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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Gastro-intestinal, Liver and Lung Disorders (DMLL) > Clinic of Visceral Surgery and Medicine > Visceral Surgery

UniBE Contributor:

Friess, Helmut and Büchler, Markus Wolfgang

ISSN:

0001-544X

Publisher:

Springer-Verlag

Language:

German

Submitter:

Markus Müller

Date Deposited:

10 Jul 2018 16:42

Last Modified:

23 Oct 2019 15:00

Publisher DOI:

10.1007/BF02621314

BORIS DOI:

10.7892/boris.117722

URI:

https://boris.unibe.ch/id/eprint/117722

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