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The Relationship Between Klk3 Rs17632542 and Prncr1 Rs16901979 Polymorphisms With Susceptibility to Prostate Cancer Publisher



Yazdani M1 ; Angaji A1 ; Abolhasani M2, 3 ; Fathi Z4 ; Madjd Z2, 5 ; Roviello G6 ; Roudi R2 ; Asgari M2, 3
Authors
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Authors Affiliations
  1. 1. Department of Cell and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran
  2. 2. Oncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Hasheminejad Kidney Center, Iran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Medical Genetics and Molecular Biology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Health Sciences, University of Florence, viale Pieraccini, 6, Florence, 50139, Italy

Source: Meta Gene Published:2019


Abstract

Purpose: Prostate cancer (PCa) is known as the most prevalent type of cancer in men worldwide. Prostate-specific antigen (PSA) serum levels are used to screen patients in the early stages of the disease. However, due to the heterogeneity of the disease, studies have shown that the given method is not sufficient in this domain. Therefore, developing an appropriate method for identifying this group of patients is of paramount importance. Experimental design: The status of 2 single nucleotide polymorphisms, including rs17632542 in KLK3 and rs16901979 in PRNCR1, were screened in 100 PCa patients and 100 patients with benign prostatic hyperplasia as control group using the amplification-refractory mutation system (ARMS) polymerase chain reaction (PCR) method. Results: The findings of this study revealed that 86% of the PCa patients had TT genotype and 14% had CT heterozygote for rs17632542 in KLK3, but no one in the patient group had CC genotype. The analysis indicated no significant difference between case and control groups in terms of mutated and non-mutated status in KlK3 (OR [95% CI] = 1.872 [0.748–4.684] and p-value = .175). Also, 37.5% and 14.28% of the individuals with affected genotype (CT + CC) in control and case groups had lower levels of PSA and free PSA, respectively. In rs16901979 of PRNCR1, 90% of the PCa patients had CC genotype, 9% had CA heterozygote and 1% had been affected by AA homozygote. The analysis indicated no significant difference between case and control groups in terms of mutated and non-mutated status in PRNCR1 (OR [95% CI] = 1.123 [0.436–2.895] and p-value = .809). Furthermore, 66% of the control group and all the PCa patients with affected genotype (CA + AA) had higher levels of PSA and free PSA serum levels. Conclusion: It seems that the effect of rs17632542-C in KLK3 on the incidence of PCa follows a specific pattern in Iranians. Also, the PSA levels for the participants were not similar to those of most populations. With respect to rs16901979 of PRNCR1, the results were similar to the data obtained from other populations and there was a rising trend in PSA serum levels in affected individuals. © 2019