Shuting Jia1, Wenru Tang2, Ying Luo2. 1. Laboratory of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Faculty of Environmental Science and Engineering, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Chenggong County, Kunming, 650500, Yunnan, China. lilith-jia@hotmail.com. 2. Laboratory of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Faculty of Environmental Science and Engineering, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Chenggong County, Kunming, 650500, Yunnan, China.
Abstract
BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant neoplasms worldwide. The p53 gene is frequently mutated in some histological subtypes of HCC. The role of p53 mutations and polymorphic variant of codon 72 in the prognosis of disease is still unclear. The p53 tumor suppressor gene Arg72Pro polymorphism has been associated with HCC. However, results were inconsistent. This meta-analysis was performed to estimate the association between p53 Arg72Pro polymorphism and HCC or HCC infected by HBV/HCV. METHODS: Electronic search of PubMed was conducted to select studies. Studies containing available genotype frequencies of Arg72Pro were chosen, and pooled odds ratio (OR) with 95 % confidence interval (CI) was used to assess the association. RESULTS: Ten published studies, including 1,371 HCC cases and 2,517 controls were identified. The overall results suggested that the variant genotypes were associated with the HCC risk (Pro/Pro vs. Pro/Arg + Arg/Arg: OR 1.355, 95 % CI 1.041-1.764, p = 0.024). In the stratified analysis, individuals with the Pro/Pro in the recessive model had increased risk of HCC (OR 1.927, 95 % CI 1.127-3.297, p = 0.017) in Caucasian. A symmetric funnel plot, the Begg's test, was suggestive of the lack of publication bias. There was no association between the p53 codon 72 polymorphism and HBV/HCV-positive HCC. CONCLUSION: This meta-analysis suggests that p53 condon 72 Pro/Progenotypes are associated with increased risk of HCC in Caucasian. To validate this association, further studies with larger participants worldwide are needed to examine the associations between this polymorphism and HCC.
BACKGROUND:Hepatocellular carcinoma (HCC) is one of the most common malignant neoplasms worldwide. The p53 gene is frequently mutated in some histological subtypes of HCC. The role of p53 mutations and polymorphic variant of codon 72 in the prognosis of disease is still unclear. The p53tumor suppressor gene Arg72Pro polymorphism has been associated with HCC. However, results were inconsistent. This meta-analysis was performed to estimate the association between p53 Arg72Pro polymorphism and HCC or HCC infected by HBV/HCV. METHODS: Electronic search of PubMed was conducted to select studies. Studies containing available genotype frequencies of Arg72Pro were chosen, and pooled odds ratio (OR) with 95 % confidence interval (CI) was used to assess the association. RESULTS: Ten published studies, including 1,371 HCC cases and 2,517 controls were identified. The overall results suggested that the variant genotypes were associated with the HCC risk (Pro/Pro vs. Pro/Arg + Arg/Arg: OR 1.355, 95 % CI 1.041-1.764, p = 0.024). In the stratified analysis, individuals with the Pro/Pro in the recessive model had increased risk of HCC (OR 1.927, 95 % CI 1.127-3.297, p = 0.017) in Caucasian. A symmetric funnel plot, the Begg's test, was suggestive of the lack of publication bias. There was no association between the p53 codon 72 polymorphism and HBV/HCV-positive HCC. CONCLUSION: This meta-analysis suggests that p53 condon 72 Pro/Progenotypes are associated with increased risk of HCC in Caucasian. To validate this association, further studies with larger participants worldwide are needed to examine the associations between this polymorphism and HCC.
Authors: A Storey; M Thomas; A Kalita; C Harwood; D Gardiol; F Mantovani; J Breuer; I M Leigh; G Matlashewski; L Banks Journal: Nature Date: 1998-05-21 Impact factor: 49.962
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Authors: R Birgander; A Själander; A Rannug; A K Alexandrie; M I Sundberg; J Seidegård; G Tornling; G Beckman; L Beckman Journal: Carcinogenesis Date: 1995-09 Impact factor: 4.944
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