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Ludwig Institute for Cancer Research, Imperial College School of Medicine, St Marys Hospital, London W2 1PG, England [L. A. B., J. O., P. J. F., T. C.]; Department of Gynaecological Oncology, University of Sheffield, Northern General Hospital, Sheffield S5 7AU, England [J. A. T.]; University of Glasgow, Pathology Department, Western Infirmary, Glasgow G11 6NT, Scotland [B. G.]; Birmingham Clinical Trials Unit, University of Birmingham, Birmingham B15 2TT, England [L. H.]; UO Oncologia Medica, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo, Italy [M. G.]; and Dana-Farber Cancer Institute, Boston, Massachusetts 02115 [M. C. M., W. G. K.]
We have sought to determine the basis for preferential loss of the codon 72 proline (72P) rather than the arginine (72R) allele in squamous cell carcinoma of the vulva with loss of heterozygosity (LOH) in p53. The proportion of cases containing human papillomavirus (HPV) 16 was not statistically different among individuals with either 72RR or 72RP in the germ line (P > 0.99), but p53 LOH was significantly more common in individuals heterozygous 72RP than in 72RR individuals (P = 0.04). LOH more commonly involved the 72P allele in both HPV-positive and HPV-negative cancers. Our results imply that preferential loss of the 72P allele in vulval squamous cell carcinoma occurs by HPV-dependent and -independent mechanisms.
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