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Presence of HPV-16 may increase HNSCC risk
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The detection of HPV-16 in the oral cavity appeared associated with a significantly increased risk for oropharyngeal squamous cell carcinoma, according to the results of a nested case-control study.
The researchers further observed associations with other oral HPVs — including gamma11-HPV and gamma12-HPV species and beta1-HPV-5 type — and the risk for head and neck squamous cell carcinoma (HNSCC).
Little research has examined the relationship between oral HPV and HNSCC risk, according to study background. Further, the associations between other oral HPV types — including the alpha-, betta- and gamma-HPV types — and HNSCC is unknown.
Thus, Ilir Agalliu, MD, ScD, assistant professor of urology, epidemiology and population health at Albert Einstein College of Medicine, and colleagues sought to examine the associations between HPV detection in the oral cavity and incident HNSCC.
Agalliu and colleagues accessed data from two prospective cohort studies — the American Cancer Society Cancer Prevention Study II Nutrition Cohort and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial — for a total population of 96,650 participants.
All participants included had available mouthwash samples and were cancer free at baseline.
The identification of incident HNSCC — including cancers of the oropharynx, oral cavity and larynx — served as the primary endpoint.
The researchers identified 132 incident cases of HNSCC (men, n = 103; median age at baseline, 66.5 years) in both cohorts during a median follow-up of 3.9 years. They then selected three age-, sex-, race/ethnicity- and time-matched controls per case (n = 396) through incidence density sampling.
The detection of oral HPV-16 appeared associated with incident HSNCC (OR = 7.1; 95% CI, 2.2-22.6), with a positive association for oropharyngeal squamous cell carcinoma (OR = 22.4; 95% CI, 1.8-276.7).
However, this association did not persist for oral cavity squamous cell carcinoma (OR = 4.5; 95% CI, 0.6-34.7) or for laryngeal squamous cell carcinoma (OR = 0.11; 95% CI, 0.01-834.8).
Further, the detection of other HPV types — including beta1-HPV-5, beta2-HPV-38, gamma11-HPV and gamma12-HPV — showed positive associations with incident HNSCC (P < .01 for all).
Beta1-HPV-5 appeared to increase risk for oropharyngeal squamous cell carcinoma (OR = 7.42; 95% CI, 0.98-56.82), oral cavity squamous cell carcinoma (OR = 5.34; 95% CI, 1.51-18.8) and laryngeal squamous cell carcinoma (OR = 2.71; 95% CI, 1-7.43)
Gamma11-HPV appeared associated with oral cavity squamous cell carcinoma (OR = 7.47; 95% CI, 1.21-46.17) and laryngeal squamous cell carcinoma (OR = 7.49; 95% CI, 1.1-51.04), as did gamma12-HPV (OR for oral cavity = 6.71; 95% CI, 1.47-30.75; OR for laryngeal = 5.31; 95% CI, 1.13-24.95)
Study limitations included the small sample size and the lack of sequential mouthwash samples.
“This study is the first to our knowledge to demonstrate that alpha-HPV-16 detection precedes the incidence of oropharyngeal cancers,” Agalliu and colleagues wrote. “The use of easily collected oral mouthwash samples can provide a prospective marker for HNSCC risk and for oropharyngeal squamous cell carcinoma.”
Maura L. Gillison
More research is needed to fully determine the association between HPV-16 detection and HNSCC, Dana E. Rollison, PhD, vice president and chief health information officer at Moffitt Cancer Center, and Maura L. Gillison, MD, PhD, professor of internal medicine and Jed Coughlin chair of cancer research at The Ohio State University, wrote in an accompanying editorial.
“Additional studies will be necessary to investigate the complex interrelationships (confounding, mediation, effect modification) among tobacco and alcohol use, beta- and gamma-HPV infections, immune response factors, and HNSCC,” Rollison and Gillison wrote. “If oral beta- and gamma-HPV infection is indeed a risk factor for HNSCC, then the high prevalence of these infections, coupled with the rising incidence of HNSCC, would translate into a large attributable faction of disease. ... If smoking is a necessary co-carcinogen for beta- and gamma-HPV infection, then the critical public health message remains unchanged: refrain from tobacco smoking.” – by Cameron Kelsall
Disclosure: The researchers, Rollison and Gillison report no relevant financial disclosures.
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