation of pieces; gene activity that is higher or lower than normal; and changes in DNA methylation -- turning genes on or off without affecting their structure.The researchers also had access to information on how the patients who donated the samples had fared, including how they responded to certain drugs.Automated machines at three Genome Sequencing Centers, including the Broad Institute center led by Eric S. Lander, Broad Institute director, were set to work reading the DNA messages in the cancer cells' nuclei. Of the roughly 20,000 protein-coding genes in the tumor cells, 601 genes were selected by the GBM disease working group for detailed sequencing -- determining the order of chemical "letters" in the DNA -- and comparison. A second installment of genes is already being sequenced, and Chin and her group are working on additional gene lists for mutational analyses.Five major gene mutations have previously been identified in glioblastoma cells; the new sequencing effort revealed three that hadn't been discovered. One mutation affects the NF1 gene, which causes neurofibromatosis. A second mutation is in the ERBB2 gene known to be involved in breast cancer. The third affects a gene in the PIK3 signaling pathway that is abnormally activated in a number of cancers, but this particular gene, PIK3R1, had been only rarely implicated in any cancer. "Each of these mutated genes defines a new target for glioblastoma treatment," said Meyerson.As they examined the data, the researchers found that three signaling pathways -- networks of genes and proteins that act together to carry out a cellular function -- were disrupted in more than three-quarters of the GBM tumors. They are known as the cyclin-dependent kinase/retinoblastoma pathway that regulates cell division; the p53 tumor suppressor pathway, which is involved in response to DNA damage and cell death; and the receptor tyrosine kinase pathway that carries signals that control cell growth.Chin said that the most exciting finding is that this multipronged study design also enabled the scientists to make a potentially important connection between a methylation change in the glioblastoma cells and which drugs should be used for treatment. Brain tumors that contain a methylated, or silenced, form of a gene known as MGMT are known to be more susceptible to cancer drug temozolomide (Temodar). Therefore, Temodar is routinely given along with radiation to patients with MGMT methylation.But the analysis of methylation in the glioblastoma tumors, when matched with the patients' medical history, revealed a cautionary sign. When such patients were treated with Temodar and subsequently had a recurrence of the tumor, it was very likely to become resistant to treatment because of "hypermutation" -- an increased rate of gene changes that led to the tumor's ability to evade the drugs."This could have immediate clinical applications," said Chin.The discoveries in the paper are only the tip of an expected iceberg, said the authors. The "most powerful impact" is expected to come from further research studies carried out by scientists who make use of the data released freely by TCGA, they said.More than 21,000 new cases of brain cancer are expected to be diagnosed in the United States this year, and more than 13,000 people are likely to die from the disease."These impressive results from TCGA provide the most comprehensive view to date of the complicated genomic landscape of this deadly cancer," said NIH Director Elias A. Zerhouni, M.D. "The more we learn about the molecular basis of glioblastoma multiforme, the more swiftly we can develop better ways of helping patients with this terrible disease. Clearly, we should move ahead and apply the power of large-scale, genomic research to many other types of cancer."Chin is co-principal investigator of a TCGA center with Raju Kucherlapati of HMS, and Meyerson is principal investigator of a TCGA Cancer Genome Characterization Center at the Broad Institute. Chin is the scientific director of the Belfer Cancer Genomics Center in the Center for Applied Cancer Science at Dana-Farber, and Meyerson directs the Center for Cancer Genome Discovery at Dana-Farber.The research was funded by grants from the NIH.Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.The Broad Institute of MIT and Harvard was founded in 2003 to bring the power of genomics to biomedicine. It pursues this mission by empowering creative scientists to construct new and robust tools for genomic medicine, to make them accessible to the global scientific community, and to apply them to the understanding and treatment of disease. The Institute is a research collaboration that involves faculty, professional staff and students from throughout the MIT and Harvard academic and medical communities. It is jointly governed by the two universities. Organized around Scientific Programs and Scientific Platforms, the unique structure of the Broad Institute enables scientists to collaborate on transformative projects across many scientific and medical disciplines. For further information about the Broad Institute, go to http://www.broad.mit.edu.

Researchers Find Mechanism To Target Brain Tumor Cells

2008-12-04T05:13:00.000-08:00

Researchers Find Mechanism To Target Brain Tumor Cells

Researchers at Duke University Medical Center and the University of North Carolina, Chapel Hill are exploiting an "Achilles Heel" of brain tumors that may selectively kill tumor cells while sparing surrounding brain tissue. Although most cancer cells thrive by avoiding the normal process of programmed cell death, or apoptosis, the researchers found a way to turn this normal cell suicide way up for brain cancer cells. "In collaboration with Dr. Deshmukh's lab at UNC, we attempted to come up with a way to specifically target tumor cells without damaging surrounding cells," said Sally Kornbluth, Ph.D., Professor of Pharmacology and Cell Biology and Vice Dean of Basic Sciences. In addition to turning off normal cell death, brain cancers, such as glioblastomas and medulloblastomas, are generally resistant to traditional chemotherapy. And chemotherapy and radiation can also lead to significant neurological defects because they kill both cancerous and healthy brain. In their study, published in the December issue of the Proceedings of the National Academy of Sciences, the researchers found that brain tumor cells are particularly sensitive to a protein called cytochrome c, which is involved in programmed cell death. Because of this difference, lab-cultured, human brain tumor cells treated with cytochrome c were killed, while mature neurons were not affected. "This work highlights a previously unappreciated vulnerability within tumor cells. It also suggests a powerful technique by which new chemotherapeutic agents could act," Kornbluth said. "Apoptosis could be induced within brain tumors by small molecules that mimic cytochrome c," said Mohanish Deshmukh of UNC, co-seniorauthor of the study. All types of brain tumors appear to share this vulnerability, Kornbluth said. The next step toward a real-world treatment would be to determine how to deliver cytochrome c directly to brain cells without affecting other cells in the body. Indeed, much of conventional chemotherapy's more debilitating side effects, including extreme fatigue and low blood-cell counts, come from the inadvertent elimination of healthy cells. The study was supported by grants from the National Institutes of Health and the Pediatric Brain Tumor Foundation.

Role of Hypnosis in Surgical Recovery for Patients with Head and Neck Cancer

2008-12-02T10:37:00.000-08:00

Role of Hypnosis in Surgical Recovery for Patients with Head and Neck Cancer

Surgery is a very common occurrence in the United States. Surgeries are performed to diagnose and/or treat a condition. The three major concerns with any type of surgery are pain, bleeding, and infection. Taking small steps such as mandating hypnotherapy sessions for patients going through such tough procedures can have beneficial affects on both the patients’ physical and mental well-being, along with their finances.A study was performed in 1991 involving 36 patients who had head and neck cancer and were undergoing surgery to treat it. An article about the study appeared in the International Journal of Clinical and Experimental Hypnosis. The study was conducted to see whether hypnosis played a role in recovery after surgery for patients suffering from 2 particular types of cancers.The study consisted of 36 participants who were diagnosed with head and neck cancer and were undergoing surgery. Twenty-one patients served as the control group and received no hypnosis. Fifteen patients received hypnotherapy. The researchers wanted to compare length of hospital stay, surgical complications, and blood loss between the hypnosis group and the control group.Results from this study were significant between the two groups. Researchers found that those who received hypnotherapy had a much shorter hospital stay than the control group who received standard care.Researchers also found some differences among the group that received hypnosis. Those who were more highly hypnotizable experienced fewer complications after the surgery. Also, the researchers found that those who were more hypnotizable also had less blood loss during the surgery.The study concluded that hypnosis can help prevent postoperative complications. A reduction in complications after surgery also reduces the length of hospital stay after the operation. Fewer complications also suggest a quicker recovery time. A shorter hospital stay means lower medical bills.Patients going through cancer treatment already experience a high level of stress and anxiety with rehabilitation. Hypnotherapy ensures that the healing time and treatment period is shorter and more easily dealt with. The procedure may not only show physical improvements, but emotional ones as well. By taking such a small step, doctors can now further help improve the lives of their patients. Financial, physical, and emotional strains may be lifted with the help of hypnotherapy.

New Evidence Linking Meat To Cancer

2008-12-02T10:20:00.000-08:00

New Evidence Linking Meat To Cancer

Diets high in red and processed meats have long been associated with cancer of the large intestine. Now, however, for the first time scientists have looked at whether eating meat and other animal fats is also linked to cancers of the small intestine. Their findings show yet again what natural health advocates have said for years: red meat and diets high in animal fats are a good way to promote cancer, not wellness.The new study, just published in the Cancer Research, a journal of the American Association for Cancer Research, strongly suggests eating diets high in meat and other saturated fats is associated cancer of the small intestine -- a kind of cancer that has been steadily increasing since the l970s. If a person gets this type of cancer, they are at increased risk of also developing a second malignancy, an often deadly colorectal cancer."Identifying modifiable risk factors for cancer of the small intestine is important not only because the incidence of this cancer is on the rise, but it may enable us to further understand other gastrointestinal malignancies," Amanda Cross, Ph.D., a National Cancer Institute researcher and the study’s lead author, said in a statement to the media.Cross and her research team used food frequency questionnaires to document the food intake of a half million men and women enrolled in the NIH -AARP ( National Institutes of Health and American Association of Retired People) Diet and Health study over about eight years. Their findings strongly indicate the risk for a type of tumor called a carcinoid in the small intestine was associated with consuming saturated fats. Carcinoid tumors are a slow-growing type of cancer that can arise in several places throughout the body but are most often found in the gastrointestinal tract. They produce and release hormones into the body that cause symptoms such as diarrhea or skin flushing but these problems rarely show up until late in the disease.“There is some evidence to suggest that cancers of the small and large bowel both arise from adenomatous polyp precursor lesions, suggesting the adenoma-carcinoma sequence is relevant to both sites. For unknown reasons, the large intestine is much more susceptible to malignant transformation. Identifying risk factors that are unique as well as those that are similar for the two sites may aid our understanding of the comparative resistance of the small intestine to carcinogenesis,” Cross said in the press statement.She added that the associations found in the new study need to be studied further in other populations and with different types of saturated fat in order to understand the potential mechanisms involved.More cancer and saturated fat news: a study by scientists at the Tuft School of Medicine recently published in the journal Nutrition and Cancer concludes a low-fat diet may play a significant role in preventing breast cancer. The bottom line? Evidence continues to mount that by eating a diet centered on fruits and vegetables instead of fat-laden animal products, you can help control your risk of developing cancer.