Karzinogenese des Pankreaskarzinoms. Klinische Relevanz

G. Schneider; C. Lersch; R. M. Schmid

doi:10.1007/s00104-003-0618-6

Karzinogenese des Pankreaskarzinoms. Klinische Relevanz

Translated title of the contribution: Pancreatic carcinogenesis. Clinical implications

G. Schneider, C. Lersch, R. M. Schmid

Department of Internal Medicine II - Gastroenterology

Technical University of Munich

Research output: Contribution to journal › Review article › peer-review

1 Scopus citations

Abstract

Our understanding of the molecular pathology of pancreatic carcinoma has improved tremendously over the past few years due to the development of sophisticated molecular techniques.This knowledge has led to the postulation of a pancreatic tumor progression model.This article describes the molecular oncogenesis of pancreatic carcinoma and points out potential targets for therapeutic interventions. Pancreatic cancer is characterized by the sequential acquisition of somatic mutations in the proto-oncogene K-RAS and the tumor suppressors INK4a, TP53 and DPC4/SMAD4 and by epigenetic alterations, including the overexpression of the "epidermal growth factor" receptor/ligand system. These genetic changes cause a profound disturbance to cell cycle regulation and continuous growth. Further analysis of the underlying molecular mechanisms will offer new diagnostic and therapeutic options and hopefully improve the outcome of this grim disease in the future.

Translated title of the contribution	Pancreatic carcinogenesis. Clinical implications
Original language	German
Pages (from-to)	165-170
Number of pages	6
Journal	Chirurg
Volume	74
Issue number	3
DOIs	https://doi.org/10.1007/s00104-003-0618-6
State	Published - Mar 2003

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abstract = "Our understanding of the molecular pathology of pancreatic carcinoma has improved tremendously over the past few years due to the development of sophisticated molecular techniques.This knowledge has led to the postulation of a pancreatic tumor progression model.This article describes the molecular oncogenesis of pancreatic carcinoma and points out potential targets for therapeutic interventions. Pancreatic cancer is characterized by the sequential acquisition of somatic mutations in the proto-oncogene K-RAS and the tumor suppressors INK4a, TP53 and DPC4/SMAD4 and by epigenetic alterations, including the overexpression of the {"}epidermal growth factor{"} receptor/ligand system. These genetic changes cause a profound disturbance to cell cycle regulation and continuous growth. Further analysis of the underlying molecular mechanisms will offer new diagnostic and therapeutic options and hopefully improve the outcome of this grim disease in the future.",

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N2 - Our understanding of the molecular pathology of pancreatic carcinoma has improved tremendously over the past few years due to the development of sophisticated molecular techniques.This knowledge has led to the postulation of a pancreatic tumor progression model.This article describes the molecular oncogenesis of pancreatic carcinoma and points out potential targets for therapeutic interventions. Pancreatic cancer is characterized by the sequential acquisition of somatic mutations in the proto-oncogene K-RAS and the tumor suppressors INK4a, TP53 and DPC4/SMAD4 and by epigenetic alterations, including the overexpression of the "epidermal growth factor" receptor/ligand system. These genetic changes cause a profound disturbance to cell cycle regulation and continuous growth. Further analysis of the underlying molecular mechanisms will offer new diagnostic and therapeutic options and hopefully improve the outcome of this grim disease in the future.

AB - Our understanding of the molecular pathology of pancreatic carcinoma has improved tremendously over the past few years due to the development of sophisticated molecular techniques.This knowledge has led to the postulation of a pancreatic tumor progression model.This article describes the molecular oncogenesis of pancreatic carcinoma and points out potential targets for therapeutic interventions. Pancreatic cancer is characterized by the sequential acquisition of somatic mutations in the proto-oncogene K-RAS and the tumor suppressors INK4a, TP53 and DPC4/SMAD4 and by epigenetic alterations, including the overexpression of the "epidermal growth factor" receptor/ligand system. These genetic changes cause a profound disturbance to cell cycle regulation and continuous growth. Further analysis of the underlying molecular mechanisms will offer new diagnostic and therapeutic options and hopefully improve the outcome of this grim disease in the future.

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KW - Oncogenesis

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KW - Therapeutics

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M3 - Übersichtsartikel

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ER -

Karzinogenese des Pankreaskarzinoms. Klinische Relevanz

Abstract

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