Genetic variants in cell cycle control pathway confer susceptibility to lung cancer

摘要: Purpose: To test the hypothesis that common sequence variants of cell cycle control genes may affect lung cancer predisposition. Experimental Design: We explored risk associations 11 polymorphisms in seven a large case-control study including 1,518 Caucasian patients and controls. Results: When individuals with variant-containing genotypes were compared homozygous wild-type carriers, significantly increased was identified for p53 intron 6 [rs1625895; odds ratio (OR), 1.29; 95% confidence interval (95% CI), 1.08-1.55] p27 5′ untranslated region (UTR; rs34330; OR, 1.27; CI, 1.01-1.60). Compared wild-types, variant STK15 F31I CCND1 G870A associated altered ORs 0.58 0.37-0.90) 1.26 1.03-1.53), respectively. assess cumulative effects all investigated on carcinogenesis, we conducted combined analysis found low-risk few adverse alleles, more alleles had an significant dose-dependent manner ( P trend = 0.041). This pattern evident ever smokers 0.037), heavy 0.020), older subjects 0.011). Higher-order gene-gene interactions evaluated using classification regression tree analysis, which indicated might be carcinogenesis never/light-smokers smokers, respectively. Conclusions: Our results suggest gene smoking function collectively to modulate cancer.