Objectives: The objectives of this study are to document the status of p53 expression and mutation in cervical cancer at protein, RNA and DNA levels and to relate this to the presence of HPV. Materials and methods: Biopsy specimens from one hundred and three squamous cell carcinoma of the cervix and histologically normal ectocervix were analysed. Fresh tissues were extracted for protein, RNA IntroductionThere is a strong association between infection with certain types of genital human papillomaviruses (HPVs) and the subsequent development of cervical cancer.' The evidence supporting this association has been comprehensively reviewed recently2 and HPV types 16 and 18 are considered to be human carcinogens. In the majority of cervical carcinomas viral DNA sequences are integrated into the host genome3 resulting in deregulation of the viral oncogenes E6 and E7. The E6 oncoprotein of the high risk types has been shown in in vitro studies to bind to the p53 protein and degrade it via the ubiquitin pathway.4 These and other observations suggest that p53 inactivation in HPV containing cervical cancers is effected via E6 binding and implies that p53 mutation is unlikely to play a role in malignant progression in the cervix. Previous studies indicated that p53 mutation in cervical cancer was
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