OBJECTIVE: Sinonasal oncocytic papilloma (SOP) is a rare subtype of sinonasal papilloma. There are currently few reports on its clinical features and outcomes after endoscopic surgical resection. This study aims to explore the clinical characteristics of SOP and potential factors predicting tumor recurrence through a single-center retrospective case series analysis.
METHODS: We conducted a retrospective analysis of 69 patients who underwent endoscopic surgery of SOP from June 2012 to April 2019. The data of patients\' demographics, clinical features, follow-up period, and treatment outcomes were collected.
RESULTS: The series includes 43 males and 26 females with an average age of 60.2 years. The tumor commonly involved the nasal cavity (n = 59; 89.4%), followed by maxillary sinus (n = 31; 44.9%), ethmoid sinus (n = 28; 40.6%), frontal sinus (n = 6; 8.7%) and sphenoid sinus (n = 6; 8.7%). The follow-up period ranged from 3 months to 96 months (mean, 34.6 months) and nine patients (13%) developed tumor recurrence during the follow-up period. Univariate analysis found that the recurrence of SOP was significantly related to tumor attachment site, Oikawa tumor stage, and histological dysplasia (p<0.05). Multivariate COX regression analysis found that Oikawa staging system (p = 0.024) and presence of dysplasia (p = 0.04) were significantly related to tumor recurrence.
CONCLUSIONS: SOP had low recurrence rate which was comparable to sinonasal inverted papilloma in the endoscopic era. Our findings also demonstrated that presence of dysplasia is an independent prognostic factor for recurrence free survival.

The aim of this study was to investigate the role of human papillomavirus (HPV) in sinonasal inverted papilloma (SIP) and sinonasal oncocytic papilloma (SOP) from a single institution and whether p16 can serve as a surrogate marker for HPV infection. This study included 49 subjects with SIP and 36 subjects with SOP. Formalin-fixed paraffin-embedded tissues were used to extract genomic DNA, and HPV detection was performed by utilizing a valid nested polymerase chain reaction approach that can detect all known HPV subtypes. Immunohistochemistry was used to evaluate the expression of p16 in all tumor sections. The presence of HPV DNA was found in 6.1% (3/49) of the SIP patients and 11.1% (4/36) of the SOP patients. All identified HPV subtypes in SIP were high-risk HPV, including HPV-16 (two patients) and HPV-58 (one patient). Regarding SOP, there were three patients positive for HPV-16 and one with low-risk HPV (type 6). In total, 11/49 (22.4%) SIP lesions and 10/36 (27.8%) SOP lesions were considered p16 positive, with p16 staining in more than 70% of tumor cells. There was only one SIP and one SOP that were positive for both HPV (high-risk HPV type 16) and p16 staining. HPV does not play an etiologic role in inverted papilloma or oncocytic papilloma of the sinonasal region. p16 immunostaining should not be used as a surrogate marker to evaluate the HPV infection status in these lesions.

OBJECTIVE: Sinonasal inverted papilloma (SIP) and sinonasal oncocytic papilloma (SOP) are uncommon, benign epithelial neoplasms located in the sinonasal region, that have the potential for malignant transformation. A recent study reported that EGFR and KRAS mutations occurred in the majority of Western patients with SIP and SOP, respectively. The aims of this study were to investigate the prevalence of KRAS and EGFR mutations in Chinese SIP and SOP patients, and to study the association between molecular alterations and their clinical features.
RESULTS: We retrospectively collected 80 sinonasal papilloma specimens, including 44 cases with SIP, 33 cases with SOP, and three cases with mixed sinonasal papilloma, which harboured elements of both inverted and oncocytic types. Formalin-fixed paraffin-embedded tissues were used to extract genomic DNA, and EGFR and KRAS mutations were evaluated with direct Sanger sequencing. Thirty-five (78%) SIP patients harboured EGFR mutations, and all mutations were exon 20 insertions, whereas no KRAS mutations were detected. In contrast, KRAS mutations were detected in 82% of SOP patients, but no EGFR mutations were detected. Among the three mixed-type cases, two harboured both EGFR exon 20 insertions and KRAS mutations. Another case harboured a KRAS mutation, but no EGFR mutation was detected.
CONCLUSIONS: SIP and SOP are two clinical entities with different genetic mutational patterns of EGFR and KRAS. Mixed types with elements of both SIP and SOP may harbour both EGFR and KRAS mutations.