Human papillomavirus: An unlikely etiologic factor in sinonasal inverted papilloma

被引:27
作者
Mohajeri, Sepideh [1 ]
Lai, Chi [2 ]
Purgina, Bibianna [2 ]
Almutairi, Dakheelallah [3 ]
Baghai, Tabassom [4 ,5 ]
Dimitroulakos, Jim [4 ,5 ]
Kilty, Shaun [5 ,6 ]
机构
[1] Univ Ottawa, Fac Med, Ottawa, ON, Canada
[2] Univ Ottawa, Dept Pathol, Ottawa, ON, Canada
[3] King Saud bin Abdulaziz Univ Hlth Sci, Riyadh, Saudi Arabia
[4] Univ Ottawa, Dept Biochem Microbiol & Immunol, Ottawa, ON, Canada
[5] Ottawa Hosp Res Inst, Ottawa, ON, Canada
[6] Univ Ottawa, Dept Otolaryngol Head & Neck Surg, Ottawa, ON, Canada
关键词
Inverted papilloma; human papillomavirus; p16; squamous cell carcinoma; polymerase chain reaction; IN-SITU HYBRIDIZATION; HPV DNA; PREVALENCE; MANAGEMENT; RECURRENCE; TUMORS; RISK;
D O I
10.1002/lary.27207
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objectives/Hypothesis Study Design 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. Retrospective surgical specimen tumor sample analysis. Methods Results 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. 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 Level of Evidence 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. NA Laryngoscope, 2443-2447, 2018
引用
收藏
页码:2443 / 2447
页数:5
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