Cervical Cancer causes are the factors that initiate and promote malignant transformation of the cervical epithelium. The principal and necessary cause is persistent infection with high-risk human papillomavirus, a sexually transmitted DNA virus; types such as 16 and 18 are responsible for most cases. While most HPV…
Cervical Cancer causes are the factors that initiate and promote malignant transformation of the cervical epithelium. The principal and necessary cause is persistent infection with high-risk human papillomavirus, a sexually transmitted DNA virus; types such as 16 and 18 are responsible for most cases. While most HPV infections clear spontaneously, persistence of a high-risk genotype drives carcinogenesis through expression of the viral oncoproteins E6 and E7, which inactivate the p53 and retinoblastoma tumor-suppressor pathways, deregulate the cell cycle, and impair apoptosis and genomic stability. These events promote stepwise progression from normal epithelium through cervical intraepithelial neoplasia to invasive carcinoma, with activation of downstream signaling pathways, including PI3K/AKT/mTOR, contributing to tumor development. Cofactors that increase the likelihood of persistence and progression include early or multiple sexual partners and other sexually transmitted infections, immunosuppression, tobacco use, long-term hormonal influences, high parity, and limited access to screening that would otherwise detect and treat precancerous lesions. Because the underlying cause is a vaccine-preventable infection, primary prevention through HPV vaccination and secondary prevention through HPV-based and cytologic screening are central to reducing incidence. Research examines the role of HPV in virus-induced carcinogenesis, the signaling alterations found in cervical tumors, and the behavioral and access-related cofactors that shape disease risk.
6 peer-reviewed articles, ranked by relevance. Each links to its DOI.