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KUANetal.
TABLE V.5 Evidence surrounding smoking as a risk factor for sinonasal malignancies.
Clinical endpoints
Study
Year LOE Study design Study groups
Conclusion
Greiser et al. 94
1. Smoking increased SNM risk and peaked after 21.75 pack-years 2. Smokers who quit ≥ 28 years ago were at lower risk than those whoquit < 15 years ago Smoking significantly increased SNM risk in males
1. OS 2. Occupational exposure profile
2012 3
Case–control
Bavaria registry
( n = 2828 men only; 427 cases and 2401 controls)
Comba et al. 85
1992 3
Case–control
Multicenter cohort of SNM( n = 332; 78 cases and 254 controls) case–control series (160 SNM, 290 controls, 1970–180) Multicenter
1. OS 2. Occupational exposure profile 1. OS 2. Occupational exposure profile
Brinton et al. 92
Smoking tobacco increased the risk of SCC two- to threefold
1984 3
Case–control
Abbreviations: OS, overall survival; SNM, sinonasal malignancy.
TABLE V.6 Evidence surrounding viral infections as a risk factor for sinonasal malignancies.
Clinical endpoints Conclusion
Study
Year LOE Study design Study groups
Ferreli et al. 97
1. HPV infection increased the risk for IP malignancy 2. High-risk HPV types were associated with greater malignancy risk 38.8% cases tested HPV positive
Riskof
31 studies included 163 malignant and 961 nonmalignant IPs
2022 2
Systematic
malig nancy
reviewand meta analysis
Syrjänen and Syrjänen 95
2013
2
Systematic
1956 sinonasal
HPVstatus
reviewand meta analysis
papillomas from 90 studies between 1950 and 2012 Single center study on 54 patients (25 IPs, five oncocytic papillomas, and 35 SNSCC) Single center study on 161 SNM
Sahnane et al. 96
HPVstatus
High risk HPV was detected in 13% of IP-SCC and 8% de novo-SCC
2019 3
Retrospective cohort
Bishop et al. 65
2013
4
Retrospective case series
HPVstatus
1. 21% SCC were positive for high-risk HPV DNA, including type 16 (82%), types 31/33 (12%), and type 18 (6%) 2. HPV was detected in nonkeratinizing SCC (34%), but none in keratinizing SCC group
Abbreviations: IP-SCC, inverted papilloma-associated squamous cell carcinoma; SCC, squamous cell carcinoma; SNM, sinonasal malignancy.
studies have demonstrated EGFR overexpression in about 40% of SCCs and in 20%–33% of ITACs, which is lower than that in histologically similar head and neck and colorectal cancers. 103–105 ACC is the most common salivary-type sinonasal tumor. 106 EN1 , DLX6 , and OTX1 represent potential drivers and therapeutic targets for ACC. 107 NOTCH1 mutations were identified in poorly differentiated ACC and associ
ated with poorer prognosis, higher tendency to metastasize to liver and bone, and possible responsiveness to NOTCH1 inhibitors. 108 In addition, EGFR and c-Kit genetic abnor malities have been observed in sporadic cases. 109 Even though numerous studies report ONB cytogenetic and genomic alterations, common findings include the positive association of chromosome 11 deletion and chro mosome 1p gain with poor ONB survival and TP53 gene
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