Head and neck squamous cell cancer and the human papillomavirus: Summary of a National Cancer Institute State of the Science Meeting, November 9–10, 2008, Washington, D.C.

Adelstein, David J.; Ridge, John A.; Gillison, Maura L.; Chaturvedi, Anil K.; D’Souza, Gypsyamber; Gravitt, Patti E.; Westra, William H.; Psyrri, Amanda; Kast, W. Martin; Koutsky, Laura A.; Giuliano, Anna R.; Krosnick, Steven; Trotti, Andy; Schuller, David E.; Forastiere, Arlene A.; Ullmann, Claudio Dansky

doi:10.1002/hed.21269

Cited by 254 publications

(282 citation statements)

References 52 publications

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“…Inactivation of Rb, in particular, leads to marked overexpression of the tumor suppressor protein p16, for which transcription is normally repressed by Rb. This marked overexpression, which is very uncommon in non-HPV-related SCC, makes p16 a good surrogate marker of HPV, but more importantly, a good marker of transcriptionally-active HPV [18], because while HPV DNA can be found in a relatively high numbers of head and neck SCC of all anatomic subsites, the ones with better clinical outcomes have only been those where HPV is present in the tumor and in transcriptionally active form [12]. It is generally accepted that if one finds evidence of high risk HPV in a tumor that coexistent overexpression of p16 and/ or significant expression of HPV E6 and E7 transcripts, this indicates biologically and clinically significant role of HPV in the tumor.…”

Section: Discussionmentioning

confidence: 99%

“…These tumors may present as different variants distinct from the typical keratinizingtype SCC, including nonkeratinizing [5,6], basaloid [7,8], and papillary SCC [9] and also undifferentiated carcinoma [10]. It has also been documented in several studies that HPV-related carcinomas of the upper aerodigestive tract have more favorable prognosis than HPV negative ones [11][12][13]. Most previous studies investigated HPV in tumors using DNA-based polymerase chain reaction (PCR) [14] while in more recent years DNA-based in situ hybridization (ISH) has been used [5,13,15].…”

Section: Introductionmentioning

confidence: 99%

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Adenosquamous Carcinoma of the Head and Neck: Relationship to Human Papillomavirus and Review of the Literature

Masand

El‐Mofty

et al. 2011

Head and Neck Pathol

129

106

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Adenosquamous carcinoma (ADSC) of the head and neck is an aggressive variant of squamous cell carcinoma (SCC). Certain variants of head and neck SCC are human papillomavirus (HPV)-related and have better prognosis. The relationship of HPV to head and neck ADSC has not been investigated. We searched our files for the term ''adenosquamous'' and head and neck subsites and found cases from 1998 to 2009. The requisite histologic criteria were the presence of SCC combined with distinct gland formation and/or intracellular mucin. DNA in situ hybridization for high-risk HPV, RNA in situ hybridization for high risk HPV E6 and E7 transcripts, and immunohistochemistry for p16 and p53 were performed. The existing literature on ADSC was also reviewed. Of the 18 cases, eight were from the larynx and hypopharynx, four from the oral cavity, three from the oropharynx, and three from the nasal cavity. Three cases (16%) showed both high risk HPV E6 and E7 and p16 expression, one from the nasal cavity and two from the oropharynx. Both oropharyngeal carcinoma patients were alive and disease free at 34 and 103 months, respectively. ADSCs of the head and neck are a heterogeneous group of tumors. A small minority of cases harbor HPV and most of these, particularly those occurring at sites with known high prevalence of HPV, show active viral transcription with detectable E6 and E7 and overexpression of p16. The HPV-related oropharyngeal cases, though rare, appear to do very well clinically, while the remaining cohort of ADSC patients do quite poorly. Head and neck ADSC appears to be a mixed variant that can be further classified according to its HPV status.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Adenosquamous Carcinoma of the Head and Neck: Relationship to Human Papillomavirus and Review of the Literature

Masand

El‐Mofty

et al. 2011

Head and Neck Pathol

129

106

View full text Add to dashboard Cite

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“…The overall incidence of HNC has changed little over the last 20 years, with an estimated age standardised rate of 11 per 100,000 in Europe in 2012 [2]. However, the emergence of human papilloma virus (HPV)-related HNC means that the traditional pattern of higher incidence in older people, often associated with tobacco and alcohol use, is changing [3,4]. Since HPV-related HNC occurs primarily among younger individuals, and the incidence of these tumours is rising [4], an increasing number of HNC will be diagnosed in people of working age.…”

Section: Long Term Workforce Participation Patterns Following Head Anmentioning

confidence: 99%

Long-term workforce participation patterns following head and neck cancer

et al. 2014

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“…Human papillomavirus (HPV) is now well established as an important cause of head and neck cancer [1][2][3], but its distribution is highly restricted by anatomic site and tumor type. It is detected in 50-80 % of oropharyngeal cancers where it tracks with the non-keratinizing squamous cell phenotype, but it is not frequently detected in head and neck squamous cell carcinomas arising outside of the oropharynx [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Mucoepidermoid Carcinoma Does Not Harbor Transcriptionally Active High Risk Human Papillomavirus Even in the Absence of the MAML2 Translocation

Bishop

Yonescu

Batista

et al. 2014

Head and Neck Pathol

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High risk human papillomavirus (HPV) is firmly established as an important cause of oropharyngeal carcinoma. Recent studies have also implicated HPV as a cause of mucoepidermoid carcinoma (MEC)-a tumor of salivary gland origin that frequently harbors MAML2 translocations. The purpose of this study was to determine the prevalence of transcriptionally active HPV in a large group of MECs and to determine whether HPV infection and the MAML2 translocation are mutually exclusive events. Break-apart fluorescence in situ hybridization for MAML2 was performed on a tissue microarray containing 92 MECs. HPV testing was performed using RNA in situ hybridization targeting high risk HPV mRNA E6/E7 transcripts. Of the 71 MECs that could be evaluated by FISH, 57 (80 %) harbored the MAML2 rearrangement. HPV was not detected in any of the 57 MECs that contained a MAML2 rearrangement, in any of the 14 MECs that did not contain the rearrangement, or in any of the 21 MECs where MAML2 status was unknown. High risk HPV does not appear to play any significant role in the development of MEC. It neither complements nor replaces MAML2 translocation in the tumorigenesis of MEC.

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Head and neck squamous cell cancer and the human papillomavirus: Summary of a National Cancer Institute State of the Science Meeting, November 9–10, 2008, Washington, D.C.

Cited by 254 publications

References 52 publications

Adenosquamous Carcinoma of the Head and Neck: Relationship to Human Papillomavirus and Review of the Literature

Adenosquamous Carcinoma of the Head and Neck: Relationship to Human Papillomavirus and Review of the Literature

Long-term workforce participation patterns following head and neck cancer

Mucoepidermoid Carcinoma Does Not Harbor Transcriptionally Active High Risk Human Papillomavirus Even in the Absence of the MAML2 Translocation

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