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Z Gastroenterol 2002; 40(S2): 58-61
DOI: 10.1055/s-2002-35904
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© Karl Demeter Verlag im Georg Thieme Verlag Stuttgart · New York

Pathogenese des Pankreaskarzinoms

R. M. Schmid
  • 1II Medizinische Klinik und Poliklinik, Technische Universität München
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Publication History

Publication Date:
04 December 2002 (online)

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Zusammenfassung

Im Gegensatz zum übrigen Gastrointestinaltrakt findet sich im normalen Pankreas eine sehr geringe Proliferationsrate, daher kann man davon ausgehen, dass der Eintritt von Pankreaszellen in den Zellzyklus den ersten Schritt in der Tumorentwicklung darstellt. Im Zellzyklus gibt es Kontrollpunkte, so genannte „Checkpoints”, an denen das Durchlaufen des Zellzyklus überwacht wird, um die korrekte Verdopplung des gesamten Genoms bei der Zellteilung zu gewährleisten. Der Verlust eines oder mehrerer dieser Kontrollpunkte führt zur Akkumulation von strukturellen genetischen Veränderungen, die letztlich zur malignen Entartung führen. Maligne Zellen sind durch ungehindertes Wachstum charakterisiert, durch Eindringen in das umliegende Gewebe und durch Metastasierung. Alle diese Eigenschaften können auf genetische Veränderungen und deren funktionelle Konsequenz zurückgeführt werden. Die Aktivierung des Proto-Oncogens K-Ras und die Inaktivierung der Tumorsuppressorgene INK4a, p53 und SMAD4 sind charakteristisch für das Pankreaskarzinom. Es wurde ein Tumorprogressionsmodell aufgestellt, in dem duktale intraepitheliale Neoplasien die Vorläuferläsionen darstellen. Eine sequenzielle Abfolge von genetischen Ereignissen wird derzeit erarbeitet. Keimbahnmutationen in spezifischen Genen wurden bei familiären Formen des Pankreaskarzinoms nachgewiesen.

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Prof. Dr. Roland M. Schmid

Direktor der II. Medizinischen Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München

Isamninger Straße 22

81675 München

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