Human papillomavirus type 16 in head and neck carcinogenesis

Chen, Renwei; Aaltonen, Leena‐Maija; Vaheri, Antti

doi:10.1002/rmv.471

Cited by 33 publications

(28 citation statements)

References 169 publications

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“…Low-risk viruses, which include HPV 6 and 11, typically cause benign warts and are rarely associated with malignancy [2,3,14]. In contrast, infection with high-risk viruses, including HPV 16, 18, 31 and 45, has been linked to the development of cervical carcinoma as well as other genital malignancies [14,15] and head and neck cancers [16].…”

Section: The Human Papillomavirus Life Cyclementioning

confidence: 98%

Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity

Hebner

Laimins

2005

Reviews in Medical Virology

313

251

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Human papillomaviruses (HPVs) are small double-stranded DNA viruses that infect the cutaneous and mucosal epithelium. Infection by specific HPV types has been linked to the development of cervical carcinoma. HPV infects epithelial cells that undergo terminal differentiation and so encode multiple mechanisms to override the normal regulation of differentiation to produce progeny virions. Two viral proteins, E6 and E7, alter cell cycle control and are the main arbitrators of HPV-induced oncogenesis. Recent data suggest that E6 and E7 also play a major role in the inhibition of the host cell innate immune response to HPV. The E1 and E2 proteins, in combination with various cellular factors, mediate viral replication. In addition, E2 has been implicated in both viral and cellular transcriptional control. Despite decades of research, the function of other viral proteins still remains unclear. While prophylactic vaccines to block genital HPV infection will soon be available, the widespread nature of HPV infection requires greater understanding of both the HPV life cycle as well as the mechanisms underlying HPV-induced carcinogenesis.

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Section: The Human Papillomavirus Life Cyclementioning

confidence: 98%

Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity

Hebner

Laimins

2005

Reviews in Medical Virology

313

251

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“…Recent data have now attributed a viral etiology to a subset of head and neck squamous cell carcinoma (HNSCC), and there is sufficient evidence to support the hypothesis of a role for Human papillomavirus (HPV) in the development of HNSCC [2][3][4]. According to Robert Koch's postulates of germ theory an organism is the cause of disease if certain requirements are fulfilled (Table 1) [5].…”

Section: Introductionmentioning

confidence: 97%

Evidence for a causal association for HPV in head and neck cancers

Sudhoff

Schwarze

Winder

et al. 2011

Eur Arch Otorhinolaryngol

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Current data have now attributed a viral etiology and causality of Human papillomavirus (HPV). Epidemiological analysis of the last decade demonstrates a rapid increase of HPV-associated HNSCC. Genomic detection of HPV DNA in the nuclei of certain oro-pharyngeal cancer cells gives strong evidence of a viral etiology in HNSCC. Non-smokers, non-drinkers, and a sexual debut at a younger age and other sexual risk factors have an increased risk of HPV-positive oropharyngeal cancer. Sexual transmission is considered to play a causal role. In contrast to HPV-negative HNSCC most studies reveal a favorable prognosis for HPV-positive tumors. There is evidence of alterations in the p53 pathway through expression of E6 oncogene with subsequent induction of tumor cell proliferation. Synergies between viral oncogenes and other carcinogens are hypothesized. HPV alone appears to be insufficient as the sole cause of HNSCC; this may explain the long latency period between HPV infection and cancer development. There is now sufficient evidence for a causal role for HPV in HNSCC. As in cervical cancer, HPV requires oncogenes and co-factors for tumor development. Thus, inhibition or loss of such co-factors may lead to tumor regression. The vast amounts of epidemiological, molecular pathological and in vitro experimental data are consistent with the hypothesis that HPV does indeed have a causal role. We await final validation from animal experimentation in which regression of HPV-positive tumors will follow from loss or inhibition of E6 and E7.

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“…Infection with high-risk human papillomavirus (HPV) types, particularly HPV16, has been associated with increased risk for HNSCC, and DNA from this virus has been detected in tumors of HNSCC patients (11)(12)(13)(14)(15)(16). Antibodies to the L1 protein of HPV16 reflect the presence of viral DNA and have also been associated with risk for HNSCC.…”

Section: Introductionmentioning

confidence: 99%

Global DNA Methylation Level in Whole Blood as a Biomarker in Head and Neck Squamous Cell Carcinoma

Hsiung

Marsit²,

Houseman³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

274

257

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Background: Head and neck squamous cell carcinoma (HNSCC) is commonly associated with tobacco and alcohol exposures, although dietary factors, particularly folate, and human papillomavirus, are also risk factors. Epigenetic alterations are increasingly implicated in the initiation and progression of cancer. Genome-wide (global) hypomethylation seems to occur in early neoplasia and is a feature of genomic DNA derived from solid tumor tissues, including HNSCC. This study aimed to determine whether global methylation in DNA derived from whole blood, a proxy tissue, is associated with HNSCC and to assess potential modification of this property by environmental or behavioral risk factors. Methods: Global DNA methylation levels were assessed using a modified version of the combined bisulfite

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Human papillomavirus type 16 in head and neck carcinogenesis

Cited by 33 publications

References 169 publications

Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity

Human papillomaviruses: basic mechanisms of pathogenesis and oncogenicity

Evidence for a causal association for HPV in head and neck cancers

Global DNA Methylation Level in Whole Blood as a Biomarker in Head and Neck Squamous Cell Carcinoma

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