Molecular alterations in pancreatic cancer

Friess, Helmut; Berberat, P.; Büchler, Markus Wolfgang (1997). Molecular alterations in pancreatic cancer. Acta Chirurgica Austriaca, 29(5), pp. 245-247. Springer-Verlag 10.1007/BF02621314

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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.

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