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.
First principles
HPV oncoproteins directly disable the cell's tumour-suppressor brakes
High-risk HPV types, especially 16 and 18, produce the E6 and E7 oncoproteins once infection becomes persistent rather than transient. E6 promotes degradation of p53 and E7 inactivates the retinoblastoma protein, removing the two central checks on uncontrolled cell cycle progression and DNA damage repair. This is the true mechanistic root of cervical carcinogenesis, and it explains why persistence of infection, not simply exposure to the virus, is what matters.
Educational content pending clinical review. Not medical advice.