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Association between PARP‐1 V762A polymorphism and cancer susceptibility: a meta‐analysis
Author(s) -
Yu Hongping,
Ma Hongxia,
Yin Ming,
Wei Qingyi
Publication year - 2012
Publication title -
genetic epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.301
H-Index - 98
eISSN - 1098-2272
pISSN - 0741-0395
DOI - 10.1002/gepi.20663
Subject(s) - meta analysis , genetics , biology , oncology , medicine
Poly(ADP‐ribose) polymerase‐1 (PARP‐1 catalyzes poly(ADP‐ribosyl)ation to various proteins involved in many cellular processes, including DNA damage detection and repair and cell proliferation and death. PARP‐1 has been implicated in human carcinogenesis, but the association between the most‐studied PARP‐1 V762A polymorphism (rs1136410) and risk of various cancers was reported with inconclusive results. The aim of this study was to assess the association between the PARP‐1 V762A polymorphism and cancer risk. A meta‐analysis of 21 studies with 12,027 cancer patients and 14,106 cancer‐free controls was conducted to evaluate the strength of the association using odds ratio (OR) with 95% confidence interval (CI). Overall, no significant association was found between the PARP‐1 V762A polymorphism and cancer risk. In the stratified analyses, however, it was found that the variant A allele of the PARP‐1 V762A polymorphism was associated with an increased risk of cancer among Asian populations (VA + AA vs. VV: OR = 1.11, 95% CI: 1.01–1.23; P heterogeneity = 0.210), but a decreased risk of cancer (VA + AA vs. VV: OR = 0.89, 95% CI: 0.80–1.00; P heterogeneity = 0.004) among Caucasian populations, especially for glioma risk (OR = 0.79, 95% CI: 0.69–0.90; P heterogeneity = 0.800). This meta‐analysis found evidence for an association of the PARP‐1 V 762A polymorphism with increased risk of cancer among Asians, but decreased risk of cancer among Caucasians, particularly of glioma. Further well‐designed studies with large sample sizes of different ethnic populations and different cancer types are warranted to confirm these findings. Genet. Epidemiol . 36 : 56–65 2012. © 2011 Wiley Periodicals, Inc.