TUESDAY, Oct. 7 (HealthDay News) -- Men who drink a moderate amount of red wine may lower their risk of lung cancer, even if they smoke, researchers report.

"An antioxidant component in red wine may help to prevent lung cancer," said lead researcher Chun Chao, a research scientist with the Kaiser Permanente Southern California Department of Research and Evaluation. "The findings provide an impetus for future research to find out if there is something in red wine that may help to either prevent or treat lung cancer."

But the researchers cautioned that the findings don't mean that it's OK to smoke.

For the study, Chao's group collected data on 84,170 men who participated in the California Men's Health Study. Among these men, the researchers identified 210 cases of lung cancer.

The researchers found that there was, on average, a 2 percent lower risk of lung cancer associated with each glass of red wine consumed per month.

The greatest reduction was among men who smoked and drank one to two glasses of red wine a day. These men lowered their risk for lung cancer by 60 percent, Chao's group found.

The reduction wasn't as pronounced among nonsmokers who drank one to two glasses of red wine a day. And no reduction in risk for lung cancer was associated with white wine, beer or liquor, the researchers said.

Despite the findings, Chao warned against thinking that smoking and drinking red wine can actually prevent lung cancer.

"Men who smoke should stop smoking," she said. "Even men who drink one or two glasses of red wine per day still face a greater risk of lung cancer than do nonsmokers. This study should not be used as an excuse to drink more red wine. Moderation is always the best course."

The findings were published in the October issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.

Dr. Leonard Lichtenfeld, the American Cancer Society's deputy chief medical officer, doesn't think that one study proves that red wine will protect you from lung cancer.

"It's an interesting study, and it raises interesting questions about whether or not there is a cancer protective effect in red wine," he said. "It is important that this be looked at further to see if that association holds up."

Lichtenfeld noted that there have been previous reports of a benefit of red wine for cancer prevention that didn't pan out. "Before we get overly excited about this, we really need to see these effects replicated," he said.

"Clearly, we aren't recommending that smokers go out and start consuming large amounts of red wine as a potential protection from getting lung cancer," he added. "There are other research reports that show that any alcohol, including red wine, can increase the risk of other cancers such as breast cancer."

More information

For more on lung cancer, visit the National Cancer Institute.

TUESDAY, Oct. 7 (HealthDay News) -- A treatment that helps prevent one type of breast cancer in women with an evaluated risk of the disease also appears to help doctors make an earlier diagnosis of another form of breast cancer, a new study reports.

Tamoxifen previously had been shown to reduce the risk of estrogen receptor (ER) positive breast cancer in women at high risk of the disease, but not to affect the chance of developing ER-negative disease.

However, the study by researchers at the University of Texas M.D. Anderson Cancer Center in Houston found that the treatment helped doctors diagnosis women who later developed estrogen receptor (ER) negative breast cancer an average of one year sooner than the same at-risk patients who instead took a placebo.

For the study, 13,388 women at high risk of breast cancer participated in the trial; 174 women were diagnosed with ER-positive tumors and 69 women with ER-negative tumors. The median time to diagnosis for ER-negative disease was 36 months in the placebo group but only 24 months in the tamoxifen group.

The median time to diagnosis for ER-positive disease was similar in the placebo and tamoxifen groups at 43 and 51 months, respectively, which is not statistically different.

It's not clear why the diagnosis time of ER-negative tumors is so different, but the authors hypothesized that the drug may make the tumors more detectable. No evidence was found that tamoxifen altered the growth rate of ER-negative disease.

The study was published online Oct. 7 in the Journal of the National Cancer Institute.

The findings should be investigated further, the researchers concluded.

More information

The National Cancer Institute has more about tamoxifen.

MONDAY, Oct. 6 (HealthDay News) -- A new technique may help doctors diagnose a rare form of leukemia in a matter of hours instead of weeks, researchers say.

Juvenile myelomonocytic leukemia (JMML) occurs in children; symptoms include fevers, poor growth, and infections.

Early diagnosis of JMML is important, since the only cure is a bone marrow transplant. But JMML is currently diagnosed by monitoring the response of JMML cells to a growth-stimulating factor called GM-CSF, which involves two to three weeks of growing cells in the laboratory.

Now, a new study published in the Oct. 7 issue of Cancer Cell may have found a faster way to diagnose this relatively rare leukemia.

For their study, researchers used a new technique that builds on flow cytometry.

In flow cytometry, fluorescently labeled antibodies are used to classify and sort cells based on the proteins on their outer surface. The new approach goes further by sending antibodies inside the cell to bind to target proteins.

To find a way to diagnose leukemia, the researchers used an antibody that binds only to the activated form of a protein called STAT5 in cell samples of 12 patients with JMML.

Eleven of the 12 JMML cell samples displayed abnormally high levels of STAT5 in response to low doses of GM-CSF. Seven out of the eight normal bone marrow samples, and eight out of eight samples from patients with similar -- but not identical disorders -- did not have increased levels of STAT5 in response to GM-CSF.

"I was surprised how much more we can learn about the inner nature of these cells by 'interrogating' them with different conditions," senior co-author Garry Nolan, immunologist and member of the Donald E. and Delia B. Baxter Laboratory in Genetic Pharmacology at Stanford, said in a university news release. "Time and again, we are finding this to be a powerful amplifier of the fate of a diseased cell and a good way to understand why it responds to certain treatments and not others."

Since the new technique can help track disease progress, the researchers hope that it can be used to monitor the effectiveness of potential drug treatments for JMML and other disorders.

"Identifying populations of cells by their responses to specific stimuli will facilitate our ability to assess the efficacy of specific agents in relevant subsets with increased precision," senior-co-author Mignon Loh, an associate professor of clinical pediatrics at the University of California, San Francisco, said in the release.

"In an era of using increasingly sophisticated targeted agents, we hope that these studies will allow investigators to more fully appreciate the specificities of their therapies," said Loh.

More information

The American Cancer Society has more about childhood leukemia  .

THURSDAY, Sept. 4 (HealthDay News) -- Potentially groundbreaking discoveries involving genetic mutations of two deadly cancers -- the brain cancer glioblastoma and pancreatic cancer -- may lead to new treatments and even cures, researchers say.

"These studies represent the most complete genetic analysis to date of any tumor type and provide a detailed genetic map of these deadly cancers," Kenneth Kinzler, a professor of oncology at Johns Hopkins University, and co-author of the study on pancreatic cancer, said during a teleconference Wednesday.

These findings are important, because genetic mutations are involved in the development of all cancers, Kinzler said. Kinzler's study of the genetic makeup of pancreatic cancer is published in the Sept. 4 online edition of Science.

Pancreatic cancer is diagnosed in 38,000 people, and brain cancer strikes 21,000 people each year in the United States. Only about 5 percent survive these cancers, the researchers said.

For the pancreatic cancer study, the researchers looked at genes in 24 people with the disease. "Analysis of 20,000 genes in 24 pancreatic cancers provided a global overview of the molecular landscape that was previously unknown to this tumor type," Kinzler said.

The researchers found 63 genetic alterations in these pancreatic cancers. However, genes do not work alone; they work together in what are called pathways. When looked at this way, Kinzler's group found 12 altered pathways.

"This really is a new perspective on the changes that drive tumor progression and suggests that we need to rethink the optimal way of diagnosing, categorizing and treating cancer," Kinzler said.

In the second report, published in the same issue of Science, co-author Dr. Victor Velculescu, an assistant professor of oncology at Johns Hopkins University, and colleagues studied 20,000 genes from 22 patients with glioblastoma multiforme (GBM), the same type of cancer diagnosed in Sen. Edward Kennedy earlier this year.

"We found that a typical GBM contains approximately 60 genetic alterations," Velculescu said during the teleconference. "Some of these changes affected many of the same pathways as those in pancreatic cancer. But many were new and appeared to affect the processes that appear to relate to the development of GBM."

One of the important discoveries about GBM was that about 12 percent of patients have an alteration in one gene -- called IDH1 -- that had never before been implicated in any type of cancer. Patients with this particular gene alteration tended to be younger and survive longer, Velculescu said.

"GBMs used to be thought of as one disease. It is now clear that they are two," Velculescu said.

In another paper on genetic alterations involving GBM tumors, researchers also reported finding alterations that appear to be responsible for the brain cancer.

Dr. Matthew Meyerson, of the Dana-Farber Cancer Institute and Harvard Medical School, and colleagues found three major gene mutations in glioblastoma, namely NF1 (a tumor suppressor gene), ERBB2 (a protein tyrosine kinase gene), and PIK3R1 (a lipid kinase gene) among 206 GBM patients.

"These findings will guide glioblastoma therapies," Meyerson said. "Cancer genome projects can discover important new cancer-causing alterations, with clinical implications. We are on our way to understanding what causes cancer in detail," he said.

Meyerson's findings were published in the Sept. 4 online issue of the journal Nature.

The findings from all three studies could have important treatment and diagnostic implications, Dr. Bert Vogelstein, the Clayton Professor of Oncology and Pathology at Johns Hopkins University and a co-author of the Science paper on GBM, said during a teleconference.

The findings suggest that most solid tumors, particularly those of the brain and pancreas, won't respond to treatments that target a single gene, Vogelstein said. "Our work suggests that it may be more productive to screen for drugs that act against the core pathways that are disregulated in most cancers," he said.

Vogelstein said more effort needs to be placed on prevention and early detection, rather than looking for cures. This emphasis should include new ways of detecting alterations in the genetic pathways of tumors. Also, ways need to be found to detect genetic alterations when cancers are still curable, he said.

It takes many years for cancers to develop, and gene alterations could be detected long before tumors grow and spread to other parts of the body, Vogelstein noted.

"Almost all tumors, probably even those of the brain and pancreas, would be curable if they could be caught early," Vogelstein said. "One focus of future research should be to emphasize early detection using the genes and pathways that have been discovered to play a role in these tumor types," he said.

Dr. Len Lichtenfeld, deputy chief medical officer at the American Cancer Society, noted that genetic alterations may be different in different cancers and even among people with the same cancers.

"This [new research] reinforces the thought that we will eventually get to a point where we will be able to take a specimen from an individual's cancer and look at the genetic changes in the cancer and use that information and apply it to treatment that would be specific for that person's cancer," Lichtenfeld said.

However, one cancer geneticist said the new studies were too small to offer any firm conclusions.

"It's a bit disappointing that so many of the mutations in these genes have already been known. There seems to be a paucity of really new findings," said Dr. Charis Eng, the Sondra J. and Stephen R. Hardis Chair of Cancer Genomic Medicine at the Cleveland Clinic and a professor at the University of Cambridge in the United Kingdom.

"Sample sizes need to be increased, clinical annotation has to be better," she added. "This has to be done in a true international collaboration. Even then, I think, we will come up with more questions than answers."

More information

For more on cancer and genetics, visit the American Cancer Society  .