FRIDAY, Feb. 15 (HealthDay News) -- The more weight you carry on your body, the greater your odds of developing cancer, British researchers report.

This is true not only of fairly common cancers such as colon and breast, but also of lesser known varieties, including gallbladder. Moreover, the degree of risk differs between men and women and among different ethnic groups, report the authors of a comprehensive new paper appearing in this week's issue of The Lancet.

"This is a profoundly important issue. Obviously, the obesity epidemic is a huge problem itself, and the relationship to cancer is only one of the many adverse health effects of being overweight and obese," said Dr. Michael Thun, head of epidemiological research at the American Cancer Society. "The evidence has been accumulating now for over 10 years. . . This study tries to provide a quantitative measure of how much the relative risk goes up with each increment, basically jumping from one BMI [body-mass index] category to another."

Although extra fat has already been identified by research as a risk factor for several different types of cancer, Thun said, "the problem of obesity is so large and so difficult to solve that there's a very sound reason for ongoing studies of things that have become increasingly well-known, just because it helps the momentum in stimulating approaches that will actually help people maintain a healthy weight."

Last year, a report issued by the American Institute of Cancer Research and the U.K.-based World Cancer Research Fund concluded that body fat is associated with an increased risk for several different types of cancer including esophageal adenocarcinoma, as well as cancers of the pancreas, colon and rectum, breast (postmenopausal), endometrium and kidney.

Although that report was one of the most comprehensive to date, it did leave some questions unanswered. For instance, are there associations between less common cancers and body weight, and do the associations differ between the sexes and people of different ethnic backgrounds?

The issue is a pressing one, with about two-thirds of adult men and women in the United States overweight or obese. That number is only expected to increase as people continue to eat more and exercise less.

This study, from scientists at the University of Manchester, analyzed 141 articles involving 282,137 cancer cases and 20 different types of malignancies to determine the cancer risk associated with a 5 kilogram-per-meter-squared increase in BMI, roughly the increase that would bump a person from middle-normal weight into overweight.

In men, such an increase in BMI raised the risk of esophageal adenocarcinoma by 52 percent, thyroid cancer by 33 percent, and colon and kidney cancer by 24 percent each.

In women, the same increase in BMI increased the risk of endometrial and gallbladder cancer by 59 percent each, esophageal adenocarcinoma by 51 percent, and kidney cancer by 34 percent.

In men, there were weaker associations between increased BMI and rectal cancer and melanoma. In women, there were weaker associations between increased BMI and postmenopausal breast, pancreatic, thyroid and colon cancers.

In both genders, there were associations between increased BMI and leukemia, multiple myeloma and non-Hodgkin's lymphoma.

For colon cancer, the associations were stronger in men than in women (24 percent vs. 9 percent).

There were stronger associations in Asia-Pacific populations between greater BMI and both premenopausal and postmenopausal breast cancers.

Although the main message is still to maintain a healthy weight, this research might indicate earlier screening for certain cancers, said Dr. Greg Cooper, interim chief of the gastroenterology division at Ireland Cancer Center of University Hospitals and Case Comprehensive Cancer Center in Cleveland. "If someone is obese, then lower the threshold for screening," he said. "One of the cancers they identified is esophageal adenocarcinoma, which is not as common as colon cancer, but it is increasing in incidence. It is thought to be related to reflux, so as a gastroenterologist, if I have a patient who has reflux and is obese, I might lower the threshold for doing an endoscopy. For other cancers like colon cancer, those guidelines are pretty well-established, and this probably wouldn't change practice."

Experts aren't sure why extra fat can lead to malignancies, but changes in the circulating levels of various hormones (insulin, insulin-like growth factors and sex steroids) might explain the link.

Here's more bad news as the world heads for a smoke-free future: An accompanying commentary from Swedish researchers notes that as people quit smoking (the biggest cause of cancer in developed countries), weight gain may become the main lifestyle factor contributing to new cancers.

More information

Visit the American Cancer Society   for more on the different types of cancer.

TUESDAY, Feb. 12 (HealthDay News) -- Women who carry the BRCA1 or BRCA2 mutations that raise the risk for both breast and ovarian cancer should weigh a new finding that suggests having your ovaries removed provides greater protection against breast cancer if you have the BRCA2 mutation.

The preventive strategy has long been contemplated by women in this high-risk category, and this latest research might help women trying to decide whether to have the procedure, said study author Dr. Noah Kauff, a gynecologist, geneticist and assistant attending physician at Memorial Sloan-Kettering Cancer Center in New York City.

"There have been studies that looked at BRCA1 and 2 together, but not 2 alone," Kauff noted. His study is published in the March issue of the Journal of Clinical Oncology.

Women with an inherited BRCA1 or BRCA2 mutation have up to an 80 percent chance of developing breast cancer in their lifetime, according to the American Cancer Society, compared to a lifetime risk of about 12 percent in the general population.

Carriers of BRCA1 or BRCA2 mutations also have an increased risk of ovarian cancer, cancer of the fallopian tubes and another gynecologic cancer called primary peritoneal cancer. The lifetime risk of ovarian cancer for those with BRCA1 mutation is up to 46 percent, and for those with BRCA2 mutations it is up to 27 percent, compared to about a 1.5 percent risk in the general population.

Kauff and his colleagues recruited women from 11 centers across the country in late 2004. For an average of three years, they followed 509 women aged 30 or older who had a BRCA1 or BRCA2 mutation and had the ovary removal surgery (oophorectomy), comparing them with 283 women who also had the mutations but did not elect to have the surgery.

"In the women who elected oophorectomy, if we look at the entire group, 1 and 2 together, we saw that women who had their ovaries removed have an 88 percent reduction in the risk of gynecologic cancer and 47 percent [reduction of risk] in breast cancer," Kauff said.

But when the women with BRCA2 mutations were looked at separately, the researchers found the surgery reduced breast cancer risk by 72 percent -- almost twice as much as the 39 percent reduced risk in BRCA1 mutation carriers -- a reduction that didn't reach statistical significance.

The surgery reduced the risk of gynecologic cancer by 85 percent in women with a BRCA1 mutation, and was suggested in women with BRCA2 mutations, but the researchers were not able to compute the level of reduced risk, because few of these women had those cancers.

When they looked more closely, the researchers found the surgery had a protective effect on the form of breast cancer known as estrogen receptor-positive cancer, reducing risk by 78 percent in both BRCA1 and BRCA2 carriers, but had no effect on ER-negative breast cancers -- which BRCA1 mutation carriers are more likely to get.

"I don't think this is going to have a lot of clinical impact for the average person with a BRCA mutation," said Debbie Saslow, director of breast and gynecologic cancer for the American Cancer Society. "For the average person with BRCA mutation, this probably won't enter into her decision-making." For some, it may confirm surgery is the right thing to do, she added.

The study also raises some questions, said Dr. Angela R. Bradbury, director of the Margaret Dyson Family Risk Assessment Program at Fox Chase Cancer Center in Philadelphia. "This paper raises a question about whether [the surgery] really reduces the risk of ovarian cancer in BRCA2," she said. However, she added, the preventive surgery "still remains the only good option."

More information

To learn more about BRCA1 and BRCA2 mutations, visit the American Cancer Society.  

MONDAY, Feb. 11 (HealthDay News) -- Scientists have uncovered at least 10 new genetic variations associated with an increased risk for prostate cancer.

The new findings double the number of genetic variants that are known to be associated with prostate cancer. Three reports detail the discoveries in the Feb. 10 online edition of Nature Genetics.

"Predisposition to prostate cancer, at least in part, is due to variations in a person's genetic code," said Dr. Rosalind Eeles, a Reader in Clinical Cancer Genetics in The Institute of Cancer Research, in Sutton, U.K., and lead author of one of the reports.

"There are many variants in the genome which confer prostate cancer risk, and these results move us nearer to being able to develop a profile of genetic variation which predicts for increased risk of the disease. This will enable us to target screening, prevention strategies and treatment," she said.

Each of the three reports was done by a different group, one in the United States, one in Great Britain, and one in Iceland. Each group studied thousands of men with and without prostate cancer.

In the first report, Eeles, and her colleagues identified seven genetic variances that were associated with prostate cancer on chromosomes 3, 6, 7, 10, 11, 19 and X.

"We have studied hundreds of thousands of genetic variants in over 10,000 men both with and without prostate cancer," Eeles said. "We have found seven new sites in the human genome that are linked to men's risk of developing prostate cancer."

Among these new sites is one gene called MSMB which could possibly be used in screening for prostate cancer and disease monitoring, Eeles noted. "Another of the sites harbors a gene called LMTK2, which might be a target for new treatments. These newly identified genetic alterations are present in over half of all prostate cancer cases. They each increase a person's risk of the disease by up to 60 percent."

In the second report, Dr. Stephen Chanock, head of the Genomic Variation Section at the U.S. National Cancer Institute, and his colleagues found genes associated with prostate cancer on chromosomes 7, 10 and 11, as well as nine other gene locations that are suggestive of an association with prostate cancer.

"We are finding the places in the genome that are associated with the risk for prostate cancer," Chanock said. "The reason this is so important is that prostate cancer is a complex disease and is not due to one genetic defect or one environmental exposure," he said.

Similar findings are being reported with breast cancer, colon cancer and lung cancer, Chanock said. "The same thing is happening in other diseases, such as diabetes, heart disease and stroke," he said. "Most diseases are complex and associated with multiple genes."

Exactly how each of these genes contributes to the risk for prostate cancer isn't clear, Chanock said. "Some of them may be responsive to environmental triggers, such as what you eat or what you inhale," he said. "Somewhere down the line, these findings may be clinically relevant, but it's too early to do that, because we are still discovering more."

In the third report, Julius Gudmundsson's team from deCODE Genetics Corp. in Iceland, found genes associated risk of prostate cancer on chromosomes 2 and X.

Although most of the gene variants are associated with a moderate risk, they are common in the population. Some of these variants are linked to more than less aggressive disease, Gudmundsson's team noted.

A substantial number of men have many risk variants that together confer clinically significant risk. In fact, 10 percent of men are at twice the risk and 1 percent of men are at three times the risk of developing the disease in the general population, Gudmundsson's group said.

One expert thinks these papers add to the general knowledge about prostate cancer's genetic underpinnings. However, how this will be translated into clinical practice is still unknown.

"These papers are adding a little bit to our knowledge of prostate cancer in the genome," said Dr. Durado Brooks, director of prostate and colorectal cancers at the American Cancer Society.

Brooks thinks the Gudmundsson paper is important, because it shows a link between genes and aggressive prostate cancer. "This is the sort of information that has the potential to be most useful in a clinical setting," he said.

Identifying which men are at risk for developing aggressive prostate cancer will be important in terms of offering care and not over treating men whose prostate cancer is less aggressive, Brooks said. "The ability to identify aggressive tumors is likely to be a great benefit," he said.

In addition, Brooks thinks that genetic information will help find ways to modify the risk of developing prostate cancer. This could involve medication and/or lifestyle changes, he said.

"This knowledge could also lead to better diagnosis and treatment," Brooks said.

More information

For more on prostate cancer, visit the U.S. National Cancer Institute.

THURSDAY, Feb. 7 (HealthDay News) -- A gene called STAT3 acts like "Jekyll and Hyde" in glioblastoma brain cancer, according to a study led by Harvard Medical School researchers.

The finding may help improve treatment of people with the deadly disease.

Glioblastoma tends to strike people in the prime of life and is almost always fatal. There are limited treatment options, which have changed little over decades.

Previous research has shown that STAT3 is an oncogene in several types of glioblastoma. An oncogene is a gene whose normal functions are disrupted and, as a result, helps promote tumor development. In such cases, blocking STAT3 would be a way of fighting these tumors.

But this new study found that STAT3 is actually a tumor-suppressor gene in other types of glioblastoma, meaning that the gene keeps renegade cancer cells in check.

So, depending on a person's genetic makeup, STAT3 can play completely different roles in glioblastoma, the researchers said.

"This discovery lays the foundation for a more tailored therapeutic intervention. And that's really important. You can't just go blindly treating people by inhibiting STAT3," study senior author Azad Bonni, an associate professor of pathology at Harvard Medical School, said in a prepared statement.

The study was published online Feb. 6 in the journal Genes & Development.

More information

The U.S. National Cancer Institute has more about brain tumors.