GENETIC POLYMORPHISMS OF DNA DAMAGE REPAIR GENES ON COLORECTAL CANCER’S RISK

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Date
2012
Authors
AHMAD AIZAT, ABDUL AZIZ
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Pusat Pengajian Sains Perubatan Universiti Sains Malaysia
Abstract
The incidence of sporadic colorectal cancer (CRC) is increasing in Asian countries, including Malaysia. Although several factors have been implicated in CRC etiology, CRC develops as a result of interaction between environmental factors and genetic predisposition. However, the genetic predisposition factors associated with CRC development remains still undetermined. In humans, there are a number of DNA repair pathways, each responsible for repairing different types of DNA damages inflicted by environmental factors. It was hypothesized that genetic variations such as single nucleotide polymorphisms (SNPs) in DNA damage repair genes could have effects on the sensitivity of the organism to environmental genotoxins and may influence CRC susceptibility. In order to test this hypothesis, a case-control study was designed and undertaken at Human Genome Centre (HGC), USM during 2010-2012. The aim was to investigate the genotype and allele frequencies of 8 SNPs of 6 genes, namely XRCC1 Arg399Gln, XPD/ERCC2 Lys751Gln, XRCC3 Thr241Met, XPC Lys939Gln, P53 Arg72Pro as well as MLH1 Asp132His, Ile219Val and Val384Asp polymorphisms in Malaysian CRC patients and healthy normal controls, and to determine whether these SNPs contribute to CRC susceptibility risk in Malaysian population. This study involved 510 study subjects, comprising of 255 histopatologically confirmed sporadic CRC patients as cases and 255 healthy normal individuals as controls. After getting informed consents from study subjects, peripheral blood samples were collected, DNA was extracted and all the above 8 polymorphisms were genotyped employing PCRRFLP method. The genotypes were categorized into homozygous wildtype, heterozygous variant and homozygous variant. On comparing the genotype frequencies of all SNPs between cases and controls, the homozygous variant genotypes P53 Pro72Pro and XPC Gln939Gln were significantly higher in cases. The risk association of all the 8 SNPs either singly and/or in combination with CRC predisposition risk was examined by using binary logistic regression and deriving odds ratios (OR) and 95% CIs. On evaluating risk associated with variant genotypes singly, homozygous variant P53 Pro72Pro and XPC Gln939Gln showed significantly higher risk association with CRC susceptibility. When analyzed in 2 way combinations, the genotype combinations of XPD/ERCC2 Ly/Lys+XPC Gln/Gln; XRCC3 Thr/Thr+P53 Pro/Pro; XPC Gln/Gln+ MLH1 Asp/Asp; XPC Gln/Gln+ MLH1 Ile/Ile; P53 Arg/Arg+ XPC Gln/Gln; P53 Pro/Pro+ MLH1 Asp/Asp; P53 Pro/Pro+ MLH1 Ile/Ile and P53 Pro/Pro+ MLH1 Val/Val emerged as high risk combination genotypes associated with CRC susceptibility. Finally, in 3 way genotype combinations, the genotype combinations of P53 Pro/Pro+XPC Lys/Lys+XRCC3 Thr/Thr; P53 Pro/Pro+XPC Lys/Gln+XRCC3 Thr/Thr; P53 Arg/Arg+XPC Gln/Gln+MLH1 Asp/Asp; P53 Arg/Arg+XPC Gln/Gln+MLH1 Ile/Ile and P53 Pro/Pro+XPC Lys/Lys+MLH1 Val/Val, were found to be associated with higher CRC susceptibility risk. Furthermore, several genotypes such as XRCC1 Arg/Gln genotype singly and combination genotypes such as XRCC1 Arg/Arg+XPD Lys/Gln, XRCC1 Arg/Gln+XPC Gln/Gln, XRCC1 Arg/Arg+XRCC3 Thr/Thr, XRCC1 Arg/Arg+P53 Arg/Pro, XRCC1 Arg/Gln+P53 Arg/Arg, XRCC1 Gln/Gln+P53 Arg/Pro, XRCC1 Arg/Gln+MLH1 Asp/Asp, XRCC1 Arg/Pro+MLH1 Ile/Val, XRCC1 Gln/Gln+MLH1 Ile/Ile, XRCC1 Arg/Gln+MLH1 Val/Val and XPD Lys/Lys+ XRCC3 Thr/Met were observed to show low risk association. From the present study results it is suggested that variant genotypes of P53 (P53 Pro/Pro) and XPC (XPC Gln/Gln) either singly and/or in combination, may be considered as high risk genotypes associated with CRC susceptibility.
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Human Genome
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