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Human papillomavirus (HPV) is the only DNA tumour virus where a large body of evidence implicates it in human cancers. The evidence for a causative role of HPV in human cervical cancer, was recently reviewed by zur Hausen, (1) and is the following: (1) expression of specific HPV genes (such as E6 and E7) were shown in cervical cancer cell lines and cancer biopsies (2) (2) viral DNA was shown to have immortalisation properties (3,4); (3) viral oncogene expression was shown to be required for the maintenance of the malignant phenotype in specific cervical cancer cell lines (5,6); (4) a substantial number of epidemiological studies have been performed which point to high risk HPV as a primary risk factor for cervical cancer. In addition, large case-control and prospective epidemiological studies supported this idea, and indicated that persisting HPV infections were the most significant risk factor in cervical cancer. (7,8)
Different types of HPV have been identified in a high percentage of nonmelanoma skin cancers (basal and squamous cell carcinomas). However, these basal and squamous cell carcinomas occur preferentially in light exposed sites. This could suggest an interaction between ultraviolet light and a low risk (non-mutagenic) papillomavirus infection.(9) This would make it a possible candidate in pterygia, which are thought to have aetiology involving ultraviolet irradiation.
The binding to the p53 protein of the E6 oncoprotein, encoded by HPV types 16 and 18, results in the rapid degradation of p53 protein through the ubiquitin mediated pathway. This HPV infection mechanism leads to a damaged p53 dependent programmed cell death…