Analysis of XRCC2 and XRCC3 gene polymorphisms in pancreatic cancer

Talar‐Wojnarowska, Renata; Gąsiorowska, Anita; Dranka-Bojarowska, Daria; Lampe, Paweł; Smolarz, Beata; Małecka‐Panas, Ewa

doi:10.3892/br.2015.550

Cited by 9 publications

(6 citation statements)

References 21 publications

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“…11 XRCC2 p.Arg188His polymorphism located in exon3 12 has been associated with cancers like pancreatic, 13 ovarian, 14 oral 15 and upper aerodigestive tract cancers. 16 XRCC3 (chromosome location 14q32.3) encodes a 346 amino acid polypeptide 17 that participates in DNA doublestrand break repair. Variation in expression of XRCC3 has been reported in various cancers, like gastric, breast, lung, skin and colorectal.…”

Section: Introductionmentioning

confidence: 99%

Association of XRCC1, XRCC2 and XRCC3 Gene Polymorphism with Esophageal Cancer Risk

Kaur¹,

Sambyal²,

Guleria³

et al. 2020

CEG

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The X-ray repair cross-complementing (XRCC) gene polymorphisms influence esophageal carcinogenesis by altering the DNA repair capacity. The present study was designed to screen five single nucleotide polymorphisms (SNPs) of XRCC genes for their susceptibility to esophageal cancer (EC) risk. There is no previous report on these polymorphisms for EC from India, where EC frequency is high. Methods: The present study included 497 subjects (213 EC patients and 284 healthy controls). The polymorphisms were screened using the PCR-RFLP method and allele and genotype distribution were compared using chi-square test. Association analysis was done by haplotype analysis and linkage disequilibrium (LD) analysis. Gene-gene interactions were identified using multifactor dimensionality reduction (MDR). The risk was calculated using binary logistic regression. Results: For XRCC1 p.Arg399Gln, a decreased risk for EC was associated with the AA genotype [OR (95% CI): 0.53 (0.3-0.95), p=0.03] even after adjusting for various covariates [OR (95% CI): 0.49 (0.26-0.9), p=0.024] and with the recessive model [OR (95% CI): 0.49 (0.27-0.8), p=0.016]. The GA genotype of p.Arg280His was associated with an increased risk for EC [OR (95% CI): 1.7 (1.0-2.82), p= 0.045] after adjustments. The two XRCC1 polymorphisms, p.Arg399Gln and p.Arg194Trp were in slight LD among EC patients (D ̍́= 0.845, r 2 =0.042). XRCC2 and XRCC3 polymorphisms were not associated with EC risk. Conclusion: XRCC1 p.Arg399Gln plays a protective role in the development of the EC. The study is the first report from India, providing baseline data about genetic polymorphisms in DNA repair genes XRCC1, XRCC2 and XRCC3 modulating overall EC risk.

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Section: Introductionmentioning

confidence: 99%

Association of XRCC1, XRCC2 and XRCC3 Gene Polymorphism with Esophageal Cancer Risk

Kaur¹,

Sambyal²,

Guleria³

et al. 2020

CEG

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“…The promoter of the gene coding for Cox‐2 (PTGS2) contains various putative transcriptional regulatory elements , and polymorphisms in this region can potentially alter the expression of PTGS2, thereby modulating the risk for different cancer types. Two functional polymorphisms in the promoter of the PTGS2 gene (−765G>C, and −1195A>G), which modulate the risk for various cancers , have been identified .…”

Section: Introductionmentioning

confidence: 99%

Association of promoter polymorphism −765G>C in the PTGS2 gene with malignant melanoma in Italian patients and its correlation to gene expression in dermal fibroblasts

Gomez-Lira

Ferronato

Malerba

et al. 2014

Experimental Dermatology

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Prostaglandins, especially prostaglandin E synthetase (PGE2), influence carcinogenesis by promoting cell proliferation, inhibiting apoptosis, stimulating angiogenesis and mediating immune suppression. Cyclooxygenase-2, coded by the PTGS2 gene, is the key enzyme in the production of prostaglandins. In melanoma, Cox-2 is over expressed in primary malignant melanoma (MM) and in their corresponding metastases. Polymorphisms in the promoter region of PTGS2 gene can modulate gene expression and could modify individual susceptibility to MM. Two hundred and forty melanoma patients and 342 controls were genotyped for polymorphisms -765G>C (rs20417) and -1195A>G (rs689466). Allele -765C frequency was significantly higher in melanoma patients. No allele frequency differences for -1195A>G polymorphism were observed. Haplotype analysis revealed that the haplotypes carrying the minor alleles were associated to a higher risk of melanoma (P = 0.02). Expression analysis showed that allele -765C is associated to a higher gene expression and could represent a risk allele by affecting the functionality of the promoter.

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“…XRCC3 rs861539 occurred in response to the polymorphism at amino acid 241, which was changed from threonine to methionine (or the nucleotide from C to T), resulting in impaired DNA repair function via a defect in the function of XRCC3 by removing the phosphorylation site. 43 The XRCC3 homovariant Met/Met genotype has been identified with higher DNA double-strand break adducts after the same level of DNA damage challenges in the lymphocytes of investigated healthy subjects, 7 while modifying the XRCC3 levels of the Thr241Met variant cells alters their DNA repair capacity. 44 In addition, the XRCC3 heterovariant Thr241Met carriers who were exposed to ionizing radiation are associated with an increased number of micronuclei in their lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

The contribution of XRCC3 genotypes to childhood acute lymphoblastic leukemia

Pei

Chang

Hsu

et al. 2018

CMAR

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PurposeA growing body of evidence shows an association between DNA repair protein genotypes and susceptibility to various cancers. However, few studies have assessed the contribution of the genotype of XRCC3, a homologous repair gene, to the occurrence or prognosis of childhood acute lymphoblastic leukemia (ALL). In this study, we investigated the contribution of seven XRCC3 polymorphisms to childhood ALL.Patients and methodsWe recruited 266 patients with childhood ALL and 266 healthy controls. Genomic DNA was isolated from peripheral blood samples. The XRCC3 rs1799794, rs45603942, rs1799796, rs861530, rs28903081, rs861539, and rs3212057 polymorphic genotypes of each subject were determined through conventional polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis.ResultsGenotypes with the rs861539 polymorphism were significantly associated with the risk of childhood ALL. The allelic distribution analyses suggested a significant association between the T allele at rs861539 with an increased risk of childhood ALL in the Taiwanese population. Polymorphic variants of XRCC3 at rs3212057 or rs28903081 did not exist in the study population. XRCC3 rs1799794, rs45603942, rs1799796, and rs861530 were not significantly associated with the risk of childhood ALL in the Taiwanese population.ConclusionOur findings suggest that XRCC3 genotypes with polymorphisms at rs861539 may play a role in determining individual susceptibility to childhood ALL in this Taiwanese population. The polymorphism may be a potential detector and predictor of childhood ALL.

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Analysis of XRCC2 and XRCC3 gene polymorphisms in pancreatic cancer

Cited by 9 publications

References 21 publications

<p>Association of <em>XRCC1</em>, <em>XRCC2</em> and <em>XRCC3</em> Gene Polymorphism with Esophageal Cancer Risk</p>

<p>Association of <em>XRCC1</em>, <em>XRCC2</em> and <em>XRCC3</em> Gene Polymorphism with Esophageal Cancer Risk</p>

Association of promoter polymorphism −765G>C in the PTGS2 gene with malignant melanoma in Italian patients and its correlation to gene expression in dermal fibroblasts

The contribution of <em>XRCC3 </em>genotypes to childhood acute lymphoblastic leukemia

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