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dc.contributor.authorSoares, C. P. [UNESP]
dc.contributor.authorZuanon, J. A S [UNESP]
dc.contributor.authorTeresa, D. B. [UNESP]
dc.contributor.authorFregonezi, P. A. [UNESP]
dc.contributor.authorBenatti Neto, Carlos[UNESP]
dc.contributor.authorOliveira, M. R B [UNESP]
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.available2014-05-27T11:21:54Z
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.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.relation.ispartofHistology and Histopathology
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.typeArtigo
dcterms.licensehttp://revistas.um.es/analesps/about/submissions#copyrightNotice
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.scopus2-s2.0-33645758485
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Ciências Farmacêuticas, Araraquarapt
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
dc.identifier.file2-s2.0-33645758485.pdf
dc.relation.ispartofjcr2.015
dc.relation.ispartofsjr0,672
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