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Why Stopping Smoking Does Not Always Stop Cancer

Tom Gilbert
 
As researchers have long known, when cigarette smokers quit, they reduce their risk of developing many — but not all — smoking-related diseases. For example, current and ex-smokers remain at considerably greater risk for lung cancer than non-smokers.

What they did not know was why.

Now, a study published in the August, 2007 online journal, BMC Genomics, sheds some light on why former smokers remain far more susceptible to lung cancer than those who have never smoked.

A team led by Wan L. Lam and Stephen Lam from the British Columbia Cancer Agency looked at lung tissue from 24 current and former smokers, as well as from people who had never smoked. They used a technique called serial analysis of gene expression (SAGE), which helps to identify patterns of gene activity.

Only about a fifth of the genes in a human cell are active, or "switched on," at a given time, but smoking changes this. The researchers found that some of these changes are irreversible and that others can be reversed by stopping smoking. For example, some DNA repair genes are irreversibly damaged by smoking, and smoking also permanently switched off genes that help combat lung cancer.

"Those genes and functions which do not revert to normal levels upon smoking cessation may provide insight into why former smokers still maintain a risk of developing lung cancer," according to Raj Chari, also of the British Columbia Cancer Agency and first author of the study.

The study is the largest human SAGE study reported to date, and also generated a large SAGE library for future research.

Tobacco smoking accounts for 85 percent of lung cancers, with former smokers accounting for half of those diagnosed with the disease.
September 10, 2007



 
 
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