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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.