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Genetic variants in carcinogen-metabolizing enzymes, cigarette smoking and pancreatic cancer risk
Carcinogenesis, 04/16/2012
Clinical Article
Jang JH et al. – Variants of carcinogen metabolism genes are independently associated with pancreatic cancer risk and may modify the risk posed by smoking.
Methods- A population–based study was conducted with 455 pancreatic cancer cases and 893 controls.
- Epidemiological and smoking data were collected from questionnaires and variants were genotyped by mass spectrometry.
- Age– and sex–adjusted odds ratio (ASOR) and multivariate–adjusted odds ratio (MVOR) estimates were obtained using multivariate logistic regression, and interactions between each variant and smoking were investigated.
- Current smoker status [MVOR=2.29, 95% confidence interval (95% CI): 1.62, 3.22], 10–27 pack–years (MVOR=1.57, 95% CI: 1.13, 2.18), >27 pack–years (MVOR=1.77, 95% CI: 1.27, 2.46) and longer durations of smoking (19–32years: MVOR=1.46, 95% CI: 1.05, 2.05; >32years: MVOR=1.78, 95% CI: 1.30, 2.45) were associated with increased pancreatic cancer risk.
- CYP1B1–4390–GG (ASOR=0.36, 95% CI: 0.15, 0.86) and Uridine 5'–diphospho glucuronosyltransferase 1 family, polypeptide A7–622–CT (ASOR=0.77, 95% CI: 0.60, 0.99) were associated with reduced risk.
- N–acetyltransferase 1–640–GT/GG (ASOR=1.75, 95% CI: 1.00, 3.05), GSTM1 (rs737497)–GG (ASOR=1.41, 95% CI: 1.02, 1.95), GSTM1 gene deletion (ASOR=4.89, 95% CI: 3.52, 6.79) and glutathione S–transferase theta–1 gene deletion (ASOR=4.41, 95% CI: 2.67, 7.29) were associated with increased risk.
- Significant interactions were observed between pack–years and EPHX1–415 (P=0.04) and smoking status and N–acetyltransferase 2–857 (P=0.03).
