xRead - Nasal Obstruction (September 2024) Full Articles

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ICAR SINONASAL TUMORS

TABLE XXI.B.2 (Continued)

Clinical endpoints Loss ofCPP

Study

Year LOE Study design Study groups

Conclusion

Ojiri et al. 1122 1. Co-existing SCCs demonstrate distinctive imaging finding (partial or absent CCP) 2. CCP present in eight tumors (80%) 3. One tumor contained microscopic IP-SCC 4. Partial CCP detected in two tumors that contained IP-SCC Abbreviations: ADC, apparent diffusion coefficient; CCP, convoluted cerebriform pattern; DN-SCC, de novo squamous cell carcinoma; IP-SCC, inverted papilloma associated squamous cell carcinoma; OS, overall survival. 2000 4 Retrospective case series Biopsy-proven IP, previously untreated ( n = 10)

clonal precursor lesions to IP-SCC. 659,667 In contrast to IP, TP53 and/or CDKN2A mutations/deletions are present in the majority of IP-SCC, while NFE2L2 and PIK3CA mutations and EGFR , TERT , SOX2 , CCND1 , MYC , and FGFR1 amplifications have been reported in subsets of cases. 660,1138 IP-SCC shows high expression of genes associ ated with epithelial–mesenchymal transition and extracel lular matrix remodeling. 1140 Preclinical models of IP-SCC with EGFR exon 20 mutations demonstrate endoge nous EGFR, MAPK, and PI3K/AKT pathway activity and responsiveness to irreversible EGFR inhibitors (e.g., ner atinib, afatinib, dacomitinib) in vitro. 659 Table XXI.B.3 summarizes evidence surrounding histopathologic studies and molecular pathogenesis of IP-SCC. Aggregate grade of evidence : C (Level 2: one study; Level 3: five studies; Level 4: six studies) MINOR SALIVARY GLAND TUMORS OF THE SINONASAL TRACT A Intestinal-type adenocarcinoma The 5th edition of the WHO Classification of Head and Neck Tumors classifies sinonasal adenocarcinomas of sur face epithelial origin (nonsalivary-type adenocarcinomas) in intestinal and nonintestinal types. 17 ITAC is one of the most common sinonasal cancers, especially in European countries. 1141 The typical site of origin is the ethmoid, often arising from the olfactory cleft. 1142 The correlation between sinonasal ITAC and occupational exposure is well known. 1143 The most important risk factor is exposure to hardwood dusts, such as beech or oak, followed by prod ucts from the textile industry and leather dusts. 39,1144 The current staging system for sinonasal ITAC follows the AJCC TNM classification of nasal cavity and paranasal sinuses cancers (8th edition), which has been demon strated to stratify patients according to prognosis. 16,158,1144 XXII

However, the propensity of ITAC to present at a locally advanced stage supports the need for a more personal ized approach to cancer staging, since different prognostic patterns are recognizable even within the pT4a (anterior wall of the sphenoid involvement vs. lateral or poste rior sphenoid walls invasion) and the pT4b groups (focal dural invasion vs. massive dura and cerebral extension or leptomeningeal spread). 1145,1146 Tumor subtypes and grade From a histological perspective, ITAC resembles primary adenocarcinoma arising from the intestinal mucosa and consists of proliferation of dysplastic columnar cells with interspersed goblet cells forming papillae and glands. In an attempt to stratify patients according to prognosis, sev eral histologic features have been considered over the years. Historically, Barnes classified ITACs into five sub types: papillary (18%), colonic (40%), solid (20%), mucinous (14%), and mixed (8%). 1147 A few years later, Kleinsasser and Schroeder divided ITACs into four subtypes: papillary tubular cylinder cell, which was further graded from I to III; alveolar goblet; signet-ring cell; and transitional. 1148,1149 The signet-ring cell subtype represents the ITAC subtype associated with the worst prognosis. 17 In addition to mor phologic subtypes, the histological grade of differentiation (well, moderately, and poorly differentiated) can be associ ated with prognosis, with poorly differentiated ITAC being the most aggressive subtype and more prone to local and distant relapse. 362,1150 Recent evidence also suggests that P53 could play a role in disease behavior and response to treatment, with P53 status on pretreatment biopsy used to determine treatment strategy. 293 In ITACs with func tional P53 (58% of cases), including both the wild-type and the mutated protein with function preservation or gain, neoadjuvant chemotherapy with cisplatin, 5-fluorouracil, and leucovorin (PFL) resulted in complete response in 1