title: Genetic polymorphisms involved in the inflammatory response and lung cancer risk: a case-control study in Japan.
abstract: Evidence is accumulating that chronic inflammation may have an important mechanism for the development and progression of lung cancer. Therefore, genetic polymorphisms in genes that involved in the inflammatory response may be associated with lung cancer risk. We evaluated the role of tumor necrosis factor α (TNFA) rs1799724, interleukin 1β (IL1B) rs16944, IL6 rs1800796, myeloperoxidase (MPO) rs2333227 and C-reactive protein (CRP) rs2794520 in a case-control study comprised of 462 lung cancer cases and 379 controls in a Japanese population. Unconditional logistic regression was used to assess the adjusted odds ratios (OR) and 95% confidence intervals (95% CI). CRP rs2794520 (OR=1.64, 95% CI=1.19-2.26) and IL6 rs1800796 (OR=1.41, 95% CI=1.02-1.96) were associated with lung cancer risk. In addition, we assessed interactions between the polymorphisms and smoking. The polymorphisms did not significantly modify the association between smoking and lung cancer. As TNFA triggers a cytokine cascade, the modifying effect of the TNFA rs1799724 genotypes on the association of any of the remaining polymorphisms with lung cancer risk was also examined. There was a significant interaction between TNFA rs1799724 and MPO rs2333227 (Pinteraction=0.058). Future studies involving larger control and case populations will undoubtedly lead to a more thorough understanding of the role of the polymorphisms involved in the inflammation pathway in lung cancer.
authors.affiliation: Department of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan. Electronic address: chikako@phealth.med.kyushu-u.ac.jp.
authors.forename: Chikako
authors.initials: C
authors.lastname: Kiyohara
authors.forename: Takahiko
authors.initials: T
authors.lastname: Horiuchi
authors.forename: Koichi
authors.initials: K
authors.lastname: Takayama
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Nakanishi
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000235:genetics / Q000276:immunology; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000276:immunology*; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology; D007564:Japan; D008175:Lung Neoplasms / Q000235:genetics* / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009195:Peroxidase / Q000235:genetics / Q000276:immunology; D020641:Polymorphism, Single Nucleotide; D012306:Risk; D012307:Risk Factors; D012907:Smoking; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D009195:Peroxidase
keywords: Epidemiology; Genetic polymorphism; Inflammatory cytokine; Lung cancer; Smoking