Common gene boosts breast cancer risk in smokers

February 14, 2008

NEW YORK (Reuters Health) - Researchers have confirmed yet another ill effect of smoking cigarettes: it increases the risk of breast cancer in women with a common genetic variation.

The gene involved, N-acetyltransferase 2 (NAT2), is believed to help clear the body of aromatic amines, a major carcinogen in tobacco smoke. The researchers found that women with the slower-acting form of this gene -- who represent 50 percent to 60 percent of the white population and 35 percent to 40 percent of African-Americans -- are more likely to get breast cancer if they smoke.

But the study's lead author said the finding shouldn't motivate people to undergo; instead, she said, it should spur them to quit smoking. "We still know very little about what these genes do and how they might affect risk-we think the most important thing for people to do is to live a healthy lifestyle," Dr. Christine B. Ambrosone of the Roswell Park Cancer Institute in Buffalo, New York, told Reuters Health.

It has been known for years, Ambrosone noted, that the risk of bladder cancer is higher in people with the slow-acting gene version, known as the slow acetylator NAT2 genotype. However, research to date has not found any link between cigarette smoking and overall breast cancer risk. Scientists had theorized that smoking might actually reduce breast cancer risk because it can lower estrogen levels.

To investigate whether the presence of genetic mutations may influence the smoking-breast cancer relationship, Ambrosone and her colleagues analyzed data from 13 studies including a total of 11,922 women.

For women with the slow-acting gene, the researchers found, breast cancer risk increased with the number of pack years smoked, but smoking had no effect on breast cancer risk in women with the fast-acting genotype.

However, women with the slow-acting gene who smoked for at least 20 pack years -- the equivalent of a pack a day for 20 years --were 44 percent more likely to develop breast cancer than non-smokers. Theis iIncreased risk was seen for both premenopausal and postmenopausal women with the slow acetylator NAT2 gene.

"Because of the frequency of slow acetylator genotypes among non-Asian populations...smoking cessation programs need to be further targeted to women as a means for preventing breast cancer," Ambrosone and her colleagues conclude.

"What we believe is important is the public health message," the researcher said. "Here's one more adverse health outcome that smoking is likely related to."