My research is focused on airway inflammation and its role in airway epithelial carcinogenesis. Tumor-promoting inflammation is a cancer hallmark, and it is considered an enabling characteristic due to its contributions to the acquisition of core hallmark capabilities. Cigarette smoking is the principal cause of lung carcinogenesis. However, several studies have found that smokers with chronic obstructive pulmonary disease (COPD), an inflammatory disease of the lung, have an increased risk of lung cancer compared to smokers with comparable cigarette exposure but without COPD. This suggests a strong link between COPD-related airway inflammation and lung cancer. In addition, it is known that mutant epithelial cells begin to edit the microenvironment as soon as they transform but the exact mechanisms involved in this immuno-editing process from escaping the immunosurveillance to tumor progression still not well understood. We have previously shown that the numerous cytokines released during inflammation (oncogene-driven or COPD-related) promote lung tumorigenesis in a genetic mouse model of lung cancer. We are currently dissecting the sex- and cell-type specific mechanisms responsible for this phenomenon with genetic and pharmacologic approaches. This will provide a better understanding of the role of specific inflammatory pathways in lung carcinogenesis, and subsequently allow preclinical testing of the efficacy of anti-inflammatory agents in preventing lung cancer in high-risk population or patient with early metaplastic lesions. This would also have a major impact on the treatment of patients with lung cancer by providing the basis for rationally directed immunotherapeutic modalities to improve the efficacy of currently available treatment regimens.
Publications/Creative Works
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