Quantitative cell-cycle protein expression in oral cancer assessed by computer-assisted system
C.P. Soares1, J.A.S. Zuanon2, D.B. Teresa1, P.A Fregonezi1, C.B. Neto1, M.R.B. Oliveira2, E.A. Donadi4, C.P. Martinelli-Kläy3 and E.G. Soares3
1Department of Clinical Analysis, School of Pharmacy, University of São Paulo State (UNESP), Araraquara, São Paulo, Brazil, 2Department of Physiology and Pathology, School of Dentistry, University of São Paulo State (UNESP), Araraquara, São Paulo, Brazil, 3Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, SP, Brazil, 4Department of Clinical Medicine, Faculty of Medicine of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, SP, Brazil
Offprint requests to: Offprint requests to: Dr. C.P. Soares, Department of Clinical analysis, School of Pharmacy, University of São Paulo State (UNESP), Rua Expedicionários do Brasil, 1621, Zip code 14 801 902, Arangquara, São Paulo, Brasil. e-mail: soarescp@hotmail.com
Summary. The 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. Histol Histopathol 21, 721-728 (2006)
Key words: Oral cancer, p53, PCNA, Ki-67, computer-assisted analysis
DOI: 10.14670/HH-21.721