Incidence of human papillomavirus in oropharyngeal squamous cell carcinomas: now and 50 years ago

Chênevert, Jacinthe; Chiosea, Simion I.

doi:10.1016/j.humpath.2011.03.009

Cited by 34 publications

(33 citation statements)

References 30 publications

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“…The higher incidence of PI3K pathway activation in oropharyngeal SCC was previously reported [5]. Oropharyngeal SCC are increasingly associated with human papillomavirus (HPV) infection [6,7] and the higher prevalence of PI3K pathway abnormalities in these tumors was eventually linked to HPV [8,9]. …”

Section: Introductionmentioning

confidence: 94%

PIK3CA, HRAS and PTEN in human papillomavirus positive oropharyngeal squamous cell carcinoma

et al. 2013

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BackgroundRecent genomic evidence suggests frequent phosphatidylinositide 3-kinase (PI3K) pathway activation in human papillomavirus (HPV) positive oropharyngeal squamous cell carcinoma. Mutations/amplification of the gene encoding p110α catalytic subunit of phosphoinositide 3-kinase (PIK3CA), loss of phosphatase and tensin homolog (PTEN) and HRAS mutations are known to activate PI3K pathway.Methods and resultsPIK3CA mutations were identified by Sanger sequencing in 23 of 75 (31%) HPV-positive oropharyngeal carcinomas, including exon 9 (p.E545K [n = 10] and p.E542K [n = 5]) or exon 20 (p.H1047Y, n = 2) mutations. Five rare and one novel (p.R537Q) PIK3CA mutations were identified. HRAS mutation (p.Q61L) was detected in 1 of 62 tested cases. PIK3CA amplification by fluorescence in situ hybridization (FISH) was identified in 4 cases (4/21, 20%), while PTEN loss was seen in 7 (7/21, 33%) cases (chromosome 10 monosomy [n = 4], homozygous deletion [n = 3]).ConclusionsOverall, genetic alterations that likely lead to PI3K pathway activation were identified in 34 of 75 cases (45%) and did not correlate with disease specific survival. These findings offer a molecular rationale for therapeutic targeting of PI3K pathway in patients with HPV-positive oropharyngeal carcinoma.

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Section: Introductionmentioning

confidence: 94%

PIK3CA, HRAS and PTEN in human papillomavirus positive oropharyngeal squamous cell carcinoma

et al. 2013

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“…Human papilloma virus (HPV) infection has become an increasingly common cause of oropharyngeal squamous cell carcinoma (OPSCC) [1, 2]. HPV-mediated OPSCC is fairly responsive to chemoradiotherapy and has a better prognosis than HPV-unrelated OPSCC [3].…”

Section: Introductionmentioning

confidence: 99%

Staging and prognosis of oropharyngeal carcinoma according to the 8th Edition of the American Joint Committee on Cancer Staging Manual in human papillomavirus infection

Yamashita

Ikegami

Hirakawa

et al. 2018

Eur Arch Otorhinolaryngol

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PurposeThe aim of this study was to evaluate the 8th edition of the American Joint Committee on Cancer Staging Manual: Head and Neck Section on oropharyngeal squamous cell cancer (OPSCC) and to clarify the relationship between p16 overexpression and the presence of human papillomavirus (HPV) DNA using fresh frozen samples.MethodsSamples from 100 OPSCC patients were analyzed using polymerase chain reaction (PCR) and p16 immunohistochemistry.ResultsFive-year overall survival (OS) was 73.0%, 93.9%, and 62.2% in all, p16-positive (n = 34), and p16-negative (n = 66) cases, respectively. OS tended to be better aligned with stage in the 8th edition than in the 7th edition. The 5-year OS was 96.0% in never or light smokers (< 40 pack-years), and 87.5% in heavy smokers (≥ 40 pack-years) in the p16-positive group, respectively (p = 0.027). HPV infection was found in 100% of p16-positive and 21.2% of p16-negative cases. The p16-positive cases had higher viral load and integrated physical status than the p16-negative cases. Although 1 case with p16 overexpression showed no PCR amplification using consensus primers, PCR amplification was detected using HPV 16 E6-specific primers.ConclusionsThe 8th edition predicts OPSCC prognosis more accurately than the 7th edition and p16-overexpression is an excellent surrogate marker for detecting HPV infection. Although high-risk-type HPV infection was observed in p16-negative cases, it showed no significant effect in survival outcome.

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“…This epidemiologic change has been attributed to high-risk human papillomavirus (HPV) and particularly to type 16, which is now recognized as a causative agent in a growing subset of oropharyngeal squamous cell carcinomas (OPSCCs) [5]. Indeed, numerous studies have demonstrated a two to three fold increase in the prevalence of HPV-driven OPSCC over the last three decades, especially in North America and Northern Europe [6][7][8]. The underlying reasons are still poorly understood and several hypotheses have been proposed: changes in sexual behavior [9], decreased rates of tonsillectomy performed in the pediatric population since the 70s [10] and progress in the diagnostic work up and HPV testing assays [11].…”

Section: Introductionmentioning

confidence: 99%

Do high-risk human papillomaviruses cause oral cavity squamous cell carcinoma?

et al. 2015

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Incidence of human papillomavirus in oropharyngeal squamous cell carcinomas: now and 50 years ago

Cited by 34 publications

References 30 publications

PIK3CA, HRAS and PTEN in human papillomavirus positive oropharyngeal squamous cell carcinoma

PIK3CA, HRAS and PTEN in human papillomavirus positive oropharyngeal squamous cell carcinoma

Staging and prognosis of oropharyngeal carcinoma according to the 8th Edition of the American Joint Committee on Cancer Staging Manual in human papillomavirus infection

Do high-risk human papillomaviruses cause oral cavity squamous cell carcinoma?

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