Molekularbiologische charakterisierung des pankreaskarzinoms

H. Friess; M. E. Martignoni; M. W. Büchler

doi:10.1159/000012464

Molekularbiologische charakterisierung des pankreaskarzinoms

Translated title of the contribution: Molecular biological characteristics of pancreatic carcinoma

H. Friess, M. E. Martignoni, M. W. Büchler

Research output: Contribution to journal › Article › peer-review

Abstract

Molecular alterations play a key role in the pathogenesis of pancreatic cancer. These alterations stimulate tumor growth and enhance the metastatic behavior of the tumor. In this paper we describe relevant molecular alterations in pancreatic carcinoma. Overexpression of growth factors (EGF, TGF-α, TGF-β 1-3, aFGF, bFGF), growth factor receptors (EGF receptor, c- erbB2, c-erbB3, TGF-β receptors I-III), adhesion molecules (ICAM-1, ELAM- 1), factors of metastasis (uPA, uPA receptor, KAI1) and gene mutations (p53, K-ras, DCC, APC) are present in a significant number of patients with pancreatic carcinoma. These changes could explain the aggressive growth and the early metastasis of pancreatic carcinoma and may contribute to new therapy concepts.

Translated title of the contribution	Molecular biological characteristics of pancreatic carcinoma
Original language	German
Pages (from-to)	14-21
Number of pages	8
Journal	Chirurgische Gastroenterologie mit Interdisziplinaren Gesprachen
Volume	14
Issue number	1
DOIs	https://doi.org/10.1159/000012464
State	Published - Mar 1998
Externally published	Yes

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title = "Molekularbiologische charakterisierung des pankreaskarzinoms",

abstract = "Molecular alterations play a key role in the pathogenesis of pancreatic cancer. These alterations stimulate tumor growth and enhance the metastatic behavior of the tumor. In this paper we describe relevant molecular alterations in pancreatic carcinoma. Overexpression of growth factors (EGF, TGF-α, TGF-β 1-3, aFGF, bFGF), growth factor receptors (EGF receptor, c- erbB2, c-erbB3, TGF-β receptors I-III), adhesion molecules (ICAM-1, ELAM- 1), factors of metastasis (uPA, uPA receptor, KAI1) and gene mutations (p53, K-ras, DCC, APC) are present in a significant number of patients with pancreatic carcinoma. These changes could explain the aggressive growth and the early metastasis of pancreatic carcinoma and may contribute to new therapy concepts.",

keywords = "Adhesion molecules, Gene mutations, Growth factor receptors, Growth factors, Pancreatic carcinoma: molecular biology, Urokinase plasminogen activator",

author = "H. Friess and Martignoni, {M. E.} and B{\"u}chler, {M. W.}",

year = "1998",

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AU - Büchler, M. W.

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N2 - Molecular alterations play a key role in the pathogenesis of pancreatic cancer. These alterations stimulate tumor growth and enhance the metastatic behavior of the tumor. In this paper we describe relevant molecular alterations in pancreatic carcinoma. Overexpression of growth factors (EGF, TGF-α, TGF-β 1-3, aFGF, bFGF), growth factor receptors (EGF receptor, c- erbB2, c-erbB3, TGF-β receptors I-III), adhesion molecules (ICAM-1, ELAM- 1), factors of metastasis (uPA, uPA receptor, KAI1) and gene mutations (p53, K-ras, DCC, APC) are present in a significant number of patients with pancreatic carcinoma. These changes could explain the aggressive growth and the early metastasis of pancreatic carcinoma and may contribute to new therapy concepts.

AB - Molecular alterations play a key role in the pathogenesis of pancreatic cancer. These alterations stimulate tumor growth and enhance the metastatic behavior of the tumor. In this paper we describe relevant molecular alterations in pancreatic carcinoma. Overexpression of growth factors (EGF, TGF-α, TGF-β 1-3, aFGF, bFGF), growth factor receptors (EGF receptor, c- erbB2, c-erbB3, TGF-β receptors I-III), adhesion molecules (ICAM-1, ELAM- 1), factors of metastasis (uPA, uPA receptor, KAI1) and gene mutations (p53, K-ras, DCC, APC) are present in a significant number of patients with pancreatic carcinoma. These changes could explain the aggressive growth and the early metastasis of pancreatic carcinoma and may contribute to new therapy concepts.

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Molekularbiologische charakterisierung des pankreaskarzinoms

Abstract

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