WEDNESDAY, Jan. 16 (HealthDay News) -- A new blood test that looks at five genetic variants could one day predict the risk of developing prostate cancer, a new study says.

Researchers found that among men with four of the five variants, the risk of prostate cancer is increased 400 percent to 500 percent, compared to men with none of the variants. And if a man has these gene variants and a family history of prostate cancer, his risk of developing the disease increases more than 900 percent.

"There are five genetic variants that have been shown to be associated with prostate cancer risk," said lead researcher Dr. Jianfeng Xu, a professor of epidemiology and cancer biology at Wake Forest University School of Medicine.

For the study, the researchers examined DNA samples from 2,893 men with prostate cancer and compared them with DNA of 1,781 healthy men. All the men participated in a prostate cancer study in Sweden.

The researchers found that each of these common genetic variants was independently associated with prostate cancer risk. The five variants plus a family history of prostate cancer accounted for 46 percent of prostate cancer patients.

The effect of each variant is too small to be useful in predicting the risk for prostate cancer, Xu said. "But if you have four of these variants your risk is increased fourfold, which is something we have never seen before," he said.

The five genetic locations include three on chromosome 8q24, one on chromosome 17q12, and one on chromosome 17q24.3, according to the report, published online Jan. 16 in the New England Journal of Medicine.

When family history of prostate cancer is added to the mix, the results become more striking, Xu said. "Family history is the sixth factor," he said. "For a man with five gene variants and a family history the risk is increased tenfold."

Xu thinks that by using these gene variants and family history as a guide, "we can use this information to predict which men have a risk of developing prostate cancer."

Currently, age, race and family history are the three risk factors associated with increased risk of prostate cancer.

The researchers said the study is important because it's one of the first to show how a combination of several genes can affect disease risk. Genomics teams across the United States are looking for combinations of genes that may contribute to common diseases such as cancer, diabetes and asthma, according to background information for the study.

Dr. Durado Brooks, director of prostate and colorectal cancer at the American Cancer Society, said the findings are important, but it's not yet clear how they could be used in clinical practice.

"This study is helping us understand the role of genetic variants in the risk for prostate cancer," Brooks said.

But, he added, "If you develop a test and tell a man you have five times the risk of developing prostate cancer as other men, what do you do with that?"

Brooks also noted that these genetic variants don't indicate if the disease is aggressive and needs aggressive treatment, or if it's a slow-growing cancer that may not need immediate treatment.

"We still need to find markers of disease aggressiveness. We still need better treatments," he said.

Prostate cancer is the most common type of cancer in American men, other than skin cancer. It is the second leading cause of cancer death in men, behind lung cancer, according to the American Cancer Society.

The society estimates that there will be about 218,890 new cases of prostate cancer in the United States this year, and about 27,050 men will die of the disease.

More information

To learn more about prostate cancer, visit the U.S. National Cancer Institute.

WEDNESDAY, Jan. 16 (HealthDay News) -- A new genetic test that helps assess the risk of tumor recurrence and long-term survival for patients with relatively high-risk breast cancer has been approved by the U.S. Food and Drug Administration.

The TOP2A/FISH pharmDx is the first approved device to test for the TOP2A (topoisomerase 2 alpha) gene in cancer patients. The gene plays a role in DNA replication. Changes in the TOP2A gene in breast cancer cells indicate increased risk that a tumor will recur or decreased survival.

The new test, made by Dako Denmark A/S, uses fluorescently-labeled DNA probes to detect or confirm gene or chromosome abnormalities, a process called fluorescent in situ hybridization (FISH).

The FDA approval was based on a study of 767 high-risk patients in Denmark who had been treated with chemotherapy after removal of a breast tumor. The findings indicated the test was useful in estimating cancer recurrence and overall survival.

"When used with other clinical information and laboratory tests, this test can provide health care professionals with additional insights on the likely clinical course for breast cancer patients," Dr. Daniel Schultz, director of the FDA's Center for Clinical Devices and Radiological Health, said in a prepared statement.

More information

This FDA announcement has more about the approval.

WEDNESDAY, Jan. 16 (HealthDay News) -- Melanoma has joined the list of cancers that can arise from a rare population of primordial cancer stem cells, Harvard researchers report.

Even more importantly, the scientists demonstrated for the first time that targeting these cells can slow down the growth of a tumor.

"The findings validate for the first time the potential therapeutic utility of the cancer stem cell concept," explained study author Markus Frank. "To my knowledge, cancer stem cells have not been specifically targeted to date via a prospective molecular marker."

Frank and his colleagues were interested in a particular protein called ABCB5, which is expressed on the surface of some progenitor skin cells and has been shown to confer cancer drug resistance to melanoma.

Hypothesizing that the pool of ABCB5-positive cells could include cancer stem cells, the researchers separated human melanoma cells based on whether or not they expressed ABCB5, transplanted both types of cells into mice, and monitored their ability to form tumors.

Fourteen of 23 mice injected with ABCB5-positive cells developed tumors, compared to one of 23 mice injected with cells that did not express the protein.

When a mixture of both types of cells were injected into mice, the authors found the ABCB5-positive cells were more likely to fuel tumors, and they exhibited stem cell-like properties -- that is, they divided to form both the bulk of the tumor and to regenerate the stem cells themselves.

Those findings -- that a stem cell subpopulation appears to contain the ability to reconstitute a tumor -- have been observed before in colon, brain, breast and pancreatic cancers, among others, albeit using a different cellular protein. However, the Harvard researchers added a novel twist: They showed both that ABCB5 expression correlated with disease severity, and that treatment of mice with an antibody directed against ABCB5 halted growth of existing tumors and inhibited the formation of new cancers.

Dr. Jeremy Rich, a cancer stem cell researcher at Duke University Medical Center, said, "The exciting thing is they have done things others haven't, which is to ask what is the impact of the marker on disease. First, there is an increase in ABCB5 levels as malignancy increases, and second, if you block its function with an antibody, you slow the growth of these tumors."

The results were published in the Jan. 17 issue of Nature.

According to the American Cancer Society, there were an estimated 108,230 new cases of melanoma in 2007 and 8,110 deaths.

The cancer stem cell hypothesis posits that tumors (like other noncancerous tissues) derive from a small population of primitive cells, which can divide and differentiate to form both the bulk of the cancer, and also more stem cells. Because most chemotherapeutic agents kill off the tumor cells, but leave the stem cells unscathed, the cancers return and metastasize.

The bottom line, according to the researchers, is that anti-cancer strategies need to be overhauled to kill off these stem cells.

Previous cancer stem cell studies have focused on the protein CD133. But it is not clear whether CD133 plays a role in stem cell behavior. According to Rich, such markers have sometimes been compared to the stripes painted on race cars: They do not make the car go faster, but they do help to identify it.

"This time, they have found a marker that is very interesting, because it looks like it may make the car go faster," he noted.

Also interesting, Frank noted, is the potential involvement of ABCB5 in mediating the cancer's resistance to chemotherapeutic agents.

"The findings establish a direct relationship between cancer stem cells, cancer progression, and chemoresistance in a human solid malignancy," Frank said. "This is a relationship that has been invoked often, but these findings provide first evidence of such a direct link."

But first more work needs to be done characterizing these cells. The cancer stem cells identified in this study are very rare; the authors estimated they represent about one in 1 million melanoma cells overall, and about one in 100,000 ABCB5-positive cells.

In other words, Rich explained, the researchers have not so much identified the cancer stem cells, as they have narrowed the search.

"They know the ZIP code of the cancer stem cell, but the full identity remains yet to be discovered," he said.

More information

For more on melanoma, visit the American Academy of Dermatology  .

MONDAY, Jan. 7 (HealthDay News) -- Black cancer patients continue to be significantly less likely than white patients to receive treatment for lung, breast, colon and prostate cancers, new research finds.

The study also showed that few gains have been made in the provision of cancer care to Medicare beneficiaries since the early 1990s.

In an effort to find out whether cancer care has improved since 1992, a team of Yale University researchers analyzed data from the Surveillance, Epidemiology and End Results (SEER) Medicare database. They examined records of care provided for breast, colorectal, lung or prostate cancer from 1992 to 2002.

The team specifically examined data relating to treatments that were known to be provided differently according to race to find out whether those differences had changed. They compared data from almost 7,800 cases of colon cancer, close to 1,800 cases of rectal cancer, more than 11,00 cases of lung cancer, more than 40,000 cases of breast cancer and more than 82,000 prostate cancer cases.

After reviewing the results, the researchers found that there had been almost no improvement in the proportion of patients getting treated for most cancers. They also found that the differences in care provision according to race had not changed between 1992 and 2002. Racial disparities existed even among the smaller subset of patients who saw a doctor before their cancer diagnosis.

The bottom line: "Efforts in the last decade to mitigate cancer therapy disparities appear to have been unsuccessful," the authors wrote.

They recommend further efforts to address racial disparities with an emphasis on overall quality improvement.

The study is published in the Jan. 7 online edition of Cancer and was expected to be in the journal's Feb. 15 print issue.

More information

To learn more about cancer and cancer care, visit the American Cancer Society  .