Loss of heterozygosity on chromosome 17p and mutant p53 in HPV-negative cervical carcinomas

M. Kaelbling, Harold P. Klinger, R. D. Burk, A. B. Johnson, N. B. Atkin

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


Inactivation of the protein product of the wild-type tumour suppressor gene p53 through complexing of the protein with the E6 oncoprotein of human papillomaviruses (HPV) in HPV-infected cells is thought to be important in the aetiology of cervical carcinoma. Mutations of p53 have also been reported in HPV-negative carcinomas, and we now demonstrate loss of heterozygosity (LOH) of chromosome region 17p13 (in which p53 is located) in such tumours. Immunocytochemical staining with monoclonal antimutant-p53 antibody revealed that the carcinomas with LOH on 17p and completely lacking H PV DNA sequences had mutant p53. Thus the LOH had apparently resulted in the loss of the wild-type allele. Consequently, in both HPV-positive and HPV-negative tumours there is loss of function of wild-type p53, in the former because the protein product of the p53 gene complexes with that of the viral E6 gene, in the latter because the protein is altered, presumably as a result of a direct alteration of the p53 gene but possibly because of other post-translational changes. That this mutant allele of the tumour suppressor gene may sometimes behave like an oncogene is suggested by the presence of more than the expected number of copies of the remaining chromosome 17 homologue in some carcinomas.

Original languageEnglish (US)
Pages (from-to)140-142
Number of pages3
JournalThe Lancet
Issue number8812
StatePublished - Jul 18 1992

ASJC Scopus subject areas

  • Medicine(all)


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