Elevated Levels of the P53 Tumour Suppressor Protein in the Basal Layer of Recurrent Laryngeal Papillomas
A viral aetiology for recurrent respiratory papillomatosis (RRP) has long since been postulated and the human papilloma virus (HPV) types 6,11,16 and 18 have been detected reproducibly in laryngeal papillomas and squamous cell carcinomas of the head and neck (SCCs of the H & N). Whilst the underlying mechanism(s) for the abnormal proliferation of respiratory epithelial cells leading to the formation of papillomas is unknown, it is known that the above HPV types, transform keratinocytes in culture with potencies which correlate with their ability to inactivate the p53 tumour suppressor protein. The E6 proteins of HPVs 16 and 18 complex and degrade the p53 protein1,2, whereas HPV6 and 11 E6 proteins have been reported to only weakly bind p53 without degradation2.
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