Abstract
BackgroundDNA repair genes (eg: xeroderma pigmentosum group D, XPD) may affect the capacity of encoded DNA repair enzymes to effectively remove DNA adducts or lesions, which may result in enhanced cancer risk. The association between XPD gene polymorphisms and the susceptibility of prostate cancer (PCa) was inconsistent in previous studies.Methodology/Principal FindingsA meta-analysis based on 9 independent case-control studies involving 3165 PCa patients and 3539 healthy controls for XPD Gln751Lys SNP (single nucleotide polymorphism) and 2555 cases and 3182 controls for Asn312Asp SNP was performed to address this association. Meanwhile, odds ratio (OR) and 95% confidence intervals (CIs) were used to evaluate this relationship. Statistical analysis was performed with STATA10.0. No significant association was found between XPD Gln751Lys SNP and PCa risk. On the other hand, in subgroup analysis based on ethnicity, associations were observed in Asian (eg. Asn vs. Asp: OR = 1.34, 95%CI = 1.16–1.55; Asn/Asn+Asn/Asp vs. Asp/Asp: OR = 1.23, 95%CI = 1.07–1.42) and African (eg. Asn vs. Asp: OR = 1.31, 95%CI = 1.01–1.70; Asn/Asn vs. Asp/Asp: OR = 1.71, 95%CI = 1.03–7.10) populations for Asn312Asp SNP. Moreover, similar associations were detected in hospital-based controls studies; the frequency of Asn/Asn genotype in early stage of PCa men was poorly higher than those in advanced stage of PCa men (OR = 1.45, 95%CI = 1.00–2.11).Conclusion/SignificanceOur investigations demonstrate that XPD Asn312Asp SNP not the Gln751Lys SNP, might poorly increase PCa risk in Asians and Africans, moreover, this SNPs may associate with the tumor stage of PCa. Further studies based on larger sample size and gene-environment interactions should be conducted to determine the role of XPD gene polymorphisms in PCa risk.
Highlights
Prostate cancer (PCa) is the most common male nondermatological cancer in Europe and the USA, and the sixth leading cause of cancer related-deaths, accounting for 14% (903, 500) of total new diagnosed cancer cases and 6% (258, 400) of whole cancer deaths in males in 2008 [1]
We excluded 20 studies: 12 were reduplicate, one article type was review, 3 papers were about other cancer types, two were not relate to case-control studies and last article was about single-nucleotide polymorphisms (SNP)-SNP interactions not for single SNP polymorphism
Control population including all consisted of study participants with a normal digital rectal examination (DRE) and serum prostatic specific antigen (PSA) values of,4 ng/ml, as well as old matched men, not cancer family history and not previous cancer history
Summary
Prostate cancer (PCa) is the most common male nondermatological cancer in Europe and the USA, and the sixth leading cause of cancer related-deaths, accounting for 14% (903, 500) of total new diagnosed cancer cases and 6% (258, 400) of whole cancer deaths in males in 2008 [1]. Various DNA alterations can be caused by exposure to environmental and endogenous carcinogens, including ultraviolet (UV) light, cigarette smoke, dietary factors, reactive oxygen species, and carcinogens. Most of these alterations, if not repaired, can result in genetic instability, mutagenesis and cell death. Because DNA repair pathways (DRP) play a critical role in maintaining the genomic integrity in general and specialized functions of cell as well as in the prevention of carcinogenesis, the defection of those genes in DRP can lead to highter susceptibility to multiple cancers [4,5]. The association between XPD gene polymorphisms and the susceptibility of prostate cancer (PCa) was inconsistent in previous studies
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