Abstract
XRCC (X-ray cross-complementing group) genes contribute to important DNA repair mechanisms that play roles in the repair of single strand breaks (SSBs) induced by a variety of external and internal factors, including ionizing radiation, alkylating agents and reactive oxygen species. These repair genes have a pivotal role in maintaining genomic stability through different pathways of base excision repair (BER). The aim of this study was to investigate the XRCC3 Thr241Met gene polymorphism in colorectal cancer (CRC) in Kashmir. We investigated the genotype distribution of XRCC3 gene in 120 CRC cases in comparison with 150 healthy subjects and found a significant association between XRCC3 genotypes and CRC (p≤0.05). Both heterozygous genotype (Thr/Met) as well as homozygous variant genotype (Met/Met) were moderately associated with elevated risk of CRC [OR=2.53; OR=2.29 respectively]. Also, Thr/Met and Met/Met genotypes demonstrated a significant association with the risk of CRC (p=0.003). This study displayed a significantly elevated risk for CRC in individuals with XRCC3 Thr/Met and Met/Met Genotype of about 2.5 times that with the Thr/Thr wild genotype.
Highlights
Colorectal cancer (CRC) being one of the commonly diagnosed cancer in both men and women accounts for the third most common cancer in men and the second most common cancer in women worldwide (Jemal et al, 2011)
XRCC3, which participates in DNA double-strand break via homologous recombinational repair, is a member of an emerging family of Rad-51-related proteins that likely participate in homologous recombinational repair (HRR) in order to maintain chromosome stability (Tebbs et al, 1995)
We have examined whether polymorphism in DNA repair gene XRCC3, involved in the double-strand break (DSBR) DNA repair pathways, is implicated in modulating the risk of development of colorectal cancer (CRC) in Kashmiri population in continuation of our previous study on XRCC1 gene polymorphism (Nissar et al, 2013)
Summary
Colorectal cancer (CRC) being one of the commonly diagnosed cancer in both men and women accounts for the third most common cancer in men and the second most common cancer in women worldwide (Jemal et al, 2011). Genetic polymorphisms in homologous recombination repair (HRR) genes (one of the four repair pathway in cell) leading to the insufficient protein have been found to be associated with increased risk of cancer (Smilenov, 2006). DSBR pathway is responsible for repairing double-strand breaks resulting from exogenous as well as endogenous agents such as ionizing radiation or environmental carcinogens and endogenously generated ROS. They can be produced when DNA replication encounter DNA singlestrand breaks or other types of lesion (Jacobsen et al, 2004). XRCC3 along with Rad and Xrcc form the core component of DNA double strand breaks (DSBs) repair by HRR (Nissar et al, 2014)
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