Assessment of possible association between rs378854 and prostate cancer risk in the Serbian population

Prostate cancer (PCa) is the second most commonly diagnosed cancer among men worldwide. Despite its high incidence rate, the molecular basis of PCa onset and its progression remains little understood. Genome-wide association studies (GWAS) have greatly contributed to the identification of single nucleotide polymorphisms (SNP) associated with PCa risk. Several GWAS identified 8q24 as one of the most significant PCa-associated regions. The aim of this study was to evaluate the association of SNP rs378854 at 8q24 with PCa risk in the Serbian population. The study population included 261 individuals diagnosed with PCa, 257 individuals diagnosed with benign prostatic hyperplasia (BPH) and 106 healthy controls. Data quality analysis yielded results showing deviations from Hardy-Weinberg equilibrium in groups of PCa patients and BPH patients as well as in the control group. There was no significant association between alleles and genotypes of the genetic variant rs378854 and PCa risk in the Serbian population. [Projekat Ministarstva nauke Republike Srbije, br. 173016

Apoptosis and appearance of multinuclear C6 glioma cells after treatment by microtubule poisons

Microtubules play a crucial role in a large number of cellular functions, including chromosome separation during cell division. Microtubule poisons, drugs that perturb microtubule function, are used for the treatment of a number of malignant tumors, although the precise mechanisms of their cytotoxic effect are still not well understood. In this study, we have investigated the effects of two microtubule poisons, colchicine and paclitaxel, on rat astrocytoma C6 cell line in vitro. Cells were incubated 24-72 hours with, or without poisons, fixed and processed for analysis by light and electron microscopy. Both type of drugs displayed effects on the microtubule network of C6 glioma cells observed by electron microscopy. Furthermore, microtubule poisons triggered apoptotic cell death, although the extent of apoptosis was rather low, while the number of cells arrested in mitosis was significant (33% after 24h treatment with paclitaxel). The most striking effect of paclitaxel was obesreved after 72h, when over 66% of cells displayed multiple nuclei, implying that glioma cells escape mitotic arrest, that results in formation of multinucleated cells. The results showed that C6 glioma cells are largely resistant to induction of apoptosis by microtubule poisons, so further studies are needed to examine the possibilities to overcome resistance

Programmed cell death proteins and chronic leukemia

Apoptosis or programmed cell death is a genetically regulated process of cellular suicide. Apoptosis has been implicated in a wide range of pathological conditions, and mutations in apoptotic genes play important roles in the process of malignant transformation. Chronic leukemia represents a neoplastic disorder caused primarily by defective programmed cell death, as opposed to increased cell proliferation. This paper presents the main results of our ten-year research on the apoptosis of leukemia cells. The research included the morphological aspects of the process, the effect of antineoplastic agents on the induction of apoptosis in leukemia cells and expression analysis of the proteins involved in programmed cell death. Special attention was paid to the expression and interaction of the Bcl-2 family of proteins in leukemia cells. The ultimate aim of the study of apoptosis of leukemic cells is the discovery of new biological agents that might be used in the treatment of chronic leukemia

VARIABILITY OF THE CHLOROPLAST DNA OF SESSILE OAK (QUERCUS PETRAEA AGG. EHRENDORFER, 1967) IN SERBIA

Abstract — Genetic variability of sessile oak (Quercus petraea agg. Ehrendorfer, 1967) in Serbia is estimated applying cpDNA universal primer pairs that were characterized by a high informative level for chloroplast genome variability assessment in previous investigations. Five different haplotypes were detected in the analyzed sample material from populations in Serbia

Correlation between polymorphisms at promoter region of the NOS3 gene and prostate cancer in Serbian population

Objective: Prostate cancer (PC) is the most common malignant disease in men in the Western Hemisphere. The NOS3 has a role in vascular development, regulation of the vascular tone and tumor growth in PC. In previous studies, the -786 T > C polymorphism was found to be the most important promoter alteration of the NOS3 gene that may affect the PC progression. The purpose of this study was to evaluate 786 T > C, -764A > G, -714 G > T, -690 C > T and -649 G > A polymorphisms in the promoter region of NOS3 gene as genetic indicators of the relative risk of the PC occurrence in Serbian population. Method: In this study, we characterized these polymorphisms by PCR amplification, followed by capillary electrophoresis sequencing in the peripheral blood samples from 50 patients with PC, 50 benign hyperplasia patients and 50 individuals over 40 years of age who showed no clinical signs of any prostatic disease, that were used as controls. Results: Three of the analyzed polymorphisms (-764A > G, -714 G > T and -649 G > A) were not detected during this study. It is interesting to observe that when the -786 T > C polymorphism was present, -690 C > T polymorphism was also found. Conclusion: This study demonstrates no association between the -786 T > C polymorphism in the promoter of the NOS3 gene and the development of PC