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dc.contributor.authorEskiizmir, G; Vatanseuer, HS; Ozgur, E; Aslan, A; Tanyeri, G; Gozuacik, D; Ozbilgin, MK; Cingi, C
dc.date.accessioned2020-07-01T08:36:00Z
dc.date.available2020-07-01T08:36:00Z
dc.date.issuedMAR-APR
dc.date.issued2014
dc.identifier.urihttp://hdl.handle.net/20.500.12481/7041
dc.description.abstractPurpose: Jak-Stat signaling pathway is one of the major signal transduction cascades which regulates most of the cellular events such as cell proliferation, differentiation, cell migration and apoptosis. This study aims to determine the activity of Jak-Stat signaling pathway in the pathogenesis of cholesteatoma. Materials and Methods: Cholesteatoma and skin samples were obtained from 10 patients who underwent tympanomastoidectomy for chronic otitis media with cholesteatoma. Immunohistochemical analysis of cholesteatoma and skin was performed using anti-Jak1, anti-Jak2, anti-Jak3, anti-Stat1, anti-Stat2, anti-Stat3, anti-Stat4 and anti-Stat5 antibodies. The immunoreactivities in cholesteatoma and skin were quantified using H-score measurement and statistical comparison was performed. Results: Jak1, Jak2, Jak3, Stat1 and Stat3 immunoreactivities were not detected in cholesteatoma; in contrast to the skin (129.8; 226.7; 33.0; 66.4;115.9). In addition, when H-score measurements of Stat2, Stat4 and Stat5 immunoreactivities were compared between cholesteatoma (172.8; 166.7; 120.0) and skin (400.0; 284.9; 292.0), statistically significant differences were found (p < 0.0001, p < 0.0001, p < 0.0001). Conclusions: A remarkable deficiency in the family members of Jak-Stat signaling pathway was demonstrated in cholesteatoma. Therefore, perturbations in Jak-Stat signaling pathway may play a role in the pathogenesis of cholesteatoma. (C) 2014 Elsevier Inc. All rights reserved.
dc.titleJak-Stat signaling pathway may play a role in the pathogenesis of cholesteatoma
dc.title.alternativeAMERICAN JOURNAL OF OTOLARYNGOLOGY
dc.identifier.DOI-ID10.1016/j.amjoto.2013.10.005
dc.identifier.volume35
dc.identifier.issue2
dc.identifier.startpage130
dc.identifier.endpage136
dc.identifier.issn/e-issn0196-0709
dc.identifier.issn/e-issn1532-818X


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