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142

KUANetal.

TABLE XVI.2 (Continued)

Clinical endpoints

Study

Year LOE Study design Study groups

Conclusion

Jenko et al. 762

1. HPV in sinonasal IP ± SCC higher than in the control group 2. HPV DNA was not a predictor of recurrence of IP and was not a significant risk factor for associated SCC 1. AllHPV + cases were early grade (grade I or II) IP lesions. 2. No higher grade (grades III or IV) lesions showed HPV DNA 3. Five out of seven HPV + patients were high-risk subtypes and two were unspecified subtypes 1. Increase in staining of p21 and p53 was seen in IP with severe dysplasia, IP with carcinoma, and invasive SNSCC as compared to control mucosa. 2. In groups that were HPV + , a significant increase in dysplasia was seen 1. HPV infection was not detected in specimens from clinically intact mucosa or nasal polyps 2. Three out of 26 IP were HPV associated (each double infected with HPV 6 and HPV 11) 3. Four out of 20 SNSCCs were HPV 16 positive 1. Elevated MMP-2 and 9 may be associated with early events in IP carcinogenesis 2. HPV infection may contribute as an early event in this process 1. Significant increase in EGFR andTGF- α expression in IP with severe dysplasia, IP with carcinoma, and invasive SCC as compared to IP with mild dysplasia and control nasal mucosa 2. As dysplasia increased in IP, the Ki-67 increased HPV DNA was present in 6% of the benign IP, 69% of the exophytic papilloma, and 40% of the IP that contained carcinoma.

1. Malignant alteration 2. Recurrence rate

2011

4

Case–control

68 patients with

sinonasal IP and five patients with sinonasal IP associated with SCC

compared to 47 control patients

Kimet al. 763

2007 4

Case–control

57 sinonasal IP with histologic grades stage I to stage IV

1. Prevalence of HPV subtypes insamples

classified by histological grade

Katori et al. 651

Relationship

2006 4

Case–control

29 patients with IP, 12 patients with invasive SNSCC, seven patients with exophytic papilloma, and 10 inferior turbinates (control) ( n = 26), SNSCC ( n = 20), sinonasal polyps ( n = 20), and control mucosa ( n = 20) 86 patients with sinonasal IP sinonasal papilloma, 12 patients with invasive SNSCC, and 10 control patients sinonasal papilloma, 12 patients with invasive SNSCC, and 10 patients with normal mucosa (control) 32 patients with 57 IP (five associated with carcinoma), 16 exophytic papilloma, and five oncocytic papilloma 36 patients with

between p21 andp53 expression, HPV infection, and malignant transforma tion whether HPV DNA presence indicates a coincidental, persis tent/latent, or specific infection Matrix metallo proteinase (MMP)-2 and MMP-9 expression Determine

Hoffmann et al. 671

2006 4

Case–control

Katori et al. 650

2006 4

Case–control

Katori et al. 649

2005 4

Case–control

HPV status, EGFR

expression, andki-67

Buchwald et al. 764

Presence of HPV DNA

1995 4

Case–control

Abbreviations: DSS, disease-specific survival; EGFR, epidermal growth factor receptor; KRAS, Kirsten rat sarcoma viral oncogene homolog; IP, inverted papilloma; OS, overall survival; SNSCC, sinonasal squamous cell carcinoma.