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Cervical cancers are one of the main causes of cancer-related death for women.1 All cervical carcinomas evolve from lesions caused by genital human papillomaviruses (HPVs). Low-risk HPVs (such as types 6 and 11) generate benign lesions or warts whereas high-risk HPV types have the potential to progress into cancer. HPV 16 is the most common oncogenic type responsible for 50% of cervical cancers.
HPV tumourogenesis has long been linked to the ability of high-risk HPV E6 to form a trimeric complex with the tumour suppressor p533 and the ubiquitin ligase E6-associated protein (E6AP),4 which leads to ubiquitin-mediated degradation of p53 and thus loss of control over genetic integrity.