Akademik Veri Yönetim Sistemi
JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY, cilt.44, sa.3, ss.27-49, 2025 (SCI-Expanded)
Prostate cancer and inflammation mechanism are closely related because chronic inflammation causes inflammatory cells to infiltrate into prostatic atrophy areas and proliferative inflammatory atrophy is accepted as the initiator of prostate cancer. The study included 90 patients (28 patients with benign prostatic hyperplasia (BPH), 35 patients with localized prostate cancer (LPCa), and 27 patients with metastatic prostate cancer (MPCa) and 90 healthy controls. Blood samples from 90 patients and 90 healthy people were used to isolate genomic DNA. Serum protein levels were detected using the ELISA technique, and genotyping was done using the PCR-RFLP method. It was found that genotype distributions of CCR3 gene rs4987053 and the COX-2 gene rs689466 variants showed a substantial difference between the groups (Control, BPH, LPCa, MPCa) (respectively P < 0.05, P < 0.001). In addition, a important difference was determined between the non-cancerous and the prostate cancer groups in the NOD1 gene rs5743336 variant genotype distributions (P < 0.05). However, no substantial relationship was determined between the rs16969415, rs1801157, rs2228014, rs2066847, rs4986791 variants, and a risk of prostate cancer. The serum IL-1 beta, LY96, and TLR4 protein levels differed significantly between the groups (Control, BPH, LPCa, MPCa) (P < 0.001). In addition, IL-1 beta was associated with rs689466, LY96 with rs2228014, rs5743336 genotypes (P < 0.05). As a conclusion, the CCR3 gene rs4987053, COX-2 gene rs689466, and NOD1 gene rs5743336 variations were determined to be closely associated with prostate cancer risk.