Detection of human papillomavirus (HPV) structural antigens and DNA types in inverted papillomas and squamous cell carcinomas of the nasal cavities and paranasal sinuses

Abstract

To assess the suggested etiological role of human papillomavirus (HPV), biopsies from 14 patients operated on for an inverted papilloma (11 cases) and squamous cell carcinoma (3 cases) of the nasal cavity and paranasal sinuses were analysed for light microscopical evidence of HPV, by indirect immunoperoxidase (IP-PAP) to demonstrate HPV structural proteins, and using in situ DNA-hybridization to disclose the DNA of HPV types 6, 11 and 16. The majority of the inverted papillomas contained areas of metaplastic squamous cells, including koilocytes as well as dysplastic changes consistent with intra-epithelial neoplasia as described in uterine cervix. In 3 patients, frankly invasive squamous cell carcinomas were found, originating from dysplastic squamous epithelium. Of the 14 lesions, 7 (50%) expressed HPV antigens, usually confined to only a few cells close to the surface of the epithelium. None of the malignant lesions expressed HPV antigens. In situ DNA-hybridization disclosed HPV 11 DNA alone in 5 lesions, but none of the lesions contained HPV 6 DNA. HPV 16 DNA was found in 2 lesions as a single HPV type, and in 3 other lesions concomitant with HPV 11. All three carcinomas contained HPV 16 DNA. The HPV DNA distribution proved to be different from that found in the genital tract HPV lesions; HPV DNA was less abundant in the nasal papillomas, and it was also found in the basal and suprabasal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of Psychosocial Outcomes in Head and Neck Cancer Patients Receiving a Coping Strategies Intervention and Control Subjects Receiving No Intervention

“…oral cavity cancer), identifying the HPV-16 as the dominant causative type of papillomas (Capone et ~l., 2000;Forastiere et al, 2001;Gillison et al, 1999;Gillison and Shah, 2001;Miller and Johnstone, 2001). However, there is an inconsistency in prevalence estimates with the range varying from 8 to 100% in premalignant and malignant lesions (Bouda et al, 2000;Chang et al, 1991;Franceschi et al, 1996;Greer, Jr. et al, 1990;Holladay and Gerald, 1993;Miguel et al, 1998;Sand et al, 2000;Syrjanen et al, 1987) . Such a wide range may be due to the different study designs used (e.g.…”

HPV in Head and Neck Carcinomas: Different HPV Profiles in Oropharyngeal Carcinomas – Why?

“…Having presented the first evidence on the presence of HPV in OSCC, we hypothesized that these benign sinonasal lesions and their malignant counterparts could be induced by HPV, too. Accordingly, in 1983, we demonstrated first the presence of HPV antigens in sinonasal papillomas [60] and in 1987 HPV DNA in sinonasal carcinomas [24]. So far, only one meta-analysis has been published on the HPV association with sinonasal carcinomas [61].…”

A high prevalence of human papillomavirus DNA in recurrent nasal papillomas

“…A clinical tendency for the lesion to recur even after adequate removal suggests the possibility of papillomas being induced by HPV Laryngeal papillomas are classified clinically into four groups: juvenile multiple, juvenile single, adult multiple and adult single [22]. HPV type 6/11 has been detected in almost 100% of juvenile and adult multiple laryngeal papillomas, strongly suggesting a viral aetiology for these benign tumors [23-251. Conversely, the reported prevalence of HPV in fungiform exophytic and inverted nasal papillomas has varied [l, [3][4][5][6][7][8][9][10][11][12][13]151. The methods and techniques used for detection of HPV as well as the patients' geographic location seem to influence the results.…”