Soares, C. P. [UNESP]Zuanon, J. A S [UNESP]Teresa, D. B. [UNESP]Fregonezi, P. A. [UNESP]Benatti Neto, Carlos[UNESP]Oliveira, M. R B [UNESP]Donadi, E. A.Martinelli-Kläy, C. P.Soares, E. G.2014-05-272014-05-272006-07-01Histology and Histopathology, v. 21, n. 7-9, p. 721-728, 2006.0213-3911http://hdl.handle.net/11449/68968The 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.721-728engComputer-assisted analysisKi-67Oral cancerp53PCNAcell cycle proteincyclineKi 67 antigenprotein p53tumor markercarcinogenesiscell cycle regulationcomputer assisted diagnosiscomputer systemcontrolled studydiagnostic accuracydisease severityepithelium hyperplasiahistopathologyhumanhuman tissueimmunohistochemistryleukoplakiamajor clinical studymalignant transformationmouth cancerprotein expressionquantitative analysisretrospective studyrisk assessmentsquamous cell carcinomastatistical significanceenzyme immunoassaymetabolismmouth tumorpathologyCarcinoma, Squamous CellCell Cycle ProteinsDiagnosis, Computer-AssistedHumansImmunoenzyme TechniquesKi-67 AntigenLeukoplakia, OralMouth NeoplasmsProliferating Cell Nuclear AntigenRetrospective StudiesTumor Markers, BiologicalTumor Suppressor Protein p53ArtigoAcesso aberto2-s2.0-336457584852-s2.0-33645758485.pdf