Head And Neck Cancer Linked To HPV-16 Infection

Head and neck squamous cell carcinoma aetiology is associated with infection with different species of the human papillomavirus including HPV-16

medwireNews: Oral human papillomavirus (HPV)-16 may play a role in the development of head and neck squamous cell carcinoma (HNSCC), say researchers who found that patients were seven times more likely to carry the virus than those without the malignancy.

Oral HPV-16 infection was associated with a significantly increased incidence of HNSCC (odds ratio [OR]=7.1), after adjusting for alcohol and smoking habits, which the study authors say in JAMA Oncology is in line with findings from earlier smaller studies.

And there was a particularly strong association noted between HPV-16 infection and oropharyngeal SCC (OR=22.4), although the viral strain did not significantly predict the risk of oral cavity or laryngeal SCC.

The team also found that several β and γ HPV strains previously associated with skin cancer significantly predict the risk of HNSCC.

For example, individuals who carried β1-HPV-5 were significantly more likely to develop oropharyngeal, oral cavity and laryngeal SCC than those without infection, with ORs of 7.42, 5.34 and 2.71, respectively.

And those carrying γ11-HPV or γ12-HPV were significantly more likely to have oral cavity SCC (OR=7.47 and 6.71, respectively) and laryngeal SCC (OR=7.49 and 5.31, respectively) than noncarriers.

The nested case–control analysis collated data and mouthwash samples from 96,650 individuals who were free from cancer at baseline and followed up within one of two prospective cohort studies, explain Ilir Agalliu, from Albert Einstein College of Medicine in Bronx, New York, USA, and co-investigators.

In all, 132 individuals were diagnosed with HNSCC over an average of 3.9 years of follow-up and each patient was matched by age, gender and race or ethnicity to three controls.

“This study demonstrates that HPV-16 detection precedes the incidence of oropharyngeal SCC”, the authors emphasize, noting that the easily collected oral mouthwash samples offer a prospective marker for HNSCC and oropharyngeal SCC risk.

“Associations of other HPVs, including γ11- and γ12-HPV species and β1-HPV-5 type suggest a broader role for HPVs in HNSCC etiology.”

Dana Rollison, from Moffitt Cancer Center in Tampa, Florida, USA, and Maura Gillison, from The Ohio State University in Columbus, USA, say the data reported for HPV and HNSCC are “compelling” but believe that “caution is warranted in inferring a causal relationship”.

Writing in an accompanying comment, they say further research is required to unpick the complex relationships between tobacco and alcohol use, HPV infection, immune response factors and HNSCC.

“We note the relationships among β-HPV, UV exposure, and [cutaneous]SCC risk likely provide a relevant framework: local immune suppressive effects of tobacco smoking may promote β-HPV replication that in turn may modify repair of tobacco- induced DNA damage”, they suggest.

“If smoking is a necessary cocarcinogen for β- and γ-HPV infection, then the critical public health message remains unchanged: refrain from tobacco smoking.”


Agalliu I, Gapstur S, Chen Z, et al. Associations of oral α-, β-, and γ-human papillomavirus types with risk of incident head and neck cancer. JAMA Oncol 2016; Advance online publication 21 January.doi:10.1001/jamaoncol.2015.5504

Rollison DE, Gillson ML. The alpha, beta, gammas of oral human papillomavirus infection and head and neck cancer risk.JAMA Oncol 2016; Advance online publication 21 January.doi:10.1001/jamaoncol.2015.5686

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