Role of a p53 polymorphism in the development of human papilloma-virus-associated cancer

Alan Storey, Miranda Thomas, Ann Kalita, Catherine Harwood, Daniela Gardiol, Fiamma Mantovani, Judith Breuer, Irene M. Leigh, Greg Matlashewski and Lawrence Banks
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Alan Storey: Imperial Cancer Research Fund, Skin Tumour Laboratory
Miranda Thomas: International Centre for Genetic Engineering and Biotechnology
Ann Kalita: International Centre for Genetic Engineering and Biotechnology
Catherine Harwood: Imperial Cancer Research Fund, Skin Tumour Laboratory
Daniela Gardiol: International Centre for Genetic Engineering and Biotechnology
Fiamma Mantovani: International Centre for Genetic Engineering and Biotechnology
Judith Breuer: St Bartholomews and The Royal London Hospital School of Medicine and Dentistry, Queen Mary and Westfield College
Irene M. Leigh: Imperial Cancer Research Fund, Skin Tumour Laboratory
Greg Matlashewski: Institute of Parasitology and McGill Cancer Centre, McGill University, Macdonald Campus
Lawrence Banks: Institute of Parasitology and McGill Cancer Centre, McGill University, Macdonald Campus

Nature, 1998, vol. 393, issue 6682, 229-234

Abstract: The E6 oncoprotein derived from tumour-associated human papillomaviruses (HPVs) binds to and induces the degradation of the cellular tumour-suppressor protein p53. A common polymorphism that occurs in the p53 amino-acid sequence results in the presence of either a proline or an arginine at position 72. The effect of this polymorphism on the susceptibility of p53 to E6-mediated degradation has been investigated and the arginine form of p53 was found to be significantly more susceptible than the proline form. Moreover, allelic analysis of patients with HPV-associated tumours revealed a striking overrepresentation of homozygous arginine-72 p53 compared with the normal population, which indicated that individuals homozygous for arginine 72 are about seven times more susceptible to HPV-associated tumorigenesis than heterozygotes. The arginine-encoding allele therefore represents a significant risk factor in the development of HPV-associated cancers.

Date: 1998
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DOI: 10.1038/30400

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