Carcinogenic human papillomavirus infection
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 — virtu...
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Published in | Nature reviews. Disease primers Vol. 2; no. 1; p. 16086 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.12.2016
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 2056-676X 2056-676X |
DOI | 10.1038/nrdp.2016.86 |
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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.
Virtually all cervical cancers, a large fraction of other anogenital cancers and an increasing proportion of oropharyngeal cancers are caused by human papillomavirus (HPV) infection. Here, the authors describe HPV-driven carcinogenesis and discuss how developments in vaccines and screening tests could dramatically alter the landscape of HPV-related cancers worldwide. |
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AbstractList | 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. 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.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. 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.Virtually all cervical cancers, a large fraction of other anogenital cancers and an increasing proportion of oropharyngeal cancers are caused by human papillomavirus (HPV) infection. Here, the authors describe HPV-driven carcinogenesis and discuss how developments in vaccines and screening tests could dramatically alter the landscape of HPV-related cancers worldwide. 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. Virtually all cervical cancers, a large fraction of other anogenital cancers and an increasing proportion of oropharyngeal cancers are caused by human papillomavirus (HPV) infection. Here, the authors describe HPV-driven carcinogenesis and discuss how developments in vaccines and screening tests could dramatically alter the landscape of HPV-related cancers worldwide. |
ArticleNumber | 16086 |
Author | Franceschi, Silvia Wentzensen, Nicolas de Sanjosé, Silvia Monk, Bradley J. Schiffman, Mark Fakhry, Carole Doorbar, John Stanley, Margaret A. |
Author_xml | – sequence: 1 givenname: Mark surname: Schiffman fullname: Schiffman, Mark email: schiffmm@mail.nih.gov organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute – sequence: 2 givenname: John surname: Doorbar fullname: Doorbar, John organization: Department of Pathology, University of Cambridge – sequence: 3 givenname: Nicolas surname: Wentzensen fullname: Wentzensen, Nicolas organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute – sequence: 4 givenname: Silvia surname: de Sanjosé fullname: de Sanjosé, Silvia organization: Catalan Institute of Oncology, IDIBELL, Cancer Epidemiology Research Programme and CIBER Epidemiologia Y Salud Publica – sequence: 5 givenname: Carole surname: Fakhry fullname: Fakhry, Carole organization: Department of Otolaryngology, Johns Hopkins Medicine – sequence: 6 givenname: Bradley J. surname: Monk fullname: Monk, Bradley J. organization: Division of Gynecologic Oncology, US Oncology Network, University of Arizona-Phoenix – sequence: 7 givenname: Margaret A. surname: Stanley fullname: Stanley, Margaret A. organization: Department of Pathology, University of Cambridge – sequence: 8 givenname: Silvia surname: Franceschi fullname: Franceschi, Silvia organization: International Agency for Research on Cancer, Infections and Cancer Epidemiology Group |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27905473$$D View this record in MEDLINE/PubMed |
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Title | Carcinogenic human papillomavirus infection |
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