WEDNESDAY, June 11 (HealthDay News) -- A drug already approved to reduce the risk of breast cancer in high-risk women also seems to cut the risk for other women.

A new analysis finds that those who took raloxifene (Evista) regularly over a number of years were less likely to develop invasive estrogen-receptor (ER) positive breast cancer, compared with women who did not take the drug.

Raloxifene did not, however, cut the risk for noninvasive breast cancer or invasive ER-negative cancers.

"This is a reaffirmation that the drug raloxifene is a very powerful SERM [selective estrogen receptor modulator] for reducing the risk of invasive breast cancer," said Dr. Jay Brooks, chief of hematology/oncology at Ochsner Health System in Baton Rouge, La.

The study, published in the June 10 online issue of the Journal of the National Cancer Institute, was funded by Eli Lilly and Co., which makes Evista.

SERMs block the female hormone estrogen by binding to estrogen receptors; estrogen helps fuel the growth of some breast cancers. Raloxifene and other hormonal therapies have an "estrogenic tickle" effect, explained V. Craig Jordan, author of an accompanying editorial in the journal and vice president and research director for medical science at Fox Chase Cancer Center in Philadelphia. Jordan did some of the early laboratory research on raloxifene.

Raloxifene was originally developed to prevent and treat osteoporosis, and only later was found to help reduce the risk of invasive breast cancer in high-risk women.

The new study expands on the original results of the RUTH (Raloxifene Use for the Heart) trial, originally designed to see if raloxifene, which has cholesterol-lowering properties, could reduce the risk of dying from coronary heart disease.

The trial involved more than 10,000 postmenopausal women with coronary heart disease or at risk for the condition. Participants were randomly chosen to receive either daily raloxifene or a placebo and followed for a median of 5.6 years.

Raloxifene turned out not to have any effect on heart disease mortality risk, but it did reduce the risk of invasive breast cancer by 44 percent, which translates into 1.2 women per 1,000 treated for one year who were spared the agony of a breast cancer diagnosis.

The new analysis looked more specifically at raloxifene's effect on breast cancer and found a 55 percent lower incidence of invasive ER-positive tumors, but no effect on noninvasive breast cancer or invasive ER-negative breast cancer.

According to the study authors, these findings are consistent with results from other trials involving women without heart disease. This trial and others found an increased risk of blood clots and fatal strokes among women taking raloxifene, indicating that women need to weigh the risks and benefits of the drug.

Another question is how long to take raloxifene for breast cancer prevention, although the authors speculated that up to eight years might be safe and effective.

"We're learning more about this class of drugs, what works and what doesn't work," Jordan said. "[Raloxifene] is good for osteoporosis, no good for coronary heart disease, but breast cancer is inhibited."

More information

The U.S. National Cancer Institute has more on SERMs and how they work.

TUESDAY, June 3 (HealthDay News) -- The genetic makeup that increases the risk of developing colorectal cancer also seems to improve the chances of survival after treatment, a new study indicates.

People with colorectal cancer who had close relatives with the malignancy were 28 percent less likely to die or to have a recurrence after treatment, according to a report in the June 4 issue of the Journal of the American Medical Association by physicians at the Dana-Farber Cancer Institute in Boston.

It is well-known that a close relative of someone with colon cancer is more likely to develop such a cancer, "which is why we recommend that patients who have a family history of colorectal cancer get routinely screened," said study author Dr. Jennifer A. Chan, an instructor in medicine at Harvard Medical School and Dana-Farber. "That is why we did this study."

The study included 1,087 people who had undergone surgery for their cancers and began drug therapy. Over an median follow-up period of 5.6 years, 29 percent of those with a family history died or had a recurrence of cancer, compared to 38 percent of those without a family history.

The reason for the difference isn't known or understood, Chan said. The researchers did try to determine whether lifestyle factors such as diet might be the reason but found no connection.

"Our study was not able to determine the cause," she said. "What we suspect is that there might be some sort of genetic trait that not only increases the risk, but also improves the prognosis for cancer patients."

The increase in survival was associated with the strength of the family history. Participants with two or more close relatives with the cancer had a 51 percent lower risk for cancer recurrence or death than those with no family history.

The immediate impact of the discovery might be to give some reassurance to people with colorectal cancer and a family history, Chan said. "What we hope is that this observation leads to further studies to understand the biological reasons," she said. "If we understand those reasons, we might be able to make better treatment decisions."

The study "could change some expectations about colorectal cancer," said Dr. Boris Pasche, director of the cancer genetics program at Northwestern University, who wrote an accompanying editorial.

"The genetics of colorectal cancer are very clear," Pasche said. "There is an increased risk for those with a family history. But we still don't know what is causing that inheritance."

On the clinical level, the study indicates that "patients with a family history of colorectal cancer might be more treatable than whose who do not," Pasche said.

"If these intriguing findings are validated in other studies, family history may well become a new prognostic factor in colorectal cancer," he wrote. "Should this be the case, genome-wide association studies and tumor gene expression profiling studies will be warranted."

More information

Learn about colorectal cancer from the U.S. National Library of Medicine.

MONDAY, May 19 (HealthDay News) -- Lung cancer patients may be one step closer to the day when the disease can be detected early with a simple blood test.

Scientists slated to report their findings Tuesday at the American Thoracic Society's conference in Toronto say the test -- which tracks gene activity in immune-system cells -- was very good at distinguishing patients with lung cancer from those without the disease.

"The findings are important and represent progress," said Dr. Norman Edelman, chief medical officer of the American Lung Association. "They may not be good enough [yet] to change practice. I'm sure, as the researchers refine it, it'll get better and better."

Lung cancer remains the number one cancer killer of men and women. According to the National Cancer Institute, 215,020 new cases of the disease will be diagnosed in 2008, and 161,840 Americans will die of lung cancer.

Lung tumors are notoriously difficult to spot when they are still small enough to be treated effectively, leading to an astronomically high death rate from the disease.

A technology known as CT screening can detect lung cancer in 20 percent to 60 percent of people tested, but it also has a high false-positive rate, meaning that patients often have to endure repeat or follow-up testing.

"If you do a CT scan on a general population, you are going to find lots of little nodules, and the critical issue is, what's cancer and what's not," Edelman said. The CT scan method is also controversial, with one study finding that higher detection rates did not translate into lower death rates.

"If they had a minimally invasive blood test that doesn't involve a biopsy that would tell whether or not something is cancer, that would be a huge advantage," Edelman said.

Researchers have long been looking for a simple blood test to detect lung cancer, many of them trying to find proteins released into the bloodstream by the tumor. But lung cancer is so heterogeneous, involving many different cell types, that this goal has so far proved illusive.

The authors of this study followed a different strategy, measuring gene expression profiles in lymphocytes (immune system cells) to see if they correlated with the presence or absence of lung cancer. "The hypothesis is the immune system has some sort of interplay with the cancer and, from that interplay, you get changes in the genes that are expressed," said Dr. Anil Vachani, lead author of the study and assistant professor of medicine at the University of Pennsylvania School of Medicine in Philadelphia.

A 24-gene signature tested in 137 patients with early-stage lung cancer and 91 healthy controls had overall 87 percent accuracy in identifying who had cancer and who did not.

"I would say that 87 percent is very good, but it's not excellent," Vachani said. "For a test to be really useful clinically, it has to do a little bit better."

A second study, also involving genetics and also being presented at the American Thoracic Society meeting, assessed how well five different high-risk genetic signatures predicted the likelihood of a recurrence in patients who had been diagnosed early with non-small cell lung cancer and then undergone surgery.

According to a team from Columbia University, New York City, the gene signature profiles were 40 percent to 100 percent accurate in predicting a recurrence of the disease, depending on the type of tumor. This could help physicians determine who should get more aggressive therapy, the authors stated.

More information

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

FRIDAY, May 2 (HealthDay News) -- A number of potential new targets for treatments that block tumor blood vessel formation -- a key step in tumor growth and metastasis -- have been identified by researchers at the University of North Carolina at Chapel Hill.

The use of the drug bevacizumab (Avastin) to target the formation of blood vessels (angiogenesis) that feed tumors has proven successful in treating breast and colon cancer, according to background information in the study. The drug inhibits a protein called vascular endothelial growth factor (VEGF), which plays a major role in angiogenesis.

"There is a large amount of data that shows if you block angiogenesis, you can block tumor growth. But VEGF is not responsible for all of angiogenesis. We wanted to identify more targets for this therapeutic approach," study senior author Dr. Nancy Klauber-DeMore, an associate professor of surgery in the UNC School of Medicine, said in a prepared statement.

She and her colleagues identified new targets after analyzing blood vessel cells in cancerous and normal breast tissue samples. They identified 1,176 genes that differed in activity or expression between the two cell populations. Of those, 55 genes were overexpressed more than fourfold in blood vessels from breast cancer.

"The most exciting aspect of this study is that we now have a very large list of potential targets that we will continue to work on for at least the next decade," Klauber-DeMore said.

So far, she and her colleagues have only looked at seven out of the 55 potential targets.

"This work points us in the direction we need to go to develop the next generation of angiogenesis inhibitors," Klauber-DeMore said.

The study was published in the current issue of The American Journal of Pathology.

More information

The U.S. National Cancer Institute has more about angiogenesis.