Kallikarein‐related peptidase 3 (KLK3) gene polymorphisms seem to play a role in susceptibility to prostate cancer (PC). The purpose of this study was to investigate the association between rs2735839 polymorphism of KLK3 gene and risk of PC in an Iranian population. In this case‐control study, rs2735839 was genotyped in 532 patients with PC and 602 controls with benign prostate hyperplasia (BPH) using polymerase chain reaction‐restriction fragment length polymorphism assay. The frequency of GG, AG, and AA genotypes of KLK3 polymorphism was 24.6% and 76.2%, 46.6% and 21.7%, and 28.8% and 2.1%, in patients with BPH and PC, respectively (P < 0.001). The frequency of G allele in patients with BPH and PC was 47.9% and 87%, respectively (odds ratio: 7.31; confidence interval: 5.88‐9.10; P < 0.001). Patients with AG and GG genotypes had a higher total serum level of prostate‐specific antigen (PSA) compared to those with AA genotype (P < 0.001). Patients with this polymorphism had higher risk of tumor with higher grade (P = 0.23), advanced stage (P = 0.11), perineural invasion (P = 0.07), and vascular invasion (P = 0.07) compared to those without it but this difference was not statistically significant. Based on our results, KLK3 gene polymorphism was associated with the risk of PC. Higher levels of PSA in the presence of KLK3 polymorphism in patients with PC indicated that rs2735839 polymorphism could be a risk factor for increased levels of PSA.
Background Gestational diabetes mellitus (GDM) is the most popular metabolic disease during pregnancy. The aim of the present study was to investigate any possible association between eNOS Glu298Asp and ACE I/D gene polymorphisms and the risk of GDM in a group of Iranian pregnant women. Methods In this case-control study 204 pregnant women were recruited (94 cases and 110 controls). Genomic DNA was isolated from whole blood and genotyping was performed by the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) and only PCR for eNOS and ACE polymorphisms respectively. Results Frequencies of GT and TT genotype of eNOS polymorphism among women with and without GDM were 67.90% vs. 74.47 and 7.41% vs. 8.51% respectively (P = 0.4). Corresponding figures for DD genotype of ACE polymorphism among GDM patients was more than that in healthy women (51.65% vs. 63.81% respectively). Conversely, ACE heterozygote genotype was more common in diabetic women (35.16% vs. 26.67% respectively). Although these differences were not statistically significant (P = 0.2). Conclusions Our study showed that there is no association between the presence of eNOS and ACE gene polymorphisms and developing gestational diabetes mellitus among pregnant women in our population. Further longitudinal and multicenter studies should be carried out to assess the exact metabolic effects of these polymorphisms.
Background: NAT2 enzyme involved in bioconversion of aromatic amines, heterocyclic arylamines and certain drugs into electrophilic ions that can be important initiators in tumorigenesis process. Objectives: The aim of this study was to assess the possible association between NAT2 polymorphisms (857 G > A, 481 T > C, and 590 G > A) and risk of prostate cancer (PC). Methods: Totally, 207 benign prostate hyperplasia (BPH) and 147 PC Iranian patients were evaluated. NAT2 genotypes were detected by restriction fragment length polymorphism (RFLP). Multiple logistic regression models were used to estimate the odds ratios for the association between presence of each genotype and developing PC. Results: For NAT2 G857A, the frequency of AA and AG genotypes was lower among PC patients compared to those without it (1.01% vs. 0 and 55.88% vs. 54.55%, respectively; P = 0.7). For NAT2 T481c, the odds ratios for the association of TT and CT genotypes with PC were 0.65 and 0.55, respectively, which were not statistically significant (P = 0.5 and P = 0.09, respectively). For NAT2 G590a, both AA (11.11% vs. 12.87%) and AG (45.83% vs. 52.48%) genotypes were significantly more common among PC patients compared to BPC patients (P = 0.008). However, none of the relevant odds ratios were statistically significant (OR = 2.2, P = 0.2 and OR = 1.72, P = 0.1, respectively). Among PC patients, CT genotype of T481C caused more than 4-fold significant increase in the risk of developing advanced stages of PC. Conclusions: Our study represented credible evidence that carrying G857A, G590A and T481C polymorphisms of NAT2 may not affect developing PC, its grading or invasion, but heterozygote genotype of T481C polymorphism (Rapid acetylator) can be associated with more advanced stages of cancer earlier in life. Further longitudinal studies with larger sample sizes are needed to more precisely assess the genetic risk factors of PC.
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