Women's HealthPending review

Cervical cancer

Persistent infection with high-risk HPV integrates viral oncoproteins into cervical transformation-zone cells, disabling the cell's own tumour-suppressor brakes and driving progression through preinvasive change to invasive cancer over many years: a window that screening is designed to exploit.

In a nutshell

Persistent high-risk HPV infection produces E6 and E7 oncoproteins that degrade p53 and inactivate Rb in the metaplastically active transformation zone, removing the cell's normal brakes on proliferation. Progression through CIN to invasive cancer takes years, which is exactly the window the screening programme (primary HPV testing) is designed to interrupt.

Classic presentation

Postcoital or intermenstrual bleeding with an abnormal-appearing cervix; CIN itself is asymptomatic and found only through screening.

Key points

HPV 16 and 18 cause the majority of cervical cancers via E6 (degrades p53) and E7 (inactivates Rb) oncoproteins.

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Educational content pending clinical review. Not medical advice.