Tobacco Exposure And Genetics Linked To Lung Cancer RiskEditor's Choice
Main Category: Lung Cancer
Also Included In: Genetics; Cancer / Oncology
Article Date: 27 Apr 2012 - 11:00 PDT
According to a study in the April 25 issue of the Journal of the National Cancer Institute, genotype rs1051730-rs16969968 and objective measures of tobacco exposure are associated with each other. The link indicates that the risk of developing lung cancer is mostly, if not completely, caused by the level of tobacco exposure.
Scientists are aware of the link between the rs1051730-rs16969968 genotype and heaviness of smoking, an individual's risk of lung cancer and other smoking-related outcomes. Previous research was generally based on participants' self-reported smoking habits, however, this could have led to underestimating certain links and obscured the contribution of how heavy a person smokes by potentially upsetting the balance between the link to lung cancer and other health outcomes.
Marcus R. Munafò, Ph.D., of the School of Experimental Psychology at the University of Bristol, and his team decided to establish the link between the rs1051730-rs16969968 genotype and self-reported cigarette consumption and plasma or serum cotinine levels by collecting data from six independent studies that examined self-reported daily cigarette consumption and plasma or serum cotinine levels of cigarette smokers to perform a meta-analysis of pooled per-allele effects. They also used published data on the link between cotinine levels and lung cancer risk to assess the association between the genotypes and lung cancer risk.
The findings proved that even after adjusting for self-reported cigarette consumption, the rs1051730-rs16969968 genotype is strongly linked to tobacco exposure measured through cotinine levels.
The researchers declare:
"These data therefore support the conclusion that association of rs1051730-rs16969968 genotype with lung cancer risk is mediated largely, if not wholly, via tobacco exposure."
They highlight that their study had certain limitations, such as data being obtained from disparate studies from different populations, however, they note that the data is also based on current smoking measures instead of lifetime exposure, which is more strongly linked to the risk of lung cancer.
The researchers are confident that their findings are significant in demonstrating that phenotype precision is important to uphold in GWAS studies, instead of ever-larger sample sizes, saying:
"The use of objective measures of smoking behavior in genome-wide studies may reveal novel variants associated with these outcomes, which would be undetectable using conventional self-report measures."
Margaret R. Spitz, M.D., MPH, of the Department of Molecular and Cellular Biology at the Dan L. Duncan Cancer Center at Baylor College of Medicine writes in a linked editorial, these findings "confirm that cigarettes per day is an imprecise measure of nicotine consumption, and favor the interpretation that the association between these variants and lung cancer is mediated by smoking. But the degree to which the association is mediated by smoking is yet to be determined." She adds that further studies, including mouse and cellular models together with emerging metabolic markers, "may help tease apart the direct and indirect associations of these variants with lung cancer risk."
Written By Petra Rattue
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