Molecular biology of human papillomavirus infection and cervical cancer.

By J. Doorbar. Clinical science, 2006

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Regulating the p53 pathway: in vitro hypotheses, in vivo veritas (2006, background): “The importance of MDM2 and MDM4 antagonists In many tumours that express wild-type p53, the function of p53 can be compromised by viral oncogenes such as the papillomavirus E6 and adenovirus E1B proteins that induce p53 degradatio”
Human papillomavirus molecular biology and disease association (2015, background): “This requires a change in splice site usage rather than the activation of new promoters, leading to an elevation in transcripts that initiate at the late promoter (p670 in HPV 16) and which terminate at the late (rather than the early) polyadenylation site [85], an event that is facilitated by the h”
The biology and life-cycle of human papillomaviruses. (2012, background): “the infection of a basal stem cell (rather than a basal transiently amplifying cell) and that the longevity of the stem cells is a key factor in the formation of a persistent lesion [3,50,91,92].”
Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008, background): “gov/cancertopics/types/head-and-neck/">squamous cell carcinoma of the head and neck in part by inactivating RB through expression of the E7 oncoprotei”