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Human papillomavirus: An unlikely etiologic factor in sinonasal inverted papilloma
Author(s) -
Mohajeri Sepideh,
Lai Chi,
Purgina Bibianna,
Almutairi Dakheelallah,
Baghai Tabassom,
Dimitroulakos Jim,
Kilty Shaun
Publication year - 2018
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1002/lary.27207
Subject(s) - medicine , inverted papilloma , human papillomavirus , immunohistochemistry , papilloma , basal cell , hpv infection , etiology , polymerase chain reaction , biomarker , pathology , human papilloma virus , carcinoma , oncology , cancer research , cancer , cervical cancer , biology , gene , biochemistry
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