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Acta Chirurgica Austriaca

, Volume 29, Issue 5, pp 245–247 | Cite as

Molekulare Veränderungen beim Pankreaskarzinom

  • H. Friess
  • P. Berberat
  • M. W. Büchler
Themenschwerpunkt: Pankreaskarzinom: Aktuelles Aus Der Grundlagenforschung Und Neue Konzepte Zur Therapie
  • 12 Downloads

Zusammenfassung

Grundlagen: Das Pankreaskarzinom hat eine infauste Prognose. Die Ursachen für das aggressive Tumorwachstum und die frühe Metastasierung sind nur unzureichend bekannt. Mit Hilfe von modernen molekularbiologischen Untersuchungstechniken ist es in den vergangenen Jahren gelungen, einen Einblick in die Pathophysiologie dieser Erkrankung zu gewinnen.

Methodik: Im Rahmen dieser Übersicht wird die pathogenetische Bedeutung von Wachstumsfaktor-Rezeptoren (EGFR, c-erbB-2, c-erbB-3), Wachstumsfaktoren (EGF, TGF-α, Amphiregulin, Betacellulin, TGF-βs, FGFs) sowie von Genmutationen (p53, K-ras) und Adhäsionsmolekülen beim humanen Pankreaskarzinom dargestellt.

Ergebnisse: In einer signifikanten Anzahl der Pankreaskarzinome sind Wachstumsfaktorrezeptoren (EGFR, c-erbB-2, c-erbB-3), Wachstumsfaktoren (EGF, TGF-α, Amphiregulin, Betacellulin, TGF-βs, FGFs) und Adhäsionsmoleküle (ICAM-1, ELAM-1) überexprimiert sowie Genmutationen (p53, K-ras) vorhanden. Allerdings sind nicht alle diese molekularen Veränderungen mit einem schnelleren Tumorwachstum und einer schlechteren Prognose nach Tumorresektion vergesellschaftet.

Schlußfolgerungen: Molekulare Störungen in Pankreaskarzinomzellen tragen zum malignen Phänotyp bei. Diese Veränderungen erklären, warum die Pankreaskarzinomzellen schnell proliferieren und nur eine geringe Ansprechbarkeit auf adjuvante onkologische Behandlungen zeigen.

Schlüsselwörter

Pankreaskarzinom Wachstumsfaktoren Wachstumsfaktor-Rezeptoren Genmutationen 

Molecular alterations in pancreatic cancer

Summary

Background: Pancreatic cancer is a devastating disease with poor prognosis. The reasons for its aggressive growth behavior and early metastases are unknown. In the past years molecular studies have contributed to a better understanding of the pathophysiology of this disease.

Methods: In the present review we describe the role of growth factor receptors (EGFR, c-erbB-2, c-erbB-3), growth factors (EGF, TGF-α, Amphiregulin, Betacellulin, TGF-βs, FGFs), gene mutations (p53, K-ras) and adhesion molecules in human pancreatic cancer.

Results: Overexpression of growth factor receptors (EGFR, c-erbB-2, c-erbB-3), growth factors (EGF, TGF-α, Amphiregulin, Betacellulin, TGF-βs, FGFs), gene mutations (p53, K-ras) and adhesion molecules (ICAM-1, ELAM-1) are present in a significant number of these tumors. However, not all of these molecular changes contribute to faster tumor growth and poorer prognosis following tumor resection.

Conclusions: Molecular alterations in pancreatic cancer cells contribute to the malignant phenotype. These changes explain why pancreatic cancer cells grow rapidly and exhibit low sensitivity to adjuvant oncological treatment.

Key-words

Pancreatic cancer growth factors growth factor receptors gene mutations 

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Copyright information

© Blackwell Science Ltd 1997

Authors and Affiliations

  • H. Friess
    • 1
  • P. Berberat
    • 1
  • M. W. Büchler
    • 1
  1. 1.Klinik für Viszerale und TransplantationschirurgieUniversität Bern (Inselspital)BernSchweiz

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