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Der MKG-Chirurg

, Volume 11, Issue 1, pp 21–29 | Cite as

Einfluss onkogener Viren beim oralen Plattenepithelkarzinom

Leitthema

Zusammenfassung

Hintergrund

Ausgelöst durch die nun mittlerweile routinemäßige Bestimmung des Humanen Papillomavirus (HPV) beim Oropharynxkarzinom rücken onkogene Viren als Ko- oder singuläres Karzinogen in den Fokus der personalisierten Medizin. Es scheint nun Konsens darüber zu bestehen, dass die viralen onkogenen Eigenschaften des HPV auch bei bestimmten Kopf-Hals-Karzinomen ätiologisch bedeutsam sind. Hierbei spielen Lokalisation des Primärtumors und Nachweismethoden (Immunhistochemie [ICH] vs. Polymerase-Kettenreaktion [PCR] und In-Situ-Hybridisierung [ISH]) eine essenzielle Rolle. Kontrollstudien und Metaanalysen deuten darauf hin, dass bei ca. 6–25 % der oralen Plattenepithelkarzinome (OSCC) eine zusätzliche HPV-Infektion vorliegt. Bezüglich der anderen potenziellen Onkogene Epstein-Barr-Virus (EBV) und Herpes-Simplex-Typ 1-(HSV-1) sind die ätiologischen Erkenntnisse beim oralen Karzinom wesentlich fraglicher.

Methoden

Im Rahmen eines Literaturüberblicks werden die aktuell gesicherten Erkenntnisse auf tierexperimenteller und humaner Studienbasis für HPV, HSV und EBV dargestellt. Diese werden unter dem Gesichtspunkt eines möglichen ätiologischen und prognostischen Einflusses auf das OSCC bewertet.

Schlussfolgerungen

Möglicherweise spielt eine gesicherte HPV-Infektion mit den High-Risk-Subtypen 16 und 18 eine zusätzliche Rolle, wesentlich ist aber, dass gleichzeitig bekannte Noxen wie Nikotin hinsichtlich der Ätiologie definitiv überwiegen. HPV-16 ist der wichtigste Subtyp im Zusammenhang mit dem OSCC. Bei oropharyngealen oder Tonsillenkarzinomen stellt eine Infektion mit den HPV-High-Risk-Subtypen 16 und 18 dagegen ein eigenes Subkollektiv dar, für das therapeutische Modifikationen denkbar sind. Beim HSV-1 und EBV sind ätiologische Erkenntnisse in Bezug auf das OSCC sehr fraglich. Bei der HSV-1-Infektion könnte eine kokarzinogene Komponente vor allem in Kombination mit HPV-16 vorliegen, während dies beim EBV höchstwahrscheinlich vernachlässigt werden kann. Dagegen ist eine Koinfektion mit mehreren onkogenen Viren gesichert als Risikofaktor anzusehen, wobei die Gewichtung des Einflusses einzelner onkogener Viren unklar ist. Während die PCR das derzeit sensitivste Verfahren zum HPV-Nachweis darstellt, kann die IHC zu falsch-positiven Resultaten führen.

Schlüsselwörter

Kopf-Hals-Karzinome Onkogene Viren HPV 16, 18 HSV-1 EBV 

The role of oncogenic viruses in oral squamous cell carcinoma

Abstract

Background

Triggered by the now routinely performed human papillomavirus (HPV) analysis in oropharyngeal carcinoma, the consideration of oncogenic viruses as a co- or singular carcinogen is becoming a focus of personalized medicine. There now seems to be a consensus that HPV has oncogenic properties not only in cervical carcinoma but also in certain regions of head and neck carcinomas. Localization of the tumor and detection methods (immunohistochemistry [IHC] versus polymerase chain reaction [PCR] and in situ hybridization [ISH]) play an essential role as influencing factors. Control studies and meta-analyzes indicate that about 6–25% of the oral squamous cell carcinoma (OSCC) have an additional HPV infection. With regard to the other potential oncogenes EBV and HSV-1, their etiological influence in oral carcinomas is much more questionable.

Methods

In a brief review of the literature, the current findings are presented on the basis of animal experiments and human studies for HPV, HSV and EBV. They are then evaluated from the perspective of a possible etiological and prognostic impact on OSCC.

Conclusions

A confirmed HPV infection with the high-risk subtypes 16 and 18 might play an additional role, but it is essential simultaniously present history of well-known noxious agents such as nicotine definitely outweigh the latter in terms of oncogenic influence. HPV type 16 is the most common high-risk-subtype associated with OSCC. Completely different is the situation with oropharyngeal- or tonsillar carcinomas, in which an infection with the HPV high-risk subtypes 16 and 18 is a subset of its own. In HSV-1 and EBV, these etiological findings are much more questionable with respect to the OSCC. In HSV-1 infection, a co-carcinogenic component especially in case of coinfection with HPV 16 could be present, while in EBV this can certainly be neglected. Once again, it has been proven that a coinfection with several oncogenic viruses is considered a risk factor, whereas the weighting in relation to the influence of a single oncogenic virus is unclear. While PCR is currently the most sensitive method for HPV detection IHC can lead to false positive data.

Keywords

Head and neck carcinoma Oncogenic viruses HPV 16, 18 HSV-1 EBV 

Notes

Einhaltung ethischer Richtlinien

Interessenkonflikt

A. Kolk gibt an, dass kein Interessenkonflikt besteht.

Dieser Beitrag beinhaltet keine von den Autoren durchgeführten Studien an Menschen oder Tieren. Für die aufgeführten Studien gelten die jeweils dort angegebenen ethischen Richtlinien.

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Copyright information

© Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2018

Authors and Affiliations

  1. 1.Klinik und Poliklinik für Mund-Kiefer-GesichtschirurgieKlinikum rechts der Isar der Technischen Universität MünchenMünchenDeutschland

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