Fas, FasL, and cleaved caspases 8 and 3 in glioblastomas: A tissue microarray-based study

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dc.contributor.author Saggioro, Fabiano Pinto
dc.contributor.author Neder, Luciano
dc.contributor.author Stávale, João Norberto [UNIFESP]
dc.contributor.author Paixão-Becker, Aline Nazareth de Paiva
dc.contributor.author Malheiros, Suzana Maria Fleury [UNIFESP]
dc.contributor.author Soares, Fernando Augusto
dc.contributor.author Pittella, José Eymard Homem
dc.contributor.author Matias, Caio César Marconato Simões
dc.contributor.author Colli, Benedicto Oscar
dc.contributor.author Carlotti Junior, Carlos Gilberto
dc.contributor.author Franco, Marcello Fabiano de [UNIFESP]
dc.date.accessioned 2016-01-24T14:34:54Z
dc.date.available 2016-01-24T14:34:54Z
dc.date.issued 2014-01-01
dc.identifier http://dx.doi.org/10.1016/j.prp.2013.12.012
dc.identifier.citation Pathology Research and Practice. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 210, n. 5, p. 267-273, 2014.
dc.identifier.issn 0344-0338
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/37117
dc.description.abstract This investigation analyzed the immunoexpression of FasL, Fas, cleaved caspase-8, and cleaved caspase-3 in glioblastomas. Formalin-fixed and paraffin-embedded glioblastoma tissues and control brain tissues from 97 patients were analyzed by tissue microarrays and immunohistochemistry. Patients with glioblastomas that were negative or weakly stained (<50% of cells positive) for cleaved caspase-8 had worse cancer-specific overall survival (median=8.5 months) than did patients with tumors that highly expressed cleaved caspase-8 (median=11.7 months; P=0.0325), independent of clinical variables. There was no association of other markers with survival, treatment, sex, age, tumor size, and primary site. Among the tumors, there were reasonable to good positive correlations between the expression of FasL and Fas (r=0.47) and between Fas and cleaved caspase-8 (r=0.41), and there were poor positive correlations between Fas and cleaved caspase-3 (r=0.26), FasL and cleaved caspase-8 (r=0.22), and cleaved caspase-8 and -3 (r=0.31). Our results suggest that Fas-Fas-ligand signal transduction could be inhibited, especially at the stage of caspase-8 activation, thereby establishing a major mechanism for evasion of apoptosis by these tumors. the absence or low expression of cleaved caspase-8 in the tumors was a negative prognostic indicator for patient survival. (C) 2014 Elsevier GmbH. All rights reserved. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent 267-273
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Pathology Research and Practice
dc.rights Acesso aberto
dc.subject Glioblastoma en
dc.subject Cleaved caspase 8 en
dc.subject Apoptosis en
dc.subject Survival en
dc.subject Caspase 3 en
dc.title Fas, FasL, and cleaved caspases 8 and 3 in glioblastomas: A tissue microarray-based study en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Hosp Canc AC Camargo
dc.description.affiliation Univ São Paulo FMRR USP, Fac Med Ribeirao Preto, Dept Pathol, Ribeirao Preto, SP, Brazil
dc.description.affiliation Universidade Federal de São Paulo UNIFESP EPM, Dept Pathol, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo UNIFESP EPM, Dept Neurol, São Paulo, Brazil
dc.description.affiliation Hosp Canc AC Camargo, Dept Pathol, São Paulo, Brazil
dc.description.affiliation Univ São Paulo FMRP USP, Fac Med Ribeirao Preto, Dept Surg, Ribeirao Preto, SP, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP EPM, Dept Pathol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP EPM, Dept Neurol, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 04/09932-4
dc.identifier.file WOS000335206600001.pdf
dc.identifier.doi 10.1016/j.prp.2013.12.012
dc.description.source Web of Science
dc.identifier.wos WOS:000335206600001



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