HIGH-RISK HPV TYPES IN ORAL AND LARYNGEAL PAPILLOMAS AND IN LARYNGEALLEUKOPLAKIA

Citation
O. Arndt et al., HIGH-RISK HPV TYPES IN ORAL AND LARYNGEAL PAPILLOMAS AND IN LARYNGEALLEUKOPLAKIA, Laryngo-, Rhino-, Otologie, 76(3), 1997, pp. 142-149
Citations number
58
Categorie Soggetti
Otorhinolaryngology
Journal title
ISSN journal
09358943
Volume
76
Issue
3
Year of publication
1997
Pages
142 - 149
Database
ISI
SICI code
0935-8943(1997)76:3<142:HHTIOA>2.0.ZU;2-Y
Abstract
Background: Juvenile and adult laryngeal papillomas (JLP and ALP) and oral papillomas (OP) are important benign tumors of the head and neck. Laryngeal leukoplakia (LL) may be a precancerous lesion. The etiology of the papillomas is associated with human papillomavirus infection ( HPV). The important noxes for the development of laryngeal leukoplakia s are nicotine, alcohol, and HPV. Adult laryngeal papillomas and OP ca n also undergo malignant conversion. Today, there is no marker known t o distinguish in progressive lesions and in those which show a regress ion. Different types of HPV were detected in head and neck cancer too. There is a important similarity to the genesis of cervical cancer. Th e 77 known HPV types were divided into benign types, e.g., 6 and 11, a nd those with oncogene potential, e.g., 16, 18, 31, 33, and 35. The de tection of oncogene HPV may be a sensitive marker for prognosis of pri mary benign lesions. Patients and Methods: In this study, the presence of HPV genomes 6, 11, 16, 18, 31, 33, and 35 in 17 JLP, 27 ALP, 15 OP , and 11 LL was examined. DNA extracted from archived samples embedded in paraffin was amplified using the E6 specific polymerase chain reac tion (PCR). The products were visualized by electrophoresis, and posit ive identification was achieved by Southern blot analysis and hybridiz ation to specific biotinylated oligonucleotide. Results: Our data show the presence of HPV 6/11 in all JLP (17 of 17), in all ALP (27 of 27) , in 13 of 15 (87%) OP, and in seven of 11 (63%) LL. The ''malignant'' types HPV 16, 18, and 33 were found in six of 27 (22%) of the ALP, in three of 15 (20%) of the OP, and in four of 11 (36%) of the LL The do minant type was HPV 16. HPV 31 and 35 were not detectable. Three ALP, one OP, and the four LL of the cases with oncogene HPV showed histolog ic features of moderate dysplasia. Conclusions: The role of HPV in mal ignant transformation of infected cells remains unclear. It is well kn own that the carcinogenesis must depend on promoters such as alcohol, tobacco, and metabolites of chronic inflammations. All patients with p ositive biopsies confirming HPV 16, 18, or 33 must receive special car e to prevent the development of a carcinoma.