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ICAR SINONASAL TUMORS

active and transcriptionally inactive HPV infections. As such, Svajdler et al. performed a meta-analysis specif ically assessing the presence of transcriptionally active HPV within SNSCC. 1061 They identified transcriptionally active HPV in 23.5% of SNSCC cases (95% CI: 10.7%– 41.2%) and transcriptionally active high-risk HPV in 32% of patients specifically with keratinizing SNSCC. 1061 Lewis et al. reported rates of transcriptionally active high-risk HPV based on histologic subtype of SNSCC and identified HPV positivity in 75% of papillary SCC, 41.7% of basa loid SCC, 39.7% of nonkeratinizing SCC, and only 3.4% of keratinizing SCC. 664 The significance of the discrepancy between rates of HPV within keratinizing SNSCC between these two studies is not well understood. Nonetheless, HPV infection appears to play an etiologic role in approximately 25% of SNSCC. It is proposed that HPV-associated SNSCC confers an improved prognosis. 1062,1063 Similarly, EBV has been detected in SNSCC. However, EBV has also been reported in a similar proportion of nasal polyps, and thus the role of EBV in SNSCC tumorigenesis is unclear. 1064,1065 Finally, CRS, allergic rhinitis, and nasal polyposis have been suggested as possible risk factors in the development of SNSCC. 1052,1066 Chronic inflammatory states have been implicated as risk factors for tumorigenesis elsewhere in the body. However, the data for SNSCC are more limited, and a direct causative link between nonirritant chronic sinonasal inflammation and the development of SNSCC has not been established. 1067 2 Pathologic features Patients with SNSCC most often present with typical, albeit nonspecific, features. These include nasal obstruction, rhi norrhea, epistaxis, and facial pain. 1067 These symptoms are often, but not always, unilateral. The symptoms can be misinterpreted as more common benign processes, which may delay time from initial presentation to diagnosis. In the head and neck, SCC generally arises from precur sor squamous intraepithelial neoplasia. However, in the respiratory mucosa-lined sinonasal tract, squamous meta plasia must develop prior to neoplasia. Interestingly, in de novo SNSCC, dysplastic squamous epithelium/carcinoma in situ is uncommonly found in neighboring mucosa. 1068 a Histology Like at other anatomic subsites of the head and neck, the WHO classification designates a number of specific histologic subtypes of SNSCC. Most are either classified as keratinizing (conventional) or nonkeratinizing. It is estimated that 49.5% of SNSCC is keratinizing, 33.3% is nonkeratinizing, and the remaining 17% represent other subtypes. 1067 This is a distinction of potential clinical rele

vance due to a potential discrepancy of prognosis between varying subtypes. Keratinizing SCC is characterized by stellate, irregu lar nests of tumor cells in a desmoplastic stroma. These tumor cells have abundant eosinophilic cytoplasm filled with keratin filaments, prominent intercellular bridges, and keratin production. For keratinizing SNSCC, the his tologic features are very characteristic and there is no significant differential diagnosis. Keratinizing SNSCC is further classified by grade (well, moderate, or poorly differ entiated). Nonkeratinizing SCC was historically referred to as Schneiderian carcinoma, transitional cell carcinoma, or cylindrical cell carcinoma. Today, these terms are considered obsolete. The preferred terminology is nonker atinizing SCC. Nonkeratinizing SNSCC is characterized by a ‘blue cell tumor appearance’ with high nuclear to cytoplasmic ratios arranged in large, rounded nests or ribbons with little desmoplastic stroma. The nests are typi cally well demarcated with smooth borders and commonly have central necrosis. Interestingly, these tumors often have a noninvasive appearance and can actually consist of completely exophytic projections. However, in the case of nonkeratinizing SNSCC, there are no clear data to suggest these tumors are clinically or prognostically different from more obviously invasive tumors. There is no role for tumor grading classification for nonkeratinizing SCC. Importantly, other major SCC subtypes have been described in the sinonasal tract. The diagnosis of these subtypes is based on histopathologic appearance and features. These include papillary SCC, verrucous SCC, basaloid SCC, spindle cell carcinoma (sarcomatoid), and adenosquamous carcinoma. It is suggested that, like at other subsites of the aerodigestive tract, these subtypes may confer differing prognoses. 65,1069 The 5-year DSS for each of the aforementioned subtypes is 62%, 70%, 56%, 32%, and 15%, respectively. The estimated 5-year DSS for patients with keratinizing and nonkeratinizing SNSCC is 45%. 1069,1070 b Emerging subtypes Beyond these traditional pathologies, newly character ized pathologies have been described. These include HPV-related multiphenotypic sinonasal carcinoma, sinonasal renal cell-like adenocarcinoma, NUT carci noma, SCC associated with IP, SNUC, and SWI/SNF complex-deficient carcinoma. HPV-related multipheno typic sinonasal carcinoma was described first in 2013 and is now included in the new WHO classification. 17 There is a slight preponderance seen in female patients. It is characterized by cellular proliferation of basaloid cells, a solid growth pattern separated by thin fibrous bands. Additionally, there is usually surface dysplasia (carcinoma in situ), while a population of subtle eosinophilic ducts