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Association of overexpression of p53 oncoprotein with the state of cell proliferation in oral carcinoma
Author(s) -
Warnakulasuriya K. A. A. S.,
Johnson Newell W.
Publication year - 1994
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1994.tb00053.x
Subject(s) - proliferating cell nuclear antigen , cell growth , biology , immunohistochemistry , proliferation marker , phosphoprotein , cancer research , cell division , pathology , cell , carcinoma , antibody , gene , immunology , medicine , genetics
p53 is a nuclear phosphoprotein recognised as important in the regulation of normal cell growth and proliferation, the wild‐type protein suppressing cell division. Expression of presumptive mutant protein, detected by immunohistochemistry, is used increasingly as a diagnostic and prognostic marker in human neoplasms. A question arises as to whether or not p53 (over)expression in a lesion is any more or less informative than other markers of cell proliferation. Twenty well‐differentiated oral squamous cell carcinomas which had earlier been examined for immunoreactivity against a panel of p53 antibodies were examined for the status of cell proliferation – both in islands of invading neoplastic cells and in the non‐malignant epithelial margins. The status of epithelial cell proliferation was found to be significantly higher in p53‐positive tumours when enumerated by Ki‐67 antibody, both within the tumour as well as its margins. This may confer a growth advantage to these neoplasms and reflect a status of inactivated p53 protein, although the actual cause of the rapid proliferation may lie in activation/inactivation of other genes. The PCNA labelling indices, on the other hand, were closely similar in both p53‐positive and ‐negative groups, suggesting that stabilisation of p53 protein does not influence the proliterative advantage in these carcinomas via a deregulation step of PCNA‐related gene products.