The association studies between miR-34b/c rs4938723 polymorphism and cancer risk showed conflicting results. This study aimed to assess the impact of rs4938723 polymorphism on prostate cancer risk. This case-control study was done on 151 prostate cancer (PCa) patients and 152 benign prostate hyperplasia to examine whether rs4938723 polymorphism in the promoter of pri-miR-34b/c was linked to the carcinogenesis of PCa in a sample of Iranian population. Genotyping of Pri-miR-34 b/c rs4938723 polymorphism was performed by using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. The results showed that rs4938723 variant significantly increased the risk of PCa in codominant (OR = 1.92, 95% CI = 1.15 - 3.18, p= 0.012, TC vs TT), dominant (OR = 1.99, 95% CI = 1.23 - 3.24, p= 0.005, TC + CC vs TT), and allelic (OR = 1.79, 95% CI = 1.20 - 2.68, p= 0.005, C vs T) inheritance model. Our findings propose that Pri-miR-34 b/c rs4938723 variant may be a risk factor for the development of PCa in a sample of Iranian population. Larger sample sizes with different ethnicities are required to validate our findings.

Abstract. Tumor protein 53 (TP53), a tumor suppressor gene, is a vital cellular cancer suppressor in multicellular organisms. Murine double minute-2 (MDM2) is an oncoprotein that inhibits TP53 activity. A number of studies have examined the association of TP53 and MDM2 polymorphisms with the risk of common forms of cancer, but the findings remain inconclusive. The present study aimed to evaluate the impact of the 40-bp insertion/deletion (I/D) polymorphism (rs3730485) in the MDM2 promoter region and the 16-bp I/D polymorphism (rs17878362) in TP53 on the susceptibility of prostate cancer (PCa) in a sample of the Iranian population. This case-control study included 103 patients with pathologically confirmed PCa and 142 patients with benign prostatic hyperplasia. The IntroductionProstate cancer (PCa) is the most prevalent form of cancer among males in the United States (1). In Iran, the incidence of PCa is ~9.6 cases per 100,000 individuals, with a range of 3.2-16.0 per 100,000 in various geographical settings (2,3). This is comparable with the Asia-Pacific region (9.9 per 100,000), but significantly lower than in the rest of the world (32.8 per 100,000) (4). The median age at diagnosis is ~66 years and the 5-year survival rate of patients with PCa has been estimated to be 98.9% (5).The molecular mechanisms underlying the progression and carcinogenesis of PCa have not yet been clarified. Additional molecular markers that may be employed to detect PCa and to individualize patient therapy and prognosis are of great clinical importance. A number of large cohort and case-control studies with various populations suggest that family history is a primary risk factor for PCa (6-10).In humans, the tumor protein 53 (TP53) gene is located on the short arm of chromosome 17 (17p13.1) (11). TP53, an important tumor suppressor gene, is a crucial regulator of apoptosis and the cell cycle (12-15). When it is mutated, this regulation may be lost, leading to uncontrolled cell proliferation and potentially tumorigenesis (16).The human MDM2 gene is mapped on chromosome 12q14. 3-15 (17). MDM2 functions as a key negative regulator of TP53 (18)

AIMTo compare the outcomes between related and unrelated kidney transplantations.METHODSLiterature searches were performed following the Cochrane guidelines. We conducted a systematic review and a meta-analysis, which included 12 trials that investigated outcomes including the long-term (ten years), mid-term (one to five years), and short-term (one year) graft survival rate as well as the acute rejection rate. Meta-analyses were performed using fixed and random-effects models, which included tests for publication bias and heterogeneity.RESULTSNo difference in graft survival rate was detected in patients who underwent living related kidney transplantations compared to unrelated (P = 0.44) transplantations after ten years. There were no significant differences between the graft survival rate in living related and unrelated kidney transplantations after a short- and mid-term follow-up (P = 0.35, P = 0.46). There were no significant differences between the acute rejection rate in living related and unrelated kidney transplantations (P = 0.06).CONCLUSIONThe long, mid and short term follow-up of living related and unrelated kidney transplantation showed no significant difference in graft survival rate. Also, acute rejection rate was not significantly different between groups.

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MicroRNAs (miRNAs) participate in diverse biological pathways and may act as oncogenes or tumor suppressors. The single nucleotide polymorphisms (SNPs) in miRNAs potentially can alter miRNA-binding sites on target genes as well as affecting miRNAs expression. The present study aimed to evaluate the impact of miR-608 rs4919510 C > G variant on bladder cancer risk. This case-control study conducted on 233 bladder cancer patients and 252 healthy subjects. Genotyping of miR-608 rs4919510 was done using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Our findings showed that CG as well as CG + GG genotypes significantly increased the risk of bladder cancer (OR = 1.94, 95% CI = 1.28–2.94, p  = 0.002, and OR = 1.90, 95% CI = 1.26–2.86, p  = 0.002, respectively) compared to CC genotype. The G allele significantly increased the risk of bladder cancer compared to C allele (OR = 1.69, 95% CI = 1.17–2.45, p  = 0.005). Our findings proposed that miR-608 polymorphism might be associated with increased risk of bladder cancer in a sample of Iranian population. Further large-scale studies with different ethnicities are needed to verify our findings.