There is growing evidence of a malignancy-protective role for vitamin D in breast cancer. The effects of vitamin D are mediated via the vitamin D receptor (VDR) which is encoded by VDR gene. Several SNPs on VDR gene has attracted research interest, although the magnitude of the impact of VDR allelic variations on breast cancer has been controversial. In the present study, we focused on the distribution of VDR FokI and BsmI polymorphisms in Iranian breast cancer patients. A case-control study was conducted on 296 samples including 140 breast cancer patients and 156 age matched control women. Restriction fragment length polymorphism (RFLP) analysis was performed for BsmI and FokI genotyping. Randomly selected PCR products were subjected to sequencing to verify the RFLP results. A significantly increased risk of breast cancer was observed with BsmI bb or even Bb genotype (OR 2.39, CI 1.17-4.85 and OR 2.28, CI 1.16-4.47, respectively). Nevertheless, statistically significant association between FokI genotypes and breast cancer risk was not observed. This study lends support for an increased risk of breast cancer associated with the VDR BsmI polymorphism.

Background: The present research is a case-control study to analyze the influence of pre-miRNA-146a rs2910164 and pre-miRNA-499 rs3746444 polymorphisms as candidate susceptibility factors for both rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Methods: Polymorphism in miR146 and miR499 using ARMS-PCR was genotyped on 139 autoimmune disease (AD) patients (89 RA and 50 SLE) referred to Educational Hospitals of Khorramabad, Lorestan Province, west of Iran in 2018–2019 and 237 healthy control subjects. Results: A significant increase in the likelihood of carrying the GC vs. GG of pre-miR146-rs2910164 and T vs C allele of pre-miR499- rs3746444 in patients with RA was found. On the contrary, patients with RA were less likely to carry the TC + CC vs TT genotype and the C vs T allele of pre-miR499- rs374644. In females with the GC vs GG and GC+ CC vs GG genotypes, a significant association was found with the increased risk of RA. Interestingly, the genotypic combination of TC of the pre-miR499-rs374644 with GG of pre-miR146-rs2910164 more strongly decreased the risk of RA. In patients with SLE, no notable associations were found between both pre-miRNA-146a rs2910164 and pre-miRNA-499 rs3746444 with risk of disease. Conclusion: Genetic polymorphisms of miR146 rs2910164 is associated with RA susceptibility especially in females. Interestingly, there is a potential in miR499 to reduce the risk with the protective effect of gene-gene interactions on miR146 in RA disease.

The overexpression of UHRF1 was correlated with the stage and grade of gastric cancer and is associated with the genotype distribution of rs2910164.

Our study suggested that the -579 T allele may increase the relative risk for the progression of clinicopathological characteristic of tumor grade of gastric cancer patients.

Background: A growing body of literature has revealed the effective role of miR-34a, as a tumor suppressor and regulator of expression of multiple targets in tumorigenesis and cancer progression. This study aimed at evaluating the potential effects of miR-34a alone or in combination with paclitaxel on breast cancer cells. Methods: After miR-34a transduction by lentiviral vectors in two MCF-7 and MDA-MB-231 cell lines of breast cancer, effects of the elevated expression of miR-34a in the cell viability and the cell proliferation were determined using MTT assay in treated and untreated cells with paclitaxel. The mRNA level of the CCND1 gene was then measured in the two cell lines using the qRT-PCR assay. Finally, the influence of miR-34a and paclitaxel on apoptosis and cell cycle progression were examined by flow cytometry. Results: The CCND1 mRNA expression levels were significantly down-regulated by overexpressed lentiviral miR-34a in MCF-7 and MDA-MB-231 cells. Combined treatment by miR-34a and paclitaxel reduced the cell viability and proliferation compared to single-drug treatment. In addition, the cell cycle arrest appeared at two phases by the combination of miR-34a and paclitaxel in MDA-MB-231 cells. Conclusion: Our results suggest that miR34a, in combination with paclitaxel, has a potential for decreasing the cell viability and proliferation. Moreover, it can reduce the expression of CCND1 mRNA independent of the paclitaxel effect.

Background: Vesicoureteral reflux (VUR) disease is the most common type of urinary tract anomalies in children. Genetic risk factors may be associated with the etiology of VUR. The role of the Glutathione S-transferases (GSTs) as multifunctional enzymes is cellular oxidative stress handling. This is the first study aimed at evaluating the relative risk of GSTP1, GSTM1, and GSTT1 polymorphisms in VUR susceptibility in children and provides new important insights into the genetics of affected children. Methods: The study was done in 2013 in Sistan and Baluchestan University, eastern Iran. Genotyping of three GSTP1, GSTM1, and GSTT1 genes were determined using the multiplex polymerase chain reaction assay in 216 reactions for 72 VUR children and 312 reactions for 104 healthy controls. Results: The presence of GSTT1 deletion was associated with high risk of VUR in children, whereas GSTP1 and GSTM1 genotypes did not show the same effect. Furthermore, the combination of GSTT1/GSTM1 and GSTT1/ GSTP1 genotypes showed a significant influence on lower risk of VUR in children. Conclusion: Deletion of GSTT1 functional gene is a genetic risk factor causing VUR in children. Interestingly, the combination of GSTM1 and GSTP1 null genotypes with GSTT1 has shown a protective role against risk of GSTT1 deletion.

Background: Survivors of acute myocardial infarction(AMI) struggle with stressful consequences. Sense of coherence(SOC) seems to be associated with a person's capacity to face life incidents. The current study aims to evaluate SOC's correlation with the major adverse cardiac events(MACE) among the AMI survivors. The study was designed and reported following the STROBE guidelines and checklist.Methods: This study was part of the ST-elevated myocardial infarction cohort study in Isfahan(SEMI-CI) conducted on 724 AMI survivors followed for two years. The patients' demographic, medical history and follow-up manifestations were recruited. The 13-item SOC questionnaire was utilized and the Diagnostic Criteria for Psychosomatic Research(DCPR) questionnaire for psychosomatic disorders evaluation, including health anxiety, illness denial, irritable mood, and demoralization. MACE was defined as non-fatal MI, non-fatal stroke, and atherosclerosis cardiovascular disease-related death was recorded. Results: Logistic regression assessments showed that the SOC level was an independent predictor for the development of MACE(OR:0.67; 95%CI:0.40-0.85). This finding was confirmed by the controlling factors, including demographic data(OR:0.60; 95%CI:0.35-0.79), demographic factors and medical history(OR:0.62; 95%CI:0.36-0.86), the previous ones plus clinical follow-up assessments(OR:0.59; 95%CI:0.33-0.79), and all the evaluations plus psychosomatic factors(OR:0.76; 95%CI:0.42-0.92). Similar outcomes were achieved using SOC scores.Conclusion: Based on this study, SOC was an independent MACE predictor in a large population of AMI patients through a 2-year-follow-up period.