http://dspace.nbuv.gov.ua:80/handle/123456789/133137 Sun, 19 Apr 2026 13:56:43 GMT 2026-04-19T13:56:43Z http://dspace.nbuv.gov.ua:80/bitstream/id/395790/ http://dspace.nbuv.gov.ua:80/handle/123456789/133137 http://dspace.nbuv.gov.ua:80/handle/123456789/145709 Chronic periodontitis and the risk of head and neck squamous cell carcinoma: facts and figures Gondivkar, S.M.; Gondivkar, R.S.; Gadbail, A.R.; Chole, R.; Mankar, M.; Yuwanati, M. Substantial evidence supports an association between periodontal disease and several systemic diseases including cardiovascular diseases, diabetes mellitus, respiratory diseases, adverse pregnancy outcomes, osteoporosis etc. Periodontal disease, a chronic inflammatory condition, is highly prevalent in adult populations around the world, and may be preventable. Estimates of prevalence vary between races and geographic regions, with a marked increase in the occurrence of periodontal disease with advancing age. Worldwide estimates for the prevalence of severe periodontal disease generally range from 10 to 15 %. The relationship between periodontal disease and cancer has been examined for a number of specific cancer sites. The grim statistics of head and neck cancer incidence and survival have remained essentially unchanged over the past 3 decades despite the prevention efforts against known risk factors of head and neck cancer, and advances in the diagnosis and treatment, arguing forcibly for new insights regarding the etiology as well as the strategies for prevention. Recent reports have linked periodontal disease with increased risk of squamous cell carcinoma of head and neck. This review provides current literature for a role of periodontal disease in carcinogenesis of head and neck region and discusses possible biological mechanisms involved. Tue, 01 Jan 2013 00:00:00 GMT http://dspace.nbuv.gov.ua:80/handle/123456789/145709 2013-01-01T00:00:00Z http://dspace.nbuv.gov.ua:80/handle/123456789/145708 Tumor cell heterogeneity Chekhun, V.F.; Sherban, S.D.; Savtsova, Z.D. The paper deals with the analysis of literary data on the tumor cell heterogeneity. Phenotypic, genetic and epigenetic mechanisms of heterogeneity are considered. The heterogeneity of metastasis is considered too. The importance for the biology of populations of tumor cells and the sensitivity of tumors to therapeutic treatment are discussed. Key Words: primary tumor, metastasis, heterogeneity, malignant phenotype, genetic instability, epigenetic factors. Tue, 01 Jan 2013 00:00:00 GMT http://dspace.nbuv.gov.ua:80/handle/123456789/145708 2013-01-01T00:00:00Z http://dspace.nbuv.gov.ua:80/handle/123456789/145251 Molecular characterization of PH-negative myeloproliferative neoplasms in Ukraine Mishcheniuk, O.Y.; Kostukevich, O.M.; Dmytrenko, I.V.; Sholoyko, V.V.; Prokopenko, I.M.; Martіna, Z.V.; Pilipenko, G.V.; Klymenko, S.V. Aim: The aim of this study was to examine the JAK2 V617F, the G1691A allele of factor V, and the G20210A prothrombin gene mutation status, and their predictive value for thrombosis in patients with Ph-negative myeloproliferative neoplasms (MPN) in Ukraine, with special emphasize to patient exposed to ionizing radiation due to the Chernobyl accident. Materials and Methods: There were 198 patients with Ph-negative MPN included in the study. Of these, 45 patients had experienced radiation exposure due to the Chernobyl accident. The JAK2 V617F mutation, the G1691A of factor V and the G20210A of prothrombin were detected by allele-specific polymerase chain reaction. Results: The polycythemia vera and essential thrombocythemia patients in unexposed group and Chernobyl patients were comparable in terms of the JAK2 V617F mutation prevalence with the frequency of anomaly corresponding well to the published data on unselected cases of these types of Ph-negative MPN. The JAK2 V617F mutation was less common on the border of statistical significance (p = 0.08) in Chernobyl primary myelofibrosis (PMF) patients than in non-exposed patients. JAK2 V617F positive patients had higher level of leukocytes (p = 0.03), hemoglobin (p =0.04) and splenomegaly (p = 0.04) than those without mutation. The JAK2 V617F mutation was strong predictor for thrombosis in essential thrombocytemia patients (relative risk=3.1, 95% CI = 1.7–16.4, p = 0.03). In PMF, the association with thrombosis was found for the G1691A allele of factor V (p = 0.03). The risk of thrombosis associated with the inherited thrombophilia in PMF patients was 7.0-fold (95% CI = 1.41–33.1, p = 0.03) higher than in polycythemia vera patients. The inherited thrombophilia increased risk of thrombotic complication 5.4-fold (95% CI = 1.41–18.17, p = 0.01) in overall cohort of Ph-negative myeloproliferative neoplasms patients. This trend continued in Chernobyl patients (p = 0.02), but not in unexposed cases. Conclusions: Our findings confirm previous results of other studies reporting that the JAK2 V617F mutation significantly and independently influences on a disease phenotype in Ph-negative MPN. The inherited thrombophilia is important risk factors of the thrombosis development in overall cohort primary myelofibrosis patients, and especially in disease developed following radiation exposure. Tue, 01 Jan 2013 00:00:00 GMT http://dspace.nbuv.gov.ua:80/handle/123456789/145251 2013-01-01T00:00:00Z http://dspace.nbuv.gov.ua:80/handle/123456789/145250 Effects of alvocidib and carboplatin on ovarian cancer cells in vitro Baumann, K.H.; Kim, H.; Rinke, J.; Plaum, T.; Wagner, U.; Reinartz, S. Aim: Failure of platinum chemotherapy is an unresolved issue in ovarian cancer. Targeted therapy has been added to the treatment options in solid cancers. Alvocidib is a cyclin dependent kinase inhibitor. Materials and methods: This study evaluated the effects of alvocidib together with carboplatin on ovarian cancer cells (BG-1 and Skov-3) in vitro applying proliferation assays, cell cycle distribution analyses, apoptosis induction assays, and drug accumulation assay. Results: Proliferation of both cell lines was inhibited by carboplatin and alvocidib. The interaction index revealed drug synergism at distinct drug concentrations. Cell cycle distribution was altered. Alvocidib induced apoptosis in Skov-3 cells, and necrosis in BG-1 cells. Rhodamine accumulation was increased by alvocidib or both compounds together. Conclusion: These data provide evidence for antiproliferative effects of alvocidib on human ovarian cancer cells in vitro associated with changes in cell cycle distribution, the induction of apoptosis, and modulation of intracellular drug accumulation. Alvocidib and carboplatin showed some cooperative activity. Tue, 01 Jan 2013 00:00:00 GMT http://dspace.nbuv.gov.ua:80/handle/123456789/145250 2013-01-01T00:00:00Z