Overview
Why Cervical Cancer Develops
Most cervical cancers begin after persistent infection with high risk human papillomavirus (HPV), particularly HPV 16 and HPV 18.
Most cervical cancers begin after persistent infection with high-risk human papillomavirus (HPV), particularly HPV-16 and HPV-18. HPV is common and often clears without treatment. Cancer risk rises when a high-risk type remains in cervical cells long enough to disrupt normal control of cell growth. The transformation zone, where squamous and columnar cells meet on the cervix, is especially vulnerable to these changes. Abnormal cells may progress through cervical intraepithelial neoplasia (CIN), a precancerous stage. CIN is not invasive cancer: the abnormal cells have not crossed into deeper cervical tissue. Detecting and treating significant precancerous changes can prevent invasive disease. Invasive cervical cancer develops when malignant cells penetrate beyond the surface epithelium and invade cervical stroma. This slow progression explains why screening works so well. A screening test can identify cellular abnormalities or high-risk HPV before a patient develops symptoms. Smoking and immunosuppression can make persistent HPV infection and cervical dysplasia more likely. HPV infection does not imply recent sexual exposure or infidelity; the virus can remain silent for years before it is detected.