XRCC1 Arg399Gln and Arg194Trp polymorphisms in prostate cancer risk: a meta-analysis

Wei, Bo; Zhou, You; Xu, Zheng; Ruan, Jian; Zhu, Meng; Jin, Kyong-Suk; Zhou, Dong‐Hui; Hu, Qing; Wang, Q.; Wang, Zhan; Yan, Zhiqiang

doi:10.1038/pcan.2011.26

Cited by 39 publications

(27 citation statements)

References 46 publications

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“…The protein product of XRCC1 is involved in a number of DNA repair pathways, including base excision repair. A previous meta-analysis on XRCC1 and incident prostate cancer failed to identify any association, but recently rs915927 in XRCC1 was shown to be associated with lethal prostate cancer in men with a family history of prostate cancer [34,35]. Though exploratory, our finding supports the biological plausibility that DNA repair genes interact with dietary antioxidants to modulate cancer risk, and is in line with previous reports [36].…”

Section: Discussionsupporting

confidence: 91%

Associations between circulating carotenoids, genomic instability and the risk of high-grade prostate cancer

et al. 2015

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BACKGROUND Carotenoids are a class of nutrients with antioxidant properties that have been purported to protect against cancer. However, the reported associations between carotenoids and prostate cancer have been heterogeneous and lacking data on interactions with nucleotide sequence variations and genomic biomarkers. OBJECTIVE To examine the associations between carotenoid levels and the risk of high-grade prostate cancer, also considering antioxidant-related genes and tumor instability. METHODS We measured plasma levels of carotenoids and genotyped 20 single nucleotide polymorphisms (SNP) in SOD1, SOD2, SOD3, XRCC1, and OGG1 among 559 men with non-metastatic prostate cancer undergoing radical prostatectomy. We performed copy number analysis in a subset of these men (n =67) to study tumor instability assessed as Fraction of the Genome Altered (FGA). We examined associations between carotenoids, genotypes, tumor instability and risk of high-grade prostate cancer (Gleason grade ≥4 +3) using logistic and linear regression. RESULTS Circulating carotenoid levels were inversely associated with the risk of high-grade prostate cancer; odds ratios (OR) and 95% confidence intervals (CI) comparing highest versus lowest quartiles were: 0.34 (95% CI: 0.18–0.66) for α-carotene, 0.31 (95% CI: 0.15–0.63) for β-carotene, 0.55 (0.28–1.08) for lycopene and 0.37 (0.18–0.75) for total carotenoids. SNPs rs25489 in XRCC1, rs699473 in SOD3 and rs1052133 in OGG1 modified these associations for α-carotene, β-carotene and lycopene, respectively (P ≤0.05). The proportion of men with a high degree of FGA increased with Gleason Score (P <0.001). Among men with Gleason score ≤3 +4, higher lycopene levels were associated with lower FGA (P =0.04). CONCLUSION Circulating carotenoids at diagnosis, particularly among men carrying specific somatic variations, were inversely associated with risk of high-grade prostate cancer. In exploratory analyses, higher lycopene level was associated with less genomic instability among men with low-grade disease which is novel and supports the hypothesis that lycopene may inhibit progression of prostate cancer early in its natural history.

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Section: Discussionsupporting

confidence: 91%

Associations between circulating carotenoids, genomic instability and the risk of high-grade prostate cancer

et al. 2015

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“…Such polymorphisms have also been assessed in other types of cancer. Although Wei et al (2011) reported no association with prostate cancer, when they stratified by ethnicity, an in- creased risk for the 399Gln allele in Asian men has been reported. Chen et al (2012) related the Trp/Trp genotype of the XRCC1 Arg194Trp polymorphism to an increased risk of gastric cancer, while Huang et al (2009) associated dominant and recessive models for XRCC1 Arg399Gln polymorphism with breast cancer.…”

Section: Discussionmentioning

confidence: 95%

MLH1 and XRCC1 polymorphisms in Mexican patients with colorectal cancer

Muñiz-Mendoza¹,

Ml²,

Partida-Pérez³

et al. 2012

Genet. Mol. Res.

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ABSTRACT. DNA repair proteins maintain DNA integrity; polymorphisms in genes coding for these proteins can increase susceptibility to colorectal cancer (CRC) development. We analyzed a possible association of MLH1 -93G>A and 655A>G and XRCC1 Arg194Trp and Arg399Gln polymorphisms with CRC in Mexican patients. Genomic DNA samples were obtained from peripheral blood of 108 individuals with CRC (study group) at diagnosis and 120 blood donors (control group) from Western Mexico; both groups ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 11 (3): 2315-2320 (2012) R. Muñiz-Mendoza et al. 2316 were mestizos. The polymorphisms were detected by PCR-RFLP. Association was estimated by calculating the odds ratio (OR). We found that the MLH1 and XRCC1 polymorphisms were in HardyWeinberg equilibrium. The MLH1 655A>G polymorphism in the 655G allele was associated with a 2-fold increase risk for CRC (OR = 2.04 and 95% confidence interval (95%CI) = 1.12-3.69; P < 0.01), while the MLH1 -93G>A polymorphism allele was associated with a protective effect (OR = 0.60, 95%CI = 0.40-0.89; P = 0.01 in the -93A allele and OR = 0.32, 95%CI = 0.13-0.79; P = 0.01 in the AA genotype). The XRCC1 Arg194Trp and Arg399Gln polymorphisms did not show any significant associations. In conclusion, we found that MLH1 -93G>A and 655A>G polymorphisms are associated with CRC in Mexican patients.

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“…The Arg399Gln polymorphism (rs25487) is located at the region of the BRCT-I interaction domain of XRCC1 and is linked with the reduced DRC (56,57). This polymorphism has been extensively investigated for its associations with cancer risk and the results were conflicting in different types of cancer or different populations (58)(59)(60)(61); however, a meta-analysis including 7 studies indicated that Arg399Gln was not significantly associated with SCCHN risk in Caucasians and/or Asians (25), consistent with our findings in this study.…”

Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms in key DNA repair genes and risk of head and neck cancer in a Chinese population

Yuan

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. Although tobacco and alcohol consumption are the major risk factors of head and neck cancer (HNC), genetic variations of genes involved in several biological pathways, such as DNA repair genes, may affect an individual's susceptibility to HNC. However, few studies have investigated the associations between polymorphisms in DNA repair genes and HNC risk in the Chinese population. Thus, we genotyped five common, non-synonymous single-nucleotide polymorphisms (SNPs) [APEX1 (Asp148Glu), XRCC1 (Arg399Gln), ADPRT (Val762Ala), XPD (Lys751Gln) and XPG (His1104Asp)] in a hospital-based, case-control study of 397 HNC cases and 900 cancer-free controls in China. The results showed that none of the five SNPs in the DNA repair pathway was significantly associated with HNC risk, suggesting that these polymorphisms may not play a major role in HNC susceptibility in this Chinese population. IntroductionThe incidence of head and neck cancer (HNC), especially squamous cell carcinoma of the head and neck (SCCHN), has markedly increased in the past 20 years and is now the fifth most common type of cancer worldwide (1). In the United States, it is estimated that there were 48,010 new cases and 11,260 deaths from SCCHN in 2010 (2). Accumulative evidence indicates that exposure to smoking and alcohol consumption are important risk factors of HNC (3); however, only few smokers and drinkers develop HNC, suggesting an individual susceptibility to this cancer in the general population. Most association studies on cancer susceptibility have focused on identifying effects of single-nucleotide polymorphisms (SNPs) in candidate genes of several pathways. Among these, genes involved in the DNA repair pathway are the most investigated due to their vital role in protecting the genome from insults of environmental carcinogens (4,5). Studies have shown inter-individual variations of DNA repair capacity (DRC) in the general population and the effect of a suboptimal DRC on the risk of smoking-related cancers, such as lung cancer and SCCHN (6-8).Of DNA repair pathways, nucleotide excision repair (NER) is the major repair mechanism for the DNA damage caused by tobacco smoking, which deals with a wide class of DNA damages, including bulky adducts cross-links, oxidative DNA damage, thymidine dimers and alkylating damage (9). NER involves more than 20 proteins whose inactivation may lead to xeroderma pigmentosum (XP) or Cockayne syndrome (CS). For example, rare mutations in xeroderma pigmentosum complementation group D and G (XPD and XPG) give rise to a combined XP/CS phenotype and are associated with severe neurological abnormalities.The base excision repair (BER) pathway is another important mechanism that repairs DNA damage resulting from chemical alterations of a single base; a number of proteins are involved in repair steps, such as apurinic/apyrimidinic endonuclease (APE1, also known as APEX1), X-ray repair crosscomplementing 1 (XRCC1) and ADP-ribosyltransferase (ADPRT, also known as PARP1) (10). APE1 is a key member in short-patch BER, w...

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XRCC1 Arg399Gln and Arg194Trp polymorphisms in prostate cancer risk: a meta-analysis

Cited by 39 publications

References 46 publications

Associations between circulating carotenoids, genomic instability and the risk of high-grade prostate cancer

Associations between circulating carotenoids, genomic instability and the risk of high-grade prostate cancer

MLH1 and XRCC1 polymorphisms in Mexican patients with colorectal cancer

Genetic polymorphisms in key DNA repair genes and risk of head and neck cancer in a Chinese population

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