Experimental Oncology, 2013 (том 35)http://dspace.nbuv.gov.ua:80/handle/123456789/1331342024-03-29T13:35:23Z2024-03-29T13:35:23ZChronic periodontitis and the risk of head and neck squamous cell carcinoma: facts and figuresGondivkar, S.M.Gondivkar, R.S.Gadbail, A.R.Chole, R.Mankar, M.Yuwanati, M.http://dspace.nbuv.gov.ua:80/handle/123456789/1457092019-01-26T23:23:51Z2013-01-01T00:00:00ZChronic 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.
2013-01-01T00:00:00ZTumor cell heterogeneityChekhun, V.F.Sherban, S.D.Savtsova, Z.D.http://dspace.nbuv.gov.ua:80/handle/123456789/1457082019-01-26T23:23:49Z2013-01-01T00:00:00ZTumor 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.
2013-01-01T00:00:00ZMarkers of epithelial-mesenchymal transition in renal cell carcinomaDumanskiy, Y.V.Kudriashov, A.G.Vasilenko, I.V.Kondratyuk, R.B.Gulkov, Y.K.Chystiakov, R.S.http://dspace.nbuv.gov.ua:80/handle/123456789/1452872020-12-08T13:26:21Z2013-01-01T00:00:00ZMarkers of epithelial-mesenchymal transition in renal cell carcinoma
Dumanskiy, Y.V.; Kudriashov, A.G.; Vasilenko, I.V.; Kondratyuk, R.B.; Gulkov, Y.K.; Chystiakov, R.S.
Aim - to study the influence of markers of epithelial-mesenchymal transition (EMT) on a renal cell carcinoma (RCC) prognosis. The surgical material of 47 RCC patients who underwent nephrectomy was studied. RCC patients were distributed in two groups: a short-term survival group (3 - 6 months) and a long-term survival group (17 - 24 months). EMT markers expression was assessed by immunohistochemical methods. It was determined that the rate of spindle-cell EMT was 96,4 % in a short-term survival group and 42,1 % in a long-term survival group. High rate Furhman's nuclear atypia, i.e. degree 3 - 4 occurred in 100 % of cases in a short-term survival group versus 68,4 % in a longterm survival group. Conclusion: the rate of spindle-cell EMT in RCC may serve a more sensible prognostic factor than the degree of Furhman's nuclear atypia. Key Words: renal cell carcinoma, epithelial-mesenchymal transition, the degree of Furhman’s nuclear atypia.
2013-01-01T00:00:00ZExogenous nitric oxide potentiate DNA damage and alter DNA repair in cells exposed to ionising radiationMikhailenko, V.M.Muzalov, I.I.http://dspace.nbuv.gov.ua:80/handle/123456789/1452682019-01-20T23:23:40Z2013-01-01T00:00:00ZExogenous nitric oxide potentiate DNA damage and alter DNA repair in cells exposed to ionising radiation
Mikhailenko, V.M.; Muzalov, I.I.
The aim of this study was to investigate impact of exogenous nitric oxide (NO) on generation of different types of DNA damages, their transformation, and specificity of DNA repair in cells treated with ionizing radiation (IR). Methods: levels of single-strand and double-strand breaks assessed in peripheral blood lymphocytes (PBL) isolated from healthy humans and treated in vitro with NO donor — S-nitrosoglutathione (GSNO) and IR. The rate of DNA repair estimated after 30 and 60 min of PBL treatment. The visualization and measuring the number of prompt and delayed DNA damages, including strand breaks, apurinic and thermolabile sites performed with single-cell gel electrophoresis. Results: IR caused dose-dependent generation of single strand breaks (SSBs), double strand breaks (DSBs), and heat-labile sites (HLS) in cell DNA. However, particularly destructive was combined treatment IR with GSNO as NO donor that leads to a significant increase of DNA damage and a dose-dependent inhibition of the DNA repair rate. Obtained data proofs the ability of NO to inhibit fast and slow stages of SSBs, DSBs, and HLS repair resulting in significant growth of genotoxic effect. DNA breaks generation from HLS is able to affect DSBs yields especially in cells with altered DNA repair. The process of DNA repair of delayed DSBs formed from HLS was quite different from removal of DNA damages occurring immediately after treatment and was characterized by IR dose dependent inhibition of DNA repair. Conclusion: High level of DNA strand breaks, that are generated after the combined treatment with NO and IR, are accumulated for quite a long time after exposure due to altered DNA repair, indicating the development of genetic instability and increase of carcinogenic risk for organism exposed to combination of harmful environmental factors.
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