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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/68968
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dc.contributor.authorSoares, C. P.-
dc.contributor.authorZuanon, J. A S-
dc.contributor.authorTeresa, D. B.-
dc.contributor.authorFregonezi, P. A.-
dc.contributor.authorBenatti Neto, Carlos-
dc.contributor.authorOliveira, M. R B-
dc.contributor.authorDonadi, E. A.-
dc.contributor.authorMartinelli-Kläy, C. P.-
dc.contributor.authorSoares, E. G.-
dc.date.accessioned2014-05-27T11:21:54Z-
dc.date.accessioned2016-10-25T18:22:23Z-
dc.date.available2014-05-27T11:21:54Z-
dc.date.available2016-10-25T18:22:23Z-
dc.date.issued2006-07-01-
dc.identifierhttp://hdl.handle.net/11449/68968-
dc.identifier.citationHistology and Histopathology, v. 21, n. 7-9, p. 721-728, 2006.-
dc.identifier.issn0213-3911-
dc.identifier.urihttp://hdl.handle.net/11449/68968-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/68968-
dc.description.abstractThe knowledge of cell-cycle control has shown that the capacity of malignant growth is acquired by the stepwise accumulation of defects in specific genes regulating cell growth. Histologic diagnosis might be improved by a quantitative evaluation of more specific diagnosis biomarkers, which could help to precisely identify pre-malignant and malignant oral lesions. The aim of the present study is to evaluate whether computer-based quantitative assessment of p53, PCNA and Ki-67 immunohistochemical expression, could be used clinically to foresee the risk of oral malignant transformation. This retrospective study was carried out in ninety-five oral biopsies, 27 were classified as fibrous inflammatory hyperplasia, 40 as leukoplakia and 28 as oral squamous cell carcinoma. Sixteen out of the 40 leukoplakia were diagnosed as non-dysplastic leukoplakia, the other 24 being dysplastic leukoplakia, of which 50.0% were classified as moderate to severe dysplasia. Comparison of the four groups of oral tissues showed significant rises in p53 and Ki-67 positivity index, which increased steadily in the order benign, pre-malignant, and malignant. In contrast, it was not possible to relate higher PCNA levels with pre-malignant and malignant oral lesions. We therefore conclude that PCNA immunohistochemistry expression is probably an inappropriate marker to identify oral carcinogenesis, whereas joint quantitative evaluation of p53 and Ki-67, appears to be useful as a tumor marker, providing a pre-diagnostic estimate of the potential for cell-cycle deregulation of the oral proliferate status.en
dc.format.extent721-728-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectComputer-assisted analysis-
dc.subjectKi-67-
dc.subjectOral cancer-
dc.subjectp53-
dc.subjectPCNA-
dc.subjectcell cycle protein-
dc.subjectcycline-
dc.subjectKi 67 antigen-
dc.subjectprotein p53-
dc.subjecttumor marker-
dc.subjectcarcinogenesis-
dc.subjectcell cycle regulation-
dc.subjectcomputer assisted diagnosis-
dc.subjectcomputer system-
dc.subjectcontrolled study-
dc.subjectdiagnostic accuracy-
dc.subjectdisease severity-
dc.subjectepithelium hyperplasia-
dc.subjecthistopathology-
dc.subjecthuman-
dc.subjecthuman tissue-
dc.subjectimmunohistochemistry-
dc.subjectleukoplakia-
dc.subjectmajor clinical study-
dc.subjectmalignant transformation-
dc.subjectmouth cancer-
dc.subjectprotein expression-
dc.subjectquantitative analysis-
dc.subjectretrospective study-
dc.subjectrisk assessment-
dc.subjectsquamous cell carcinoma-
dc.subjectstatistical significance-
dc.subjectenzyme immunoassay-
dc.subjectmetabolism-
dc.subjectmouth tumor-
dc.subjectpathology-
dc.subjectCarcinoma, Squamous Cell-
dc.subjectCell Cycle Proteins-
dc.subjectDiagnosis, Computer-Assisted-
dc.subjectHumans-
dc.subjectImmunoenzyme Techniques-
dc.subjectKi-67 Antigen-
dc.subjectLeukoplakia, Oral-
dc.subjectMouth Neoplasms-
dc.subjectProliferating Cell Nuclear Antigen-
dc.subjectRetrospective Studies-
dc.subjectTumor Markers, Biological-
dc.subjectTumor Suppressor Protein p53-
dc.titleQuantitative cell-cycle protein expression in oral cancer assessed by computer-assisted systemen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationDepartment of Clinical Analysis School of Pharmacy University of São Paulo State (UNESP), Rua Expedicionarios do Brasil 1621, 14 801 902 Araraquara, Sao Paulo-
dc.description.affiliationDepartment of Physiology and Pathology School of Dentistry University of São Paulo State (UNESP), Rua Expedicionarios do Brasil 1621, 14 801 902 Araraquara, Sao Paulo-
dc.description.affiliationDepartment of Pathology Faculty of Medicine of Ribeirão Preto University of São Paulo (USP), Ribeirão Preto, SP-
dc.description.affiliationDepartment of Clinical Medicine Faculty of Medicine of Ribeirão Preto University of São Paulo (USP), Ribeirão Preto, SP-
dc.description.affiliationUnespDepartment of Clinical Analysis School of Pharmacy University of São Paulo State (UNESP), Rua Expedicionarios do Brasil 1621, 14 801 902 Araraquara, Sao Paulo-
dc.description.affiliationUnespDepartment of Physiology and Pathology School of Dentistry University of São Paulo State (UNESP), Rua Expedicionarios do Brasil 1621, 14 801 902 Araraquara, Sao Paulo-
dc.rights.accessRightsAcesso aberto-
dc.identifier.file2-s2.0-33645758485.pdf-
dc.relation.ispartofHistology and Histopathology-
dc.identifier.scopus2-s2.0-33645758485-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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