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Histol Histopathol ; 21(7): 721-8, 2006 07.
Article in English | MEDLINE | ID: mdl-16598671

ABSTRACT

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.


Subject(s)
Carcinoma, Squamous Cell/pathology , Cell Cycle Proteins/metabolism , Diagnosis, Computer-Assisted , Leukoplakia, Oral/pathology , Mouth Neoplasms/pathology , Biomarkers, Tumor/metabolism , Carcinoma, Squamous Cell/metabolism , Humans , Immunoenzyme Techniques , Ki-67 Antigen/metabolism , Leukoplakia, Oral/metabolism , Mouth Neoplasms/metabolism , Proliferating Cell Nuclear Antigen/metabolism , Retrospective Studies , Tumor Suppressor Protein p53/metabolism
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