AI Article Synopsis
- - The study investigates how specific genetic variations (SNPs) in the XPC gene, which is involved in DNA repair, may affect the risk of developing prostate cancer (PC) among the Tunisian population.
- Results indicate that while the XPC Lys939Gln variant doesn’t increase cancer risk, individuals with the XPC PAT I/I genotype have a significantly higher risk of developing prostate cancer (3.83 times more likely) compared to controls.
- No strong connections were found between the XPC gene variations and clinical factors like Gleason score, TNM status, or lifestyle factors such as tobacco use and alcohol consumption.
Article Abstract
Single nucleotide polymorphisms (SNP) in repair gene DNA such as XPC gene can reduce the DNA repair capacity (DRC). Reduced DRC induce genetic instability and may increase the susceptibility to prostate cancer (PC). We conducted a case-controls study to examine the relationship between XPC Lys939Gln and XPC-PAT polymorphisms and the risk for prostate cancer in Tunisian population. We have also correlated molecular results with clinical parameters (Gleason score and TNM status) and lifestyle factors (tobacco status, alcohol consumption, and exposition to professional risk factors) of prostate cancer patients. We have found that the XPC Lys939Gln polymorphism was not associated with a risk of prostate cancer. However the XPC PAT I/I genotype was found to be associated with 3.83-fold increased risk of prostate cancer compared to controls (p = 0.00006; OR 3.83; 95% CI (1.83-8.05)). The test of linkage disequilibrium showed that XPC-PAT polymorphism is in linkage disequilibrium with XPC Lys939Gln variants. The combined analysis of XPC Lys939Gln and XPC-PAT variants showed that patients who inherited (Lys/Gln + PAT D/D) genotypes were protected against prostate cancer development compared to controls. In the other hand, no significant association has been found between XPC polymorphisms and clinical parameters or between XPC polymorphisms and lifestyle factors.
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| http://dx.doi.org/10.1007/s11033-018-4572-2 | DOI Listing |
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