ROCHESTER, MN – Obese patients with colon cancer are at greater risk for death or recurrent disease compared to those who are within a normal weight range, according to a report in Clinical Cancer Research, a journal of the American Association for Cancer Research.

“Obesity has long been established as a risk factor for cancer, but our study in colon cancer patients shows that obesity predicts a poorer prognosis after the cancer is surgically removed,” said Frank A. Sinicrope, M.D., professor of medicine and oncology at the Mayo Clinic in Rochester.

There are approximately 150,000 new cases of colon cancer diagnosed each year in the United States, and colon cancer tends to affect men and women equally, said James Abbruzzese, M.D., chairman of the Department of Gastrointestinal Medical Oncology at The University of Texas M. D. Anderson Cancer Center and an editorial board member of Clinical Cancer Research.

James Abbruzzese, M.D.

“More studies are now demonstrating that obesity plays a role as an independent risk factor for poorer patient prognosis that is unrelated to stroke or heart disease,” said Abbruzzese.

Remarkably though, many patients remain unaware of the risk associated between obesity and cancer. Results of a recent survey from the American Institute for Cancer Research showed that only 51 percent of the participants knew about the link between obesity and cancer, compared with 94 percent who were aware of the increased cancer risk associated with tobacco use, and 87 percent who knew of the increased cancer risk associated with sun exposure.

For the current study, Sinicrope and colleagues evaluated 4,381 patients with stage II or stage III colon cancer who had received adjuvant chemotherapy in clinical trials. Of these patients, 20 percent were obese.

Frank A. Sinicrope, M.D.

Obesity was significantly linked with poorer overall survival and was independent of other variables analyzed. The prognostic impact was stronger in men than in women, and men in the highest body mass index category for obesity had a 35 percent increased risk of death compared to normal weight patients. The weaker effect in women is consistent with studies that have shown a lower risk of developing colon cancer in obese women compared to obese men.

“We do not know if this is due to biology or the way we measure obesity,” said Sinicrope. “Body mass index is a limited measure and there is evidence that abdominal fat may be a better predictor of colon cancer risk and perhaps prognosis in men than in women. There is also the potential influence of menopausal status and hormone replacement therapy in women.”

- MFP Wire Services
- 03-10-2010

CALGARY, ALBERTA, CANADA — Researchers in Canada have detected a novel oncolytic viral therapy against prostate cancer with use of a virus called the reovirus, according to study results published in Cancer Research, a journal of the American Association for Cancer Research.

The respiratory, enteric, orphan virus (commonly known as reovirus) is a non-attenuated, environmental virus that has shown oncolytic potential against many types of cancer, specifically lymphoid, ovarian, breast, pancreatic and high grade glioma cancer, according to the study. This is the first time the virus has been studied against prostate cancer.

“The reovirus is a very common, ubiquitous virus that most people are exposed to. As far as we know, it doesn’t cause any significant illness in humans, even though when someone is exposed to it, it manifests, at most, as a mild respiratory infection or mild diarrhea,” said researcher Don Morris, M.D., Ph.D., medical oncologist in the Department of Oncology at the Tom Baker Cancer Center in Alberta, Canada.

“For the treatment of localized prostate cancer, we found that the reovirus is safe and has evidence of specific tumor vs. normal prostate cell efficacy,” added Morris.

Using preclinical and clinical settings, Morris and colleagues examined the efficacy of the reovirus as an experimental therapeutic for prostate cancer in vitro and in vivo. Among the six patients who participated in the study, all had early-stage, organ-confined prostate cancer. Each patient underwent a single intralesional virus injection into a suitable prostate cancer nodule via transrectal ultrasound guidance. Three weeks later, Morris and colleagues removed the prostate as part of the patient’s standard treatment for correlative science analysis.

Findings showed safety and efficacy with minimal toxicity and no viral replication in the normal parts of the prostate, according to Morris. Cancer cell death was evident in the prostate. Studies to date have suggested that the virus’ side effects are relatively modest, consisting of mild, self-limiting, flu-like symptoms.

“Our results are a stepping stone into future prostate cancer clinical trials with another category of cancer therapeutics,” he said.

Robert Clarke, Ph.D., D.Sc., professor of oncology at Lombardi Comprehensive Cancer Center at Georgetown University and an editorial board member of Cancer Research, agreed, stating that he believes this study is worthy of subsequent clinical trials of the reovirus as a possible way of treating some prostate cancers.

“People have known of this application of the reovirus in trials, but no one to my knowledge has conducted studies in prostate cancer,” said Clarke, who was not associated with this study. “I think this is an interesting approach. There is not a lot done in oncolytics, but clearly it is an area that is getting increasing attention, and we need everything we can get our hands on to make a difference in these patients.”

- MFP Wire Services
- 03-10-2010

CINCINNATI, OH — Individuals with a certain type of genetic susceptibility to lung cancer face a greatly increased risk for the deadly disease with even a small exposure to cigarette smoke, a study team that includes researchers from the University of Cincinnati has concluded.

For family members who carry this genetic variant, the risk of lung cancer is similar for both light and heavy smokers, the researchers say, adding that even non-smokers who are exposed to second-hand cigarette smoke and have a family history of lung cancer should be monitored for early detection.

The study, conducted by the Genetic Epidemiology of Lung Cancer Consortium, was recently published online by Cancer Research, a publication of the American Association for Cancer Research.

Marshall Anderson, PhD, a professor in University of Cincinnati’s cancer and cell biology department, is principal investigator of the Genetic Epidemiology of Lung Cancer Consortium, whose University of Cincinnati portion is known as the Family Lung Cancer Study. Susan Pinney, PhD, an associate professor in the department of environmental health, is a co-investigator. The study’s first author is Christopher Amos, PhD, a professor and epidemiologist at the University of Texas M.D. Anderson Cancer Center in Houston.

“The study shows a strong gene-environment interaction between a region of chromosome 6q and smoking,” University of Cincinnati’s Anderson says. “People with this susceptibility locus can develop lung cancer even with a very little bit of smoking.”

According to the Centers for Disease Control and Prevention, about 200,000 cases of lung cancer were diagnosed in the United States in 2005, the most recent year for which statistics are available. More people die from lung cancer than any other type of cancer, the Centers for Disease Control and Prevention says.

To study the chromosome region’s effect on lung cancer risk, the researchers identified a haplotype (a portion of a chromosome containing genes that tend to be inherited together) that was associated with lung cancer. Collecting data from several recruitment sites including University of Cincinnati, they then divided smoking exposures into never smokers, light smokers (fewer than 20 pack years, with a pack year being the equivalent of a pack a day for 20 years), moderate smokers (20-40 pack years) and heavy smokers (40 or more pack years).

For family members without this genetic lung cancer risk, the risk of developing the disease tracked closely with the level of smoking—in other words, heavy smokers had a significantly greater risk of developing lung cancer than moderate smokers, who had a significantly greater risk than light smokers. But in family members with the genetic risk haplotype, even light smoking resulted in a greatly increased risk for developing lung cancer. From there, increasing smoking behaviors in this group of family members carried only weakly increasing risk for developing lung cancer.

“If you carried the inherited risk and then you smoked, it didn’t matter if you were a light smoker or a heavy smoker—you were significantly more likely to develop lung cancer,” Pinney says.

Adds Anderson: “If you have a family history of lung cancer, you probably should not even be around cigarette smokers.”

- MFP Wire Services
- 03-10-2010