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Mutant p53 oncogene expression in keratoacanthoma and squamous cell carcinoma
Author(s) -
STEPHENSON T.J.,
ROYDS J.,
SILCOCKS P.B.,
BLEEHEN S.S.
Publication year - 1992
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1992.tb14866.x
Subject(s) - keratoacanthoma , immunohistochemistry , oncogene , cancer research , cell , biology , mutant , epidermoid carcinoma , pathology , cancer , monoclonal antibody , tumor suppressor gene , basal cell , antibody , cell cycle , gene , medicine , carcinogenesis , immunology , genetics
Summary The tumour suppressor gene p53, located on the short arm of chromosome 17, encodes for a nuclear protein which regulates cell proliferation by inhibiting cells entering S‐phase. p53 mutations are alleged to be the commonest genetic abnormality in human cancer. We studied mutant p53 oncoprotein expression, using PAb1801 monoclonal antibody immunohistochemistry, in 25 ‘ideal’ keratoacanthomas and 26 well‐, 19 moderately and 18 poorly differentiated squamous cell carcinomas of the skin. While there was a highly significant trend in the proportion of p53 oncoprotein‐positive lesions from keratoacanthomas to poorly differentiated squamous cell carcinomas (χ 2 = 17·13, df=l, exact P =0·00003), p53 expression was inadequate for distinguishing keratoacanthoma from well‐differentiated squamous cell carcinoma (χ 2 = 2·55, df = 1, exact P = 0·18; corresponding to a sensitivity of 0·84 and a specificity of only 0·36).

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