PI: David Christiani, MD (HSPH)
Co-PI: John Wain, MD (MGH)

Description

Although up to 90% of lung cancer in the United States is attributed to cigarette smoking, only 10% of smokers develop bronchogenic carcinoma. A plausible explanation for this observation is that host factors influence an individual’s susceptibility to tobacco smoke. The secular trend in lung cancer histology indicates that the proportion and incidence of lung adenocarcinoma has been increasing markedly over the past two decades. Adenocarcinoma now predominates as the most prevalent cell type for bronchogenic carcinoma. Postulated reasons for this change have included changes in tobacco constituents, the rising proportion of former smokers, whereby the risk of having an adenocarcinoma among those developing lung cancer increases proportionally to the time since smoking cessation. Our own preliminary data suggest that younger women are at especially high risk, given the presence of certain gene polymorphisms. We propose to take advantage of a large, on-going hospital-based case-control study, and to focus our efforts on the adenocarcinoma histology with particular attention to gender. The specific aims of this project include:

1. To assess the role of germline polymorphisms in xenobiotic metabolism genes, and in genes associated with DNA repair and the p53 tumor suppressor gene pathway in lung adenocarcinoma susceptibility.
2. To assess the role of gender with regard to genetic susceptibility to lung adenocarcinoma.
3. To assess EGFR polymorphisms and outcome in treated adenocarcinoma patients. EGFR (epidermal growth factor receptor) inhibitors were approved recently by the FDA for treatment of advanced NSCLC when other chemotherapeutic agents have failed.

David Christiani, MD - http://www.hsph.harvard.edu/lungcancer/
David Christiani, MD/John Wain, MD – http://www.massgeneral.org/cancer/research/clinical_research/thoracic.asp
John Wain, MD - www.massgeneral.org/surgery/hyperhidrosis/doctors/wain.htm

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