Objectives/hypothesis: Tenuous evidence has supported the hypothesis that sinonasal inverted papilloma (SNIP) arise from human papillomavirus (HPV) infection. To clarify the role of HPV in SNIP, all known HPV sub-types were evaluated by employing a robust polymerase chain reaction-based method in a wide variety of SNIPs from a single institution.
Study design: Retrospective surgical specimen tumor sample analysis.
Methods: HPV positivity among SNIP samples and those with squamous cell carcinoma (SCC) were compared. Immunohistochemistry was used to quantify p16 (over)expression among tumors as a surrogate marker for HPV.
Results: HPV was detected in 10/76 (13%) SNIP specimens. Identified HPV subtypes included nononcogenic 6 and 11 (6/76, 8%) and oncogenic 16, 18, 45, 56 (4/76, 5%). There was no HPV positivity among SCC samples. Only 4/10 (40%) HPV + samples had > 75% p16 cell staining.
Conclusion: HPV is not supported as an etiological driver of SNIP development or progression to SCC. The p16 biomarker is not a sensitive indicator of HPV positivity in SNIP.
Level of evidence: NA Laryngoscope, 2443-2447, 2018.
Keywords: Inverted papilloma; human papillomavirus; p16; polymerase chain reaction; squamous cell carcinoma.
© 2018 The American Laryngological, Rhinological and Otological Society, Inc.