This is the authors' abstract. We don't add key points for this paper.
Human papillomavirus (HPV) is among the most prevalent sexually transmitted pathogens worldwide and an established cause of both benign proliferative lesions and malignant neoplasms. This narrative review examines the role of HPV infection in carcinogenesis at the principal anatomical sites involved and evaluates the contribution of prophylactic vaccination to disease control. A structured search of PubMed/MEDLINE, Scopus, and Web of Science was conducted for English-language publications available up to August 2026, supplemented by current guidance from international health authorities. The evidence confirms a causal role for high-risk genotypes, principally HPV-16 and HPV-18, in oropharyngeal squamous cell carcinoma and in cancers of the cervix, vulva, vagina, penis, and anus, mediated by the E6 and E7 oncoproteins through inactivation of the p53 and retinoblastoma pathways. The strength of this association is markedly site-dependent: it is well established in the oropharynx, cervix, and anus, but remains equivocal in the oral cavity and larynx. In oropharyngeal carcinoma, HPV status is an independent prognostic factor and is incorporated into current staging. Vaccination substantially reduces infection, precancerous lesions, and cervical cancer incidence, with the greatest benefit among individuals immunized before sexual debut. Vaccination and organized screening are complementary rather than alternative strategies, and suboptimal uptake-as observed in Poland-remains the principal barrier to realizing the full preventive potential of available vaccines.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Bukała et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: