Cun Liao1, Yunfei Cao, Liucheng Wu, Jiahao Huang, Feng Gao. 1. Department of Colorectal and Anal Surgery, First Affiliated Hospital, Guangxi Medical University, Nanning, People's Republic of China.
Abstract
INTRODUCTION: GSTT1 status has been extensively studied as a colorectal cancer risk factor. However, the results are inconsistent. To examine this controversy, we performed a meta-analysis to evaluate the relationship between GSTT1 polymorphism and colorectal cancer. MATERIALS AND METHODS: We performed a literature search using PUBMED, EMBASE, Cochrane Library, and HuGNet database to February 2009, with no restrictions. All articles were independent and contained the minimum information necessary to estimate the colorectal cancer risk associated with GSTT1 null. Summary odds ratio (ORs) and 95% confidence intervals (CIs) were calculated using random-effect or fixed-effect models based on the heterogeneity of included studies. RESULTS: A total of 23 case-control studies, including a total of 11,057 subjects (5,058 cases and 5,999 controls), that related to GSTT1 polymorphism and risk of colorectal cancer were identified and included for analysis. The random-effect meta-analyses of all the 23 studies suggested that there was a small increased risk of colorectal cancer for individuals with GSTT1 null (OR was 1.23; 95% CI 1.02-1.49; I (2) = 76.9%, P for heterogeneity <0.001). The fixed-effect meta-analyses reached a similar results in Caucasians populations of ten studies (OR = 1.39; 95% CI 1.21-1.59; I (2) = 29.8%, P for heterogeneity = 0.171) and Asians populations of five studies (OR = 1.23; 95% CI 1.04-1.45; I (2) = 0.0%, P for heterogeneity = 0.428), with as inversely association in the other ethnic populations from four studies (OR = 0.69; 95% CI 0.54-0.877; I (2) = 0.0%, P for heterogeneity = 0.58). CONCLUSION: There was a small increased risk of colorectal cancer for individuals with GSTT1 null, especially for Caucasians populations and Asian populations.
INTRODUCTION:GSTT1 status has been extensively studied as a colorectal cancer risk factor. However, the results are inconsistent. To examine this controversy, we performed a meta-analysis to evaluate the relationship between GSTT1 polymorphism and colorectal cancer. MATERIALS AND METHODS: We performed a literature search using PUBMED, EMBASE, Cochrane Library, and HuGNet database to February 2009, with no restrictions. All articles were independent and contained the minimum information necessary to estimate the colorectal cancer risk associated with GSTT1 null. Summary odds ratio (ORs) and 95% confidence intervals (CIs) were calculated using random-effect or fixed-effect models based on the heterogeneity of included studies. RESULTS: A total of 23 case-control studies, including a total of 11,057 subjects (5,058 cases and 5,999 controls), that related to GSTT1 polymorphism and risk of colorectal cancer were identified and included for analysis. The random-effect meta-analyses of all the 23 studies suggested that there was a small increased risk of colorectal cancer for individuals with GSTT1 null (OR was 1.23; 95% CI 1.02-1.49; I (2) = 76.9%, P for heterogeneity <0.001). The fixed-effect meta-analyses reached a similar results in Caucasians populations of ten studies (OR = 1.39; 95% CI 1.21-1.59; I (2) = 29.8%, P for heterogeneity = 0.171) and Asians populations of five studies (OR = 1.23; 95% CI 1.04-1.45; I (2) = 0.0%, P for heterogeneity = 0.428), with as inversely association in the other ethnic populations from four studies (OR = 0.69; 95% CI 0.54-0.877; I (2) = 0.0%, P for heterogeneity = 0.58). CONCLUSION: There was a small increased risk of colorectal cancer for individuals with GSTT1 null, especially for Caucasians populations and Asian populations.
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