p53 and PCNA expression in carcinogenesis of the oropharyngeal mucosa.
Hyperplastic lesions of the oral mucosa such as leukoplakia and oral lichen planus can eventually develop into squamous cell carcinomas (SCC) and provide an excellent model for multistage carcinogenesis. The development of carcinomas is assumed to be the result of interaction of genetic factors, locally applied carcinogens and immunological unresponsiveness. The purpose of this study was, therefore, to determine the role of alterations of the tumour suppressor gene p53, and the proliferation status of the lesions determined by PCNA expression. We investigated p53 and PCNA expression in 265 tissue sections of normal mucosa, premalignant, malignant and metastatic lesions of the oral mucosa by immunohistology. Quantitative analysis showed a gradual increase in PCNA expression from normal mucosa to moderately differentiated SCC. p53 expression was detectable in benign premalignant lesions. The increase in the number of p53-positive biopsies was correlated with the dysplasia and loss of differentiation in the premalignant and malignant lesions.
Girod
S C
SC
Department of Oral and Maxillofacial Surgery, University of Cologne, Germany.
Pape
H D
HD
Krueger
G R
GR
D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53; D006801:Humans; D007971:Leukoplakia / Q000235:genetics; D008010:Lichen Planus / Q000235:genetics; D009061:Mouth Mucosa / Q000378:metabolism; D009062:Mouth Neoplasms / Q000235:genetics; D009959:Oropharyngeal Neoplasms / Q000235:genetics / Q000378:metabolism*; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
D018809:Proliferating Cell Nuclear Antigen; D016159:Tumor Suppressor Protein p53