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KUANetal.

TABLE XVI.2 (Continued)

Clinical endpoints

Study

Year LOE Study design Study groups

Conclusion

1. Recurrent IPs were more often HPV + than nonrecurrent IPs 2. Low-risk HPV infection increased the risk of tumor recurrences 3. IP and oncocytic papilloma were more often high-risk HPV-associated than fungiform papilloma

1. Role of HPV infection on recurrence of sinonasal papilloma 2. Role of HPV infection on malignant

Paehler Vor der Holte 747

2021

3

Retrospective cohort

101 patients with

benign papilloma and six patients with carcinoma in situ and SCC related IP

progression of sinonasal papilloma

Hongo et al. 672

2021

3

Retrospective cohort

146 patients with SNSCC (14 with

Prognostic

1. EGFR may play a role in the pathogenicity of sinonasal IP-related SCC 2. HPV-associated SNSCC patients

significance of HPV infection, EGFR

sinonasal IP-related SCC)

mutations, andKRAS

have better prognoses than HPV-independent patients

Li et al. 748

1. Nine out of 21 (42.9%) patients experienced local recurrence 2. T4 stage and invasive orbital cavity had a significant influence on recurrence 3. DSS is favorable in patients with SCC associated with IP 1. HPV DNA was identified in 34 out of 55 (61.8%) patients with IP 2. High-risk genotypes (19/34, 55.9%) were more prevalent than low-risk genotypes (15/34, 44.1%) 1. HPV DNA was present in 6.1% (3/49) of patients with SN IP and 11.1% (4/36) of patients with oncocytic papilloma 2. 22.4% (11/49) of sinonasal IP lesions and 27.8% (10/36) of sinonasal oncocytic papilloma lesions were p16 positive

2020 3

Retrospective cohort

21 patients with SCC associated with IP

1. Rateof

recurrence 2. 1-, 3-, and 5-yearOS 3. 1-, 3-, and 5-yearDSS

Frasson et al. 749

2020 3

Retrospective cohort

55 patients with sinonasal IP

HPV status in

samples of IP

Wanget al. 750

1. Role of HPV in sinonasal IPand sinonasal oncocytic papilloma 2. Determine

2020 3

Retrospective cohort

49 patients with

sinonasal IP and 36 patients with sinonasal oncocytic papilloma

whether p16 can serve as a surrogate marker for HPV infection

(Continues)

nonkeratinizing. Keratinizing dysplasia is morphologi cally similar to that seen in other head and neck squamous pathology—orthokeratosis, cytologic atypia, squamous dysmaturation, and increased intraepithelial disorganiza tion as it progresses from low to high grade. 36,93,645,646,660 Nonkeratinizing dysplasia is more histologically subtle and is recognized by loss of neutrophilic inflammation with associated increased mitotic activity. 643 Recent

molecular profiling data indicate that TP53 and/or CDKN2A alterations are central events in malignant pro gression of sinonasal papillomas. 660 Although studies have posited a role for high-risk HPV subtypes—in particular, types 16 and 18—during malignant conversion of sinonasal papilloma, more recent meta-analytic data indicate that high-risk HPV is associated with de novo sinonasal SCC (i.e., not arising from IP). 646,656,657,661–665 Importantly,