Törüner, Gökçe Altay2016-01-082016-01-082001http://hdl.handle.net/11693/15197Ankara : The Department of Molecular Biology and Genetics and the Institute of Engineering and Science of Bilkent University, 2001.Thesis (Ph.D.) -- Bilkent University, 2001.Includes bibliographical references.The effect of the GSTM1 and GSTT1 null genotypes, the GSTP1 Ile105Val, and TP53 Arg72Pro polymorphism on bladder cancer susceptibility was investigated in a case control study of 121 bladder cancer patients, and 121 age-sex matched controls in the Turkish population. The adjusted odds ratio (for age, sex, and smoking status) for the GSTM1 null genotype is 1.94 (95% CI 1.15- 3.26) and for the GSTP1 105 Ile/Val or Val/Val genotypes is 1.75 (95% CI 1.03- 2.99). GSTT1, and TP53 loci was not shown to be associated with bladder cancer. Combination of the two high risk genotypes, GSTM1 null and GSTP1 105 Ile/Val or Val/Val, revealed that the risk increases by 3.91 times (95% CI 1.88-8.13) when compared with the combination of the low risk genotypes of these loci. In individuals with a combined risk of cigarette smoking and the GSTM1 null genotype, bladder cancer risk is 2.81 (95% CI 1.23-6.35) relative to persons who do not smoke and carry the GSTM1 present genotype. The same risk for the GSTP1 105 Ile/Val or Val/Val genotypes is 2.38 (95% CI 1.12-4.95). These findings support the role for the GSTM1 null and the GSTP1 105 Ile/Val or Val/Val genotypes in the development of bladder cancer. Furthermore, gene-gene (GSTM1- GSTP1) and gene-environment (GSTM1-smoking, GSTP1-smoking) interactions increase this risk substantially.1 volumes (various pagings), illustrationsEnglishinfo:eu-repo/semantics/openAccessWJ504 .T67 2001Bladder neoplasms.Bladder cancer.Thesis