Abstract
Background and PurposePrevious studies concerning the role of CD86 polymorphisms (rs1129055 and rs17281995) in cancer fail to provide compelling evidence. The aim of this study was to investigate the role of common polymorphisms in the risk of cancer by meta-analysis.MethodsBy using the search terms Cluster of Differentiation 86/CD86/B7-2/polymorphism/polymorphisms/cancer, we searched PubMed, Embase, CNKI, and Wanfang and identified four studies for rs1129055 (2137 subjects) and rs17281995 (2856 subjects) respectively. Cancer risk was estimated by odds ratio (OR) and 95% confidence interval (95% CI).Major FindingsOverall, we observed significant reduced risk of cancer in relation to rs1129055. Compared with the individuals with AA genotype, the individuals with GG genotype appeared to have 62% decreased risk to develop cancer (GG versus AA: OR, 0.62; 95% CI, 0.49–0.79; Phet., 0.996). Similar effects were indicated in the G versus A allele model and the GG versus GA+AA genetic model (OR, 0.83; 95% CI, 0.74–0.93; Phet., 0.987; OR, 0.63; 95% CI, 0.50–0.79; Phet., 0.973). In addition, we found genotypes of rs17281995 had a major effect on overall cancer risk (CC versus GG: OR, 2.38; 95% CI, 1.43–3.95; Phet., 0.433; C versus G: OR, 1.23; 95% CI, 1.06–1.43; Phet., 0.521; CC versus GC+GG: OR, 2.38; 95% CI, 1.45–3.93; Phet., 0.443). The association was also observed in Caucasians and colorectal cancer. No obvious publication bias was detected in this meta-analysis.ConclusionsThese data reveal that rs1129055 may have protective effects on cancer risk in Asians and that rs17281995 is likely to contribute to risk of cancer, particularly colorectal cancer in Caucasians.
Highlights
Multiple mechanisms involved in cancer have been extensively explored
Studies that met all of the following criteria were considered in the meta-analysis: a) Authors must recruit human cancer cases and well-matched controls; b) The publication must concentrate on the association of CD86 polymorphisms and cancer risk; c) Authors had to present complete data to estimate an odds ratio (OR) with 95% confidence interval (CI); d) The study must be published on line before June 30, 2013; e) The study used an independent case population without a subsequent update; if, the case panel was expanded, the study with a larger number of subjects was included
Characteristics of studies We identified six publications [8,10,11,12,13,19] of CD86 polymorphisms and cancer risk
Summary
Multiple mechanisms involved in cancer have been extensively explored. But the continually increasing global burden of cancer may reflect the presently incomplete knowledge of the pathogenesis and aetiology mechanisms [1]. Inflammation, as one of these mechanisms, plays a promotive role in several biological capabilities including sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis which are required in the multistep development of human cancers [2]. Inflammatory activation has long been known as a contributing factor for cancer promotion and progression due to the potentiality of impairing the maintenance of tissue homeostasis and repair [3]. Cluster of Differentiation 86 (CD86, known as B7-2) residing on antigen-presenting cells is a co-stimulatory molecule. It is important for autoimmunity, transplantation, and tumor immunity [4,5]. The aim of this study was to investigate the role of common polymorphisms in the risk of cancer by meta-analysis
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