MONDAY, April 20 (HealthDay News) -- Scientists looking at everyday factors that influence cancer risk are finding important new clues that could affect cancer prevention strategies.

"Many of us believe that prevention is better than trying to identify drugs for people after they get cancer," said Dr. Peter Shields, deputy director of the Lombardi Comprehensive Cancer Center and interim chairman of the Department of Medicine at Georgetown University Medical Center in Washington, D.C. "As we understand risk factors better, it may be possible to personalize cancer prevention."

Shields moderated a Monday teleconference highlighting cancer prevention-related findings that are being presented at the annual meeting of the American Association for Cancer Research, in Denver.

One study found that two common gene variants do not protect individuals from the ill effects of smoking.

In the study, smoking boosted the odds for the two most common types of colorectal polyps: adenomas and hyperplastic polyps, although the association was stronger in the latter.

People who had smoked a pack of cigarettes a day for a year had a 68 percent increased risk for adenomas but a 238 percent increased risk for hyperplastic polyps. Those still smoking had the same risk for adenomas as former smokers but a more than threefold increased risk for the second type of polyp.

Polyps can be precursors to colon cancer, but if they're detected early, the disease can often be prevented.

There was also a slight though not statistically significant risk from "charred" (well done) meat.

"Susceptibility to smoking did not vary by this gene, and everyone needs to be concerned [about the risk of smoking]," said Andrea N. Burnett-Hartman, a doctoral student at the Fred Hutchinson Cancer Research Center in Seattle.

"This gene is not going to protect you from the carcinogenic effects of smoking, at least in colorectal tissue," she said. In terms of meat consumption, she added that "everything in moderation" remains a good rule.

Another study found that specific genetic variations in the cox-1 and cox-2 genes indicate different risks for colorectal cancer. This might help determine who would benefit from the cancer-prevention benefits of nonsteroidal anti-inflammatory drugs (NSAIDs).

Although NSAIDs, including aspirin and cox-2 inhibitors, have been shown to reduce the risk of colorectal cancer, that benefit may be nullified by an increased risk of heart disease seen in some cox-2 inhibitors such as Vioxx, which was removed from the market.

Other findings being presented at the society's meeting include:

• A tool that looks simultaneously at several genetic variants and family history might more accurately predict who is at risk for prostate cancer and who could benefit from more aggressive prevention efforts. Men who had at least 15 of the gene variants included in the tool were found to have a 34 percent increased risk of developing prostate cancer in a 20-year span, or 45 percent increased risk if they had a family history of the disease. But without the combination of genetic information, their risk would have been estimated at only 13 percent.
• Rats born to mothers who had been given folic acid supplementation during and after pregnancy were found to have experienced changes in DNA methylation in both the liver and the colon. DNA methylation is a process whereby genes can be turned off or on. Folic acid is recommended before and during pregnancy to prevent neural tube defects in babies. Folic acid intake in North America has soared since these recommendations were implemented in 1998.
• Abnormal collections of cells were found in the blood of 38 percent of people with chronic lymphocytic leukemia (CLL) as early as 10 years before their diagnosis -- something that could be a clue in the so-far fruitless search for causes of the disease. "Apparently, these cells are cranking out proteins years before people get CLL," said Dr. Neil Caporaso, a section chief at the U.S. National Cancer Institute. "We can try to understand what causes people to get these abnormalities and, more importantly, what causes somebody to progress from having relatively benign protein abnormalities to developing leukemia. We can search for environmental agents and genes that could cause this next step."

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