Abstract
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.
Translated title of the contribution | Molecular alterations in pancreatic cancer |
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Original language | German |
Pages (from-to) | 245-247 |
Number of pages | 3 |
Journal | Acta Chirurgica Austriaca |
Volume | 29 |
Issue number | 5 |
DOIs | |
State | Published - 1997 |
Externally published | Yes |