Der Nachweis humaner Papillomvirus (HPV) DNA in formalinfixierten invasiven Plattenepithelkarzinomen des Larynx mit der Polymerase Chain Reaction (PCR)*

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Abstract
Es wurden insgesamt 100 formalinfixierte und paraffineingebettete Plattenepithelkarzinome des Larynx, 41 glottischen und 59 supraglottischen Ursprungs, mit der E6 spezifischen PCR auf das Vorhandensein von HPV 6/11 DNA und auf DNA der onkogenen Typen HPV 16 und 18 untersucht. 32% der Befunde waren HPV-positiv. Während 63,4% (26) der glottischen Karzinome die gesuchte HPV DNA beherbergten, waren nur 10,2% (6) der supraglottischen Befunde HPV-positiv. Alle positiven glottischen Tumoren enthielten die onkogenen Typen. HPV 16 war bei beiden Tumorlokalisationen dominant. Bei nahezu gleichem Durchschnittsalter aller Karzinomträger wiesen die Patienten mit HPV 16 und/oder 18 positiven Karzinomen ein signifikant erhöhtes exogenes Risiko in Form des Grades des Nikotin- und Alkoholabusus auf als die Träger der HPV-negativen Karzinome beider Gruppen. Statistisch bewegt sich das exogene Risiko bei den Patienten mit einem supraglottischen Befund auf einem höheren Niveau. Die Resultate erhärten den Verdacht der bedeutenden Rolle der onkogenen Papillomviren in der Ätiologie der Larynxkarzinome. Eine Differenz in der Pathogenese der supraglottischen und glottischen Karzinome ist nach den Ergebnissen wahrscheinlich. Approximately 67 different aubtypes of HPVs have now been described. Regularly most of the cervical cancers are positive for HPV 16/18. Current research also indicates that HPVs may be involved in the development of benign tumours and also squamous cell cancers of head and neck. Studies establishing the presence of different HPV subtypes in oral cancers and precancers suggest the possibility of the virus as etiological factor in oral carcinogenesis too. In this study the prevalence of HPV 6/11, 16 and 18 infection and other exogenous risk factors like nicotine and alcohol in laryngeal cancers were studied. A total of 100 formalin-fixed and paraffin-embedded cancers, 41 glottic and 59 supraglottic, in patients aged 58 years, were detected by use of the E6 specific PCR for HPV DNA. Significantly more glottic cancers, 26 of 41 (63.4%), were positive for the investigated HPVs. HPV 16 was found in all positive cancers. This predominance of HPV 16 was also present in the supraglottic carcinomas, but only 10.2% (6 of 59) of the these groups were HPV positive. In both groups the patients with HPV 16 and/or 18 positive cancers, the exogenous risk factor was higher thay with in HPV 16/18 negative tumours. Following infection, the virus either remains dormant or eise undergoes active replication resulting in the synthesis of infectious virus. The integration of virus DNA into the host cell DNA may be the result of action of nicotine and/or alcohol. The integration event is the key of the carcinogenesis. The level of the risk factor in the patients with supraglottic tumours was significantly higher. The results this paper show the possible role of HPV 16/18 in the pathogenesis of laryngeal cancers. There may be a second important way of carcinogenesis in supraglottic carcinomas.

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