Grant: CIHR Fellowship

Lung cancer represents one of the largest health burdens worldwide. Tobacco smoke is a well recognized cause of lung cancer. However, even with smoking cessation, former smokers sustain an elevated risk of developing lung cancer. In Canada alone, the population of former smokers is well over 7.5 million individuals and growing. Therefore, cancer in former smokers will remain a significant health concern for decades to come. Recent studies have discovered that while the majority of smoking-induced gene expression return to normal levels after quitting smoking, some genes are permanently damaged. Some of these irreversible genes are tumor suppressors which serve as gatekeepers of cancer development. In this study, I will first compare lung tissue from former smokers to those of current and never smokers, to identify smoke induced effects. Secondly, I will identify those genes that do not return to normal state after quitting smoking that are specific to lung cancer in former smokers. I propose that genes that are irreversibly disrupted in former smokers with lung cancer may have biological role in lung cancer development in this population. The identification of these irreversible genes will yield novel molecular targets for developing anticancer therapeutics or serve as diagnostic markers for early detection of lung cancer.