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

2016 ◽  
Vol 19 (1) ◽  
pp. 28-34 ◽  
Author(s):  
L A Henríquez-Hernández ◽  
A Valenciano ◽  
P Foro-Arnalot ◽  
M J Álvarez-Cubero ◽  
J M Cozar ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Single Nucleotide Polymorphisms ◽  
Strand Break ◽  
Spanish Population ◽  
Double Strand Break Repair ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Dna Double Strand Break ◽  
Cancer Aggressiveness ◽  
Repair Genes

scholarly journals RAD51 and XRCC3 Polymorphisms Are Associated with Increased Risk of Prostate Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Maria Nowacka-Zawisza ◽  
Agata Raszkiewicz ◽  
Tomasz Kwasiborski ◽  
Ewa Forma ◽  
Magdalena Bryś ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Repair ◽  
Strand Break ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Dna Double Strand Break ◽  
Repair Efficiency ◽  
Increased Risk ◽  
Pcr Rflp ◽  
Repair Genes

Genetic polymorphisms in DNA repair genes may affect DNA repair efficiency and may contribute to the risk of developing cancer. The aim of our study was to investigate single nucleotide polymorphisms (SNPs) in RAD51 (rs2619679, rs2928140, and rs5030789) and XRCC3 (rs1799796) involved in DNA double-strand break repair and their relationship to prostate cancer. The study group included 99 men diagnosed with prostate cancer and 205 cancer-free controls. SNP genotyping was performed using the PCR-RFLP method. A significant association was detected between RAD51 rs5030789 polymorphism and XRCC3 rs1799796 polymorphism and an increased risk of prostate cancer. Our results indicate that RAD51 and XRCC3 polymorphism may contribute to prostate cancer.

EP-1824: Quality of life of prostate cancer patients is influenced by single nucleotide polymorphisms in DNA repair genes

2014 ◽  
Vol 111 ◽  
pp. S298
Author(s):  
L. Henríquez Hernández ◽  
A. Riveros-Pérez ◽  
A. Valenciano ◽  
J.I. Rodríguez-Melcón ◽  
M. Lloret ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Prostate Cancer ◽  
Dna Repair ◽  
Single Nucleotide Polymorphisms ◽  
Cancer Patients ◽  
Dna Repair Genes ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Repair Genes

scholarly journals Single-Nucleotide Polymorphisms Sequencing Identifies Candidate Functional Variants at Prostate Cancer Risk Loci

Genes ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 547 ◽  
Author(s):  
Peng Zhang ◽  
Lori S. Tillmans ◽  
Stephen N. Thibodeau ◽  
Liang Wang
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Single Nucleotide Polymorphisms ◽  
Protein Binding ◽  
Prostate Cancer Risk ◽  
Sequencing Analysis ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Functional Variants ◽  
Dependent Protein

Genome-wide association studies have identified over 150 risk loci that increase prostate cancer risk. However, few causal variants and their regulatory mechanisms have been characterized. In this study, we utilized our previously developed single-nucleotide polymorphisms sequencing (SNPs-seq) technology to test allele-dependent protein binding at 903 SNP sites covering 28 genomic regions. All selected SNPs have shown significant cis-association with at least one nearby gene. After preparing nuclear extract using LNCaP cell line, we first mixed the extract with dsDNA oligo pool for protein–DNA binding incubation. We then performed sequencing analysis on protein-bound oligos. SNPs-seq analysis showed protein-binding differences (>1.5-fold) between reference and variant alleles in 380 (42%) of 903 SNPs with androgen treatment and 403 (45%) of 903 SNPs without treatment. From these significant SNPs, we performed a database search and further narrowed down to 74 promising SNPs. To validate this initial finding, we performed electrophoretic mobility shift assay in two SNPs (rs12246440 and rs7077275) at CTBP2 locus and one SNP (rs113082846) at NCOA4 locus. This analysis showed that all three SNPs demonstrated allele-dependent protein-binding differences that were consistent with the SNPs-seq. Finally, clinical association analysis of the two candidate genes showed that CTBP2 was upregulated, while NCOA4 was downregulated in prostate cancer (p < 0.02). Lower expression of CTBP2 was associated with poor recurrence-free survival in prostate cancer. Utilizing our experimental data along with bioinformatic tools provides a strategy for identifying candidate functional elements at prostate cancer susceptibility loci to help guide subsequent laboratory studies.

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