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Some gene damage from smoking is permanent: study
Aug. 30, 2007
Courtesy BioMed Central
and World Science staff
A new study may help explain why former smokers are still more prone to lung cancer than those who have never
smoked. It found that smoking causes some permanent genetic damage.
Quitting still offers huge health benefits, researchers stressed, as the risk to former smokers is much lower than for current smokers.
A team led by Wan Lam and Stephen Lam from the BC Cancer Agency in Vancouver, Canada, took samples from the lungs of 24 current and former smokers, as well as from people who have never smoked.
They used the samples to create libraries using a technique called serial analysis of gene expression, which helps to identify patterns of gene activity.
Only about a fifth of the genes in a cell are switched on at any given time, but smoking leads to changes in gene activity. The researchers found that some of these changes, though not all, persisted even years after quitting smoking.
The reversible genes were particularly involved in “xenobiotic” functions—managing chemicals not produced in the body—and metabolism of genetic material and mucus secretion, scientists found. The irreversible damage was to some DNA repair genes, and to the activity of genes that help fight lung cancer development.
“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,” said Raj Chari, first author of the study. Tobacco smoking accounts for 85 percent of lung cancers, and former smokers account for half of those newly diagnosed with the disease.
The gene findings are published in the Aug. 29 issue of the online research journal
BMC Genomics.
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A new study may help explain why former smokers are still more prone to lung cancer than those who have never smoked.
Researchers led by Wan Lam and Stephen Lam from the BC Cancer Agency in Vancouver, Canada, took samples from the lungs of 24 current and former smokers, as well as from people who have never smoked. They used the samples to create libraries using a technique called serial analysis of gene expression, which helps to identify patterns of gene activity.
Only about a fifth of the genes in a cell are switched on at any given time, but smoking leads to changes in gene activity. The researchers found that some of these changes, though not all, persisted even years after quitting smoking.
Quitting still offers huge health benefits, researchers stressed, as the risk to former smokers is much lower than for current smokers.
The reversible genes were particularly involved in “xenobiotic” functions—managing chemicals not produced in the body—and metabolism of genetic material and mucus secretion, scientists found. The irreversible damage was to some DNA repair genes, and to the activity of genes that help fight lung cancer development.
“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,” said Raj Chari, first author of the study. Tobacco smoking accounts for 85 percent of lung cancers, and former smokers account for half of those newly diagnosed with the disease.
The gene findings are published in the Aug. 29 issue of the online research journal BMC Genomics.
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