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<title>Experimental Oncology, 2013, № 4</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/133138" rel="alternate"/>
<subtitle/>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/133138</id>
<updated>2026-04-19T17:46:43Z</updated>
<dc:date>2026-04-19T17:46:43Z</dc:date>
<entry>
<title>Markers of epithelial-mesenchymal transition in renal cell carcinoma</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/145287" rel="alternate"/>
<author>
<name>Dumanskiy, Y.V.</name>
</author>
<author>
<name>Kudriashov, A.G.</name>
</author>
<author>
<name>Vasilenko, I.V.</name>
</author>
<author>
<name>Kondratyuk, R.B.</name>
</author>
<author>
<name>Gulkov, Y.K.</name>
</author>
<author>
<name>Chystiakov, R.S.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/145287</id>
<updated>2020-12-08T13:26:21Z</updated>
<published>2013-01-01T00:00:00Z</published>
<summary type="text">Markers 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.
</summary>
<dc:date>2013-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Exogenous nitric oxide potentiate DNA damage and alter DNA repair in cells exposed to ionising radiation</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/145268" rel="alternate"/>
<author>
<name>Mikhailenko, V.M.</name>
</author>
<author>
<name>Muzalov, I.I.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/145268</id>
<updated>2019-01-20T23:23:40Z</updated>
<published>2013-01-01T00:00:00Z</published>
<summary type="text">Exogenous 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.
</summary>
<dc:date>2013-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Evaluation of the influence of recombinant human tumor necrosis factor on adhesive ability of human fetal umbilical vein endothelial cells to К562 and L1210 cells</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/145267" rel="alternate"/>
<author>
<name>Barilka, V.A.</name>
</author>
<author>
<name>Matlan, V.L.</name>
</author>
<author>
<name>Prymak, S.V.</name>
</author>
<author>
<name>Loginsky, V.Y.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/145267</id>
<updated>2019-01-20T23:23:33Z</updated>
<published>2013-01-01T00:00:00Z</published>
<summary type="text">Evaluation of the influence of recombinant human tumor necrosis factor on adhesive ability of human fetal umbilical vein endothelial cells to К562 and L1210 cells
Barilka, V.A.; Matlan, V.L.; Prymak, S.V.; Loginsky, V.Y.
Regulation of adhesion receptors (AR) expression on endothelial cells (EC) is controlled by tumor necrosis factor (TNF), a pleiotropic cytokine, being a local mediator of cellular homeostasis and immune response. TNF is one of the first cytokines that are secreted in inflammation and lymphoid tumors (LT). The increase in TNF-α expression promotes tumour metastasis and induces the endothelial dysfunction in many pathophysiological conditions. Aim of study was to determine an adhesive ability of human fetal umbilical vein endothelial cells (НUVECs) to adhere to cells of leukemic lines К562 and L1210 after treatment with various concentrations of recombinant human TNF (rhTNF), (Sigma, USA). Materials and Methods: HUVECs were obtained as described Jaffe E.A. et al., 1973. Cell suspension of К562 or L1210 were labeled with 3H-thymidine but not activated with rhTNF before experiment and were added to the monolayer of HUVECs. The level of attachment cells was estimated as the index of adhesion (IA). Doses of rhTNF were selected according to the predefined blood level of endogenous TNF in healthy subjects and patients with hematologic diseases and have been divided into low, intermediate, high and stimulating ones (the concentration range of 0.001–6.946 ng/ml). HUVECs that were incubated in a non-rhTNF medium have been used as controls. Results: rhTNF exerted a complex dose-dependent influence on adhesive properties of HUVECs in vitro. Parameters of AI for the К562 and L1210 cells were related to the morphologic type of cell line, which was evidenced by a high statistical correlation. Cells L1210 were characterized by high IA parameters after their treatment with low or stimulating doses of rhTNF. Cells К562 adhered to HUVECs after their treatment with stimulating doses of rhTNF. Conclusion: As proven by the obtained results, the TNF cytokine-activated vascular endothelium plays a pivotal role in the initiation of adhesion, while the influence of autocrine secretion of TNF in the very moment of the formation of intercellular contacts.
</summary>
<dc:date>2013-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>A rare coincidence: facioscapulohumeral muscular dystrophy and breast cancer</title>
<link href="http://dspace.nbuv.gov.ua:80/handle/123456789/145266" rel="alternate"/>
<author>
<name>Yazici, O.</name>
</author>
<author>
<name>Aksoy, S.</name>
</author>
<author>
<name>Ozdemir, N.</name>
</author>
<author>
<name>Sendur, M.A.N.</name>
</author>
<author>
<name>Dogan, M.</name>
</author>
<author>
<name>Zengin, N.</name>
</author>
<id>http://dspace.nbuv.gov.ua:80/handle/123456789/145266</id>
<updated>2019-01-21T23:23:45Z</updated>
<published>2013-01-01T00:00:00Z</published>
<summary type="text">A rare coincidence: facioscapulohumeral muscular dystrophy and breast cancer
Yazici, O.; Aksoy, S.; Ozdemir, N.; Sendur, M.A.N.; Dogan, M.; Zengin, N.
Aim: Facioscapulohumeral muscular dystrophy (FSHD) is an autosomally inherited neuromuscular disorder and may be associated with increased cancer risk. Patient: A 69-year old female admitted to hospital with complaint of left axillary mass who had diagnosis of FSHD in her adulthood period. Results: Bilateral breast cancer diagnosis was made and the patient underwent bila­teral mastectomy. Following the operation, adjuvant chemotherapy and radiotherapy performed and hormonal therapy started. Conclusion: The patients with congenital muscular dystrophy might have an increased risk of malignancy. We consider that some genetic alterations in FSHD might have contributed to the development of bilateral breast cancer in our patient. Key Words: muscular dystrophy, breast cancer, PTEN.Aim: Facioscapulohumeral muscular dystrophy (FSHD) is an autosomally inherited neuromuscular disorder and may be associated with increased cancer risk. Patient: A 69-year old female admitted to hospital with complaint of left axillary mass who had diagnosis of FSHD in her adulthood period. Results: Bilateral breast cancer diagnosis was made and the patient underwent bila­teral mastectomy. Following the operation, adjuvant chemotherapy and radiotherapy performed and hormonal therapy started. Conclusion: The patients with congenital muscular dystrophy might have an increased risk of malignancy. We consider that some genetic alterations in FSHD might have contributed to the development of bilateral breast cancer in our patient.
</summary>
<dc:date>2013-01-01T00:00:00Z</dc:date>
</entry>
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