Association Between the XRCC6 Polymorphisms and Cancer Risks

Jia, Jun; Ren, Juan; Yan, Dongmei; Xiao, Long; Sun, Ruili

doi:10.1097/md.0000000000000283

Cited by 29 publications

(21 citation statements)

References 37 publications

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“…Surprisingly, the XRCC6 A46922G polymorphism (SNP rs132793) was found to be protective against breast carcinogenesis but associated with increased incidence of HCC and glioma [ 111 , 118 , 125 , 126 ]. Each of these XRCC6 polymorphisms was verified as affecting overall tumor risk in a systemic review and meta-analysis [ 127 ]. Only one PRKDC polymorphism, intron 8 G6721T (SNP rs7003908), has been identified to be associated with a significant increase risk in carcinogenesis (glioma, bladder, colorectal, and prostate cancer) [ 128 , 129 , 130 , 131 ].…”

Section: Core Nhej Factors In Carcinogenesis and Cancermentioning

confidence: 99%

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

Sishc

Davis

2017

Cancers

139

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DNA double-strand breaks (DSBs) are deleterious DNA lesions that if left unrepaired or are misrepaired, potentially result in chromosomal aberrations, known drivers of carcinogenesis. Pathways that direct the repair of DSBs are traditionally believed to be guardians of the genome as they protect cells from genomic instability. The prominent DSB repair pathway in human cells is the non-homologous end joining (NHEJ) pathway, which mediates template-independent re-ligation of the broken DNA molecule and is active in all phases of the cell cycle. Its role as a guardian of the genome is supported by the fact that defects in NHEJ lead to increased sensitivity to agents that induce DSBs and an increased frequency of chromosomal aberrations. Conversely, evidence from tumors and tumor cell lines has emerged that NHEJ also promotes chromosomal aberrations and genomic instability, particularly in cells that have a defect in one of the other DSB repair pathways. Collectively, the data present a conundrum: how can a single pathway both suppress and promote carcinogenesis? In this review, we will examine NHEJ’s role as both a guardian and a disruptor of the genome and explain how underlying genetic context not only dictates whether NHEJ promotes or suppresses carcinogenesis, but also how it alters the response of tumors to conventional therapeutics.

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Section: Core Nhej Factors In Carcinogenesis and Cancermentioning

confidence: 99%

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

Sishc

Davis

2017

Cancers

139

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“…According to results of a newly meta-analysis which was performed on the XRCC6 SNP polymorphisms and cancer risk, the rs2267437 polymorphism was found to be associated with a significant increase in risks of overall cancers, breast cancer, RCC, and HCC, and it might increase the cancer risk in Asian population [25]. The result of current study showed a high association between genetic polymorphism of XRCC 6 rs2267437 with male infertility, suggesting that this SNP might be a genetic risk factor for male infertility.…”

Section: Discussionmentioning

confidence: 99%

XRCC5 VNTR, XRCC6 -61C>G, and XRCC7 6721G>T Gene Polymorphisms Associated with Male Infertility Risk: Evidences from Case-Control and In Silico Studies

Jahantigh

Colagar

2017

International Journal of Endocrinology

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We evaluate the association between genetic polymorphisms of XRCC5 VNTR, XRCC6 -61C>G, and XRCC7 6721G>T with male infertility susceptibility. A total of 392 men including 178 infertile males (102 idiopathic azoospermia and 76 severe oligozoospermia) and 214 healthy controls were recruited. XRCC6 -61C>G and XRCC7 6721G>T genotyping was performed by PCR-RFLP whereas XRCC5 VNTR was performed by PCR. The 2R allele and 2R allele carriers of XRCC5 VNTR polymorphism significantly decreased risk of male infertility. The mutant GG genotypes and carriers of the CG and GG genotypes of XRCC6 -61C>G showed increased risk for the male infertility. Furthermore, the G allele of the XRCC6 -61C>G was correlated with increased susceptibility to male infertility. Likewise, the T allele of the XRCC7 6721G>T polymorphism was associated with increased susceptibility to male infertility in azoospermia. In silico analysis predicted that the presence of tandem repeats in XRCC5 gene prompter can be sequence to bind to more nuclear factors. Also, rs2267437 (C>G) variant was located in a well-conserved region in XRCC6 promoter and this variation might lead to differential allelic expression. The XRCC7 6721G>T gene polymorphism occurred in an acceptor-splicing site, but this polymorphism has no severe modification on XRCC7 mRNA splicing. Our results indicate the association of XRCC5 VNTR, XRCC6 -61C>G, and XRCC7 6721G>T gene polymorphisms with male infertility in Iranian men.

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“…The rs2267437 polymorphism has been investigated as risk factor for cancer risk with inconsistent results. However, a recent systematic review and meta-analysis concluded that rs2267437 SNP is associated with a significant increase in risk of breast cancer, renal cell carcinoma and hepatocellular carcinoma 36 .…”

Section: Discussionmentioning

confidence: 99%

Association between single-nucleotide polymorphisms in DNA double-strand break repair genes and prostate cancer aggressiveness in the Spanish population

Henríquez-Hernández

Valenciano

Arnalot

et al. 2016

Prostate Cancer Prostatic Dis

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Association Between the XRCC6 Polymorphisms and Cancer Risks

Cited by 29 publications

References 37 publications

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

The Role of the Core Non-Homologous End Joining Factors in Carcinogenesis and Cancer

XRCC5 VNTR, XRCC6 -61C>G, and XRCC7 6721G>T Gene Polymorphisms Associated with Male Infertility Risk: Evidences from Case-Control and In Silico Studies

Association between single-nucleotide polymorphisms in DNA double-strand break repair genes and prostate cancer aggressiveness in the Spanish population

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