Veränderungen der Expression von Wachstumsfaktoren und ihrer Rezeptoren sowie Genmutationen spielen eine wesentliche Rolle in der Pathogenese von malignen gastrointestinalen Tumoren. Wir beschreiben in dieser Übersicht die wichtigsten molekularen Veränderungen beim menschlichen Pankreaskarzinom. In einer signifikanten Anzahl dieser Tumoren sind Wachstumsfaktoren [epidermal growth factor (EGF), transforming growth factor-α (TGF-α), Amphiregulin, Betacellulin, heparin-binding EGF like growth factor (HB-EGF), TGF-βs, acidic und basic fibroblast growth factor (aFGF, bFGF), kreatinocyte growth factor (KGF), platelet derived growth factors (PDGFs)] und Wachstumsfaktor-rezeptoren (EGF-Rezeptor, c-erbB-2- und c-erbB-3-Rezeptor, TGF-β-Rezeptor-2, FGF-Rezeptor, PDGF-Rezeptoren) überexprimiert sowie Genmutationen vorhanden (p53 und K-ras). Diese Veränderungen können das Tumorwachstum und seine Metastasierung stimulieren. Eine verkürzte postoperative Überlebensperiode der Patienten konnte bei einer Überexpression des EGF-Rezeptors zusammen mit EGF, TGF-α und/oder Amphiregulin, einer Überexpression des c-erbB-3-Rezeptors, bFGF, TGF-β und Mutationen des p53-Gens beobachtet werden. Diese Daten deuten darauf hin, daβ molekulare Störungen in den Pankreaskarzinomzellen eine wesentliche Ursache für die klinische Aggressivität dieser Tumorerkrankung darstellen.

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