title: Carcinogenic human papillomavirus infection.
abstract: Infections with human papillomavirus (HPV) are common and transmitted by direct contact. Although the great majority of infections resolve within 2 years, 13 phylogenetically related, sexually transmitted HPV genotypes, notably HPV16, cause - if not controlled immunologically or by screening - virtually all cervical cancers worldwide, a large fraction of other anogenital cancers and an increasing proportion of oropharyngeal cancers. The carcinogenicity of these HPV types results primarily from the activity of the oncoproteins E6 and E7, which impair growth regulatory pathways. Persistent high-risk HPVs can transition from a productive (virion-producing) to an abortive or transforming infection, after which cancer can result after typically slow accumulation of host genetic mutations. However, which precancerous lesions progress and which do not is unclear; the majority of screening-detected precancers are treated, leading to overtreatment. The discovery of HPV as a carcinogen led to the development of effective preventive vaccines and sensitive HPV DNA and RNA tests. Together, vaccination programmes (the ultimate long-term preventive strategy) and screening using HPV tests could dramatically alter the landscape of HPV-related cancers. HPV testing will probably replace cytology-based cervical screening owing to greater reassurance when the test is negative. However, the effective implementation of HPV vaccination and screening globally remains a challenge.
authors.affiliation: National Cancer Institute, Division of Cancer Epidemiology and Genetics, Room 6E544, 9609 Medical Center Drive, Rockville, Maryland 20850, USA.
authors.forename: Mark
authors.initials: M
authors.lastname: Schiffman
authors.affiliation: Department of Pathology, University of Cambridge, Cambridge, UK.
authors.forename: John
authors.initials: J
authors.lastname: Doorbar
authors.affiliation: National Cancer Institute, Division of Cancer Epidemiology and Genetics, Room 6E544, 9609 Medical Center Drive, Rockville, Maryland 20850, USA.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Wentzensen
authors.affiliation: Catalan Institute of Oncology, IDIBELL, Cancer Epidemiology Research Programme and CIBER Epidemiologia Y Salud Publica, Barcelona, Spain.
authors.forename: Silvia
authors.initials: S
authors.lastname: de Sanjosé
authors.affiliation: Department of Otolaryngology, Johns Hopkins Medicine, Baltimore, Maryland, USA.
authors.forename: Carole
authors.initials: C
authors.lastname: Fakhry
authors.affiliation: Division of Gynecologic Oncology, US Oncology Network, University of Arizona-Phoenix, Phoenix, Arizona, USA.
authors.forename: Bradley J
authors.initials: BJ
authors.lastname: Monk
authors.affiliation: Department of Pathology, University of Cambridge, Cambridge, UK.
authors.forename: Margaret A
authors.initials: MA
authors.lastname: Stanley
authors.affiliation: International Agency for Research on Cancer, Infections and Cancer Epidemiology Group, Lyon, France.
authors.forename: Silvia
authors.initials: S
authors.lastname: Franceschi
mesh_terms: D002273:Carcinogens; D055088:Early Detection of Cancer / Q000379:methods; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D008403:Mass Screening / Q000379:methods / Q000592:standards; D027383:Papillomaviridae / Q000276:immunology / Q000472:pathogenicity; D030361:Papillomavirus Infections / Q000150:complications* / Q000453:epidemiology / Q000503:physiopathology*; D053918:Papillomavirus Vaccines / Q000276:immunology / Q000627:therapeutic use; D002583:Uterine Cervical Neoplasms / Q000209:etiology / Q000517:prevention & control
chemical_list: D002273:Carcinogens; D053918:Papillomavirus Vaccines