Abstract
Any association between the CYP1A1 Ile462Val polymorphism and endometrial cancer risk remains inconclusive. For a more precise estimate, we performed the present meta-analysis. PUBMED, OVID and EMBASE were searched for the studies which met inclusion criteria. Data in all eligible studies were evaluated and extracted by two authors independently. The meta-analysis estimated pooled odds ratio (OR) with 95% confidence interval (CI) for endometrial cancer risk attributable to the CYP1A1 Ile462Val polymorphism. A total of 7 studies were included in this meta-analysis. The results indicated no association between endometrial cancer risk and the CYP1A1 Ile462Val polymorphism (for Val vs Ile allele model [OR 1.09, 95% CI 0.73-1.62]; for Val.Val vs Ile.Ile genotype model [OR 1.54, 95% CI 0.56-4.23]; for (Ile.Val + Val.Val) vs Ile.Ile genotype model [OR 1.08, 95% CI 0.71-1.63]; for Val.Val vs (Ile.Ile + Ile.Val) genotype model [OR 1.46, 95% CI 0.53-4.04]). This meta-analysis suggests that there is no association between endometrial cancer risk and the CYP1A1 Ile462Val polymorphism.
Highlights
It is reported that endometrial cancer is the most frequent “estrogen-sensitivemalignancy” in women (Key et al, 1988) and that estrogen and its metabolites are known to be both inducers and promoters of endometrial cancer (Herrington et al, 2001)
The results indicated no association between endometrial cancer risk and the CYP1A1 Ile462Val polymorphism (for Val vs Ile allele model [odds ratio (OR) 1.09, 95% confidence interval (CI) 0.73-1.62]; for Val.Val vs Ile.Ile genotype model [OR 1.54, 95% CI 0.56-4.23]; for (Ile.Val + Val.Val) vs Ile.Ile genotpye model [OR 1.08, 95% CI 0.71-1.63]; for Val.Val vs (Ile.Ile + Ile.Val) genotype model [OR 1.46, 95% CI 0.53-4.04])
Inclusion criteria Eligible study must meet all the following inclusion criteria: (a) case–control study evaluating the CYP1A1 Ile462Val polymorphism and endometrial cancer risk; (b) listing the frequency of case and control according to different genotype; (c) full text articles; (d) literature published in English. (e) genotype distribution in the control of the study was in agreement with HardyWeinberg equilibrium (HWE)
Summary
It is reported that endometrial cancer is the most frequent “estrogen-sensitivemalignancy” in women (Key et al, 1988) and that estrogen and its metabolites are known to be both inducers and promoters of endometrial cancer (Herrington et al, 2001). Prolonged estrogen stimulation factors, including stimulation by nulliparity, late menopause, and obesity, have been identified as risk factors for the development of endometrial cancer (La Vecchia et al, 1986; Elwood et al, 1977). People with these high risk factors should greatly care for their behavior and lifestyle. It is obviously that genes encoding for enzymes involved in estrogen metabolism such as CYP1A1 have been hypothesized to be involved in the etiology of these pathologies (Herrington et al, 2001). The potential effect of CYP1A1 polymorphism on endometrial cancer risk is under the hypothesis that increased exposure to 2-OH estrogen might decrease, and increased exposure to 4-OH estrogen might increase, endometrial cancer risk (Doherty et al, 2005)
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