Human papillomavirus and cervical carcinogenesis.
Epidemiological studies show that infection with a subset of genital human papillomavirus (HPV) infections is the major risk factor for the subsequent development of cervical cancer. Experimental studies show that that the E6 and E7 genes of these high risk HPVs are oncogenes that deregulate key cell cycle controls. In the normal infectious cycle high level expression of these genes is confined to non-dividing differentiated cells: HPV oncogenesis requires deregulation of viral and cellular genes permitting inappropriate expression of E6 and E7. These are rare events but viral persistence and chronic exposure to steroid hormones increase the probability of this deregulation.
Stanley
M A
MA
Department of Pathology, Tennis Court Road, Cambridge, CB2 1QP, UK.
D002453:Cell Cycle / Q000235:genetics; D005260:Female; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000235:genetics; D027383:Papillomaviridae / Q000235:genetics; D050725:Papillomavirus E7 Proteins; D030361:Papillomavirus Infections / Q000150:complications* / Q000453:epidemiology; D012097:Repressor Proteins; D012307:Risk Factors; D014412:Tumor Virus Infections / Q000150:complications* / Q000453:epidemiology; D002583:Uterine Cervical Neoplasms / Q000453:epidemiology / Q000821:virology*
C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D012097:Repressor Proteins; C059731:oncogene protein E7, Human papillomavirus type 16