Metabolic gene polymorphisms and lung cancer risk in non-smokers
2005; Elsevier BV; Volume: 592; Issue: 1-2 Linguagem: Inglês
10.1016/j.mrfmmm.2005.06.002
ISSN1873-135X
AutoresSara Raimondi, Paolo Boffetta, Sisko Anttila, Jürgen Brockmöller, Dorota Butkiewicz, Ingolf Cascorbi, Margie L. Clapper, Tommaso A. Dragani, Seymour Garte, Andre Gsur, Gerald Haidinger, Ari Hirvonen, Magnus Ingelman‐Sundberg, I Kalina, Qing Lan, Vera P. Leoni, Loı̈c Le Marchand, Stephanie J. London, Monica Neri, Andrew C. Povey, Agneta Rannug, Edyta Reszka, David Ryberg, Angela Risch, Marjorie Romkes, Alberto Ruano‐Raviña, Bernadette Schoket, Monica Spinola, Haruhiko Sugimura, Xifeng Wu, Emanuela Taioli,
Tópico(s)BRCA gene mutations in cancer
ResumoSince genetic factors may play an important role in lung cancer development at low dose carcinogen exposure, non-smokers are a good model to study genetic susceptibility and its interaction with environmental factors. We evaluated the role of the metabolic gene polymorphisms CYP1A1MspI, CYP1A1Ile462Val, GSTM1, and GSTT1 in non-smoker lung cancer patients from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC). Non-smokers (defined as subjects who never smoked on a regular basis) were selected from the GSEC database. We pooled the raw data from 21 case-control studies for a total of 2764 Caucasians (555 cases and 2209 controls) and 383 Asians (113 cases and 270 controls). Tests of heterogeneity and of inclusion bias were performed. A significant association between lung cancer and CYP1A1Ile462Val polymorphism was observed in Caucasians (adjusted OR = 2.04, 95% CI 1.17–3.54). GSTT1 deletion seems to be a risk factor for lung cancer in Caucasian non smokers only when the analysis was restricted to studies including healthy controls (adjusted OR = 1.66, 95% CI 1.12–2.46). A protective effect on lung cancer was observed with the combination of CYP1A1 wild type, GSTM1 null, and GSTT1 non-null genotypes. None of the analysed polymorphisms were associated with lung cancer in Asian non-smokers. Our analysis confirms previous findings that CYP1A1Ile462Val polymorphism may play a role in lung carcinogenesis in Caucasian non-smokers.
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