Smoking tobacco is no longer considered sexy, but it may prove a permanent turn on for some genes. Research published today in the online open access journal BMC Genomics could help explain why former smokers are still more susceptible to lung cancer than those who have never smoked.
A Canadian team led by Wan L Lam and Stephen Lam from the BC Cancer Agency, took samples from the lungs of 24 current and former smokers, as well as from non-smokers who have never smoked. They used these lung samples to create libraries using 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 cell are switched on at any given time, but environmental changes such as smoking lead to changes in gene activity. The researchers found changes that were irreversible, and some changes that were reversed by stopping smoking. The reversible genes were particularly involved in xenobiotic functions (managing chemicals not produced in the body), nucleotide metabolism and mucus secretion. Some DNA repair genes are irreversibly damaged by smoking, and smoking also switched off genes that help combat lung cancer development.
The researchers identified a number of genes not previously associated with smoking that are switched on in active smokers. One example is CABYR, a gene involved in helping sperm to swim and associated with brain tumours, which may have a ciliary function. The team also further investigated changes in genes involved in airway repair and regeneration, and within this group identified genes that fell into three categories following cessation of smoking: reversible (TFF3, encoding a structural component of mucus; CABYR, in it's newly discovered bronchial role), partially reversible (MUC5AC, a mucin gene) and irreversible (GSK3B, involved in COX2 regulation). These findings were tested against a second cohort of current, former and non-smokers.
"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, 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, and former smokers account for half of those newly diagnosed with the disease.
Effect of active smoking on the human bronchial epithelium transcriptome
Raj Chari, Kim M Lonergan, Raymond T Ng, Calum MacAulay, Wan L Lam and Stephen Lam
BMC Genomics (in press)
After the embargo, article available from the journal website at: http://www.biomedcentral.com/bmcgenomics/
Article citation and URL available on request at email@example.com on the day of publication
For author contact details please contact Jinny Wu (Press Office, BC Cancer Agency) by phone +001 604.877.6272 or via email firstname.lastname@example.orgBioMed Central (http://www.biomedcentral.com) is an independent online publishing house committed to providing open access to peer-reviewed biological and medical research. This commitment is based on the view that immediate free access to research and the ability to freely archive and reuse published information is essential to the rapid and efficient communication of science.
BioMed Central currently publishes over 160 journals across biology and medicine. In addition to open-access original research, BioMed Central also publishes reviews, commentaries and other non-original-research content. Depending on the policies of the individual journal, this content may be open access or provided only to subscribers.
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.