Prostate cancer is the most common cancer among men in many countries. Although the etiology of prostate cancer largely is unknown, both genetic and environmental factors may be involved. Advanced age, androgen metabolism, and heredity-race have been reported to be possible risk factors. On the other hand, several studies indicate that genetic polymorphisms in biotransformation enzymes play a role in prostate cancer development. In this study, association of the prostate cancer risk with genotype frequencies of the Phase I (CYP1A1) and Phase II (GSTM1 and GSTT1) biotransformation enzymes was investigated in 321 Turkish individuals (152 prostate cancer patients and 169 age-matched male controls). The presence or absences of the GSTM1 and GSTT1 genes were determined by a PCR-based method. Genotypes of CYP1A1 were determined by MspI-RFLP. The prevalence of GSTM1 null genotype in the cases was 64 percent, compared to 31 percent in the control group, indicating a strong association (OR = 4.08, 95%CI = 2.50–6.69). No association was observed between either GSTT1 null genotype or CYP1A1 polymorphism and prostate cancer incidence. No statistically significant association was observed between smoking status of the patients and any of the polymorphisms studied. In conclusion, results of this study indicate that only the GSTM1 null genotype may play an important role as a risk factor for prostate cancer development in Turkish population.

Objectives: This study aims to compare the serum calcitonin gene-related peptide (CGRP) and CGRP receptor protein levels between patients with fibromyalgia syndrome (FM) and healthy control subjects. Patients and methods: The study included 88 patients (7 males, 81 females; mean age 44.5±9.1 years; range, 20 to 72 years) newly-diagnosed with FM according to the 2010 American College of Rheumatology criteria and 88 healthy volunteers (6 males, 82 females; mean age 43.0±6.1 years; range, 20 to 57 years). Venous blood samples were collected from both groups for the measurement of the levels of serum CGRP and CGRP receptor proteins (receptor component protein [RCP], receptor activity modifying protein 1 [RAMP 1] and calcitonin receptor-like receptor [CLR]). Results: A comparison of the serum CGRP, CLR and RCP levels of the FM and control groups revealed a statistically significant difference (p=0.001, p=0.005, p=0.001, respectively). The difference between the groups in respect of the serum RAMP 1 levels was not statistically significant (p=0.107). Conclusion: The serum CGRP, CLR and RCP levels were found to be higher in the FM patients, but no difference was determined between the FM patients and the healthy control group in respect of the RAMP 1 level. These results can be of guidance for further clinical studies of the etiopathogenesis and treatment of FM.

Myeloperoxidase (MPO) is a phase I enzyme that can bioactivate many specific procarcinogens, including polycyclic aromatic hydrocarbons and aromatic amines. The MPO gene contains a common single nucleotide polymorphism, for which the -463G>A substitution within the promoter region has been shown to reduce MPO expression and activity. We investigated the association between the MPO -463G>A polymorphism and lung and prostate cancer in a Turkish population. MPO genotypes in the study populations were determined using polymerase chain reaction-based restriction fragment length polymorphism assay. The allelic frequency was significantly different between the cases and controls for lung cancer (p=0.02), but not prostate cancer (p=0.30). No significant difference was noted between the lung and prostate cancer cases and control populations in terms of genotype distribution (p=0.07, p=0.53, respectively). Control groups of lung and prostate cancer were in Hardy-Weinberg equilibrium (p=0.87 and p=0.41, respectively). To determine the protective effect against lung cancer among individuals with the -463A allele, G/A and A/A genotypes were combined. Comparison of the G/G and G/A + A/A genotypes between the lung cancer cases and control groups showed a statistically significant relationship (p=0.032, OR=0.60, 95% CI 0.38-0.95). No gender-specific difference was found in terms of genotype distribution between the lung cancer patients and the controls (female, p=0.20; male, p=0.34). In the case of smokers, a difference in genotype distribution between the lung cancer patients and the controls was statistically significant (p=0.02), although this difference was not statistically significant for non-smokers (p=0.90). Overall, no statistically significant difference was found between the prostate cancer cases and the controls in terms of genotype combination (p=0.46, OR=0.83, 95% CI 0.51-1.36). Additionally, in smokers and non-smokers, no significant relationship was determined between the prostate cancer patients and the control population (p=0.21, p=0.91, respectively). These results suggest that the MPO -463A allele significantly contributes to a protective effect overall and in smokers against lung cancer.

Prostate cancer is caused by uncontrolled growth of cells in the prostate gland. The aim of this study was to determine the cytotoxic activity of titanium dioxide (TiO2) and zinc oxide (ZnO) nanoparticles (NPs) and TiO2 + ZnO nanocomposite (NC) in human prostate cancer cell line (DU-145) and healthy mouse fibroblast cell line (L-929). In the study, TiO2 and ZnO NPs and TiO2 + ZnO NC were synthesized. Cytotoxic activities of NC and NPs was then analyzed in human prostate cancer cell line (DU-145) and healthy mouse fibroblast cell lines (L-929) using the MTT method. TiO2, ZnO and TiO2 + ZnO IC50 values were determined in DU-145 and L-929 cell cells (n = 6). TiO2 + ZnO NC in the Du-145 cell line was found as the most active, having statistically significant (***p < 0.0001, **p ˂ 0.001 and **p ˂ 0.01).

Sulfotransferase 1A1 (SULT1A1) is a member of the sulfotransferase family that plays an important role in the biotransformation of numerous carcinogenic and mutagenic compounds through sulfation. A transition, G to A at position 638, in the SULT1A1 gene, results in the Arg213His change. This single nucleotide polymorphism reduces the activity and thermostability of the SULT1A1 enzyme. In the present study, the relationship between the SULT1A1 Arg213His polymorphism and prostate cancer was investigated using PCR-RFLP. No significant difference in genotype and allele distribution was noted between the prostate cancer and control populations (P=0.072; P=0.099, respectively). The risk of prostate cancer in individuals carrying the SULT1A1*2 allele (His213 allele) was determined by combining the SULT1A1*1/SULT1A1*2 (Arg/His213) and SULT1A1*2/SULT1A1*2 (His/His213) genotypes. No association was observed between SULT1A1 Arg213His polymorphism and prostate cancer incidence (P=0.24; OR, 1.36; 95% CI, 0.84–2.25). However, the His213 allele was found to increase the risk of prostate cancer by 1.36-fold. In smoker and non-smoker populations, no significant relationship was determined between the prostate cancer and control population (P=0.45; P=0.34, respectively).