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Molecular mechanisms of carcinogenesis in gastric cancer
Heinz Höfler1, Karl-Friedrich Becker
1Technische Universitaet Muenchen, Institut fuer Pathologie, Klinikum rechts der Isar, Trogerstrasse 18, 81675 Munich, Germany.
Abstract:
The catalog of gene alterations in human cancer grows rapidly. Gastric cancer is no exception and displays gene changes in multiple oncogenes, suppressor genes, and DNA repair genes. Clinically relevant molecules whose expression or structure is altered include the plasminogen activator (uPA) and its inhibitor PAI-1 (plasminogen activator inhibitor type 1), the cell-cycle regulator cyclin E, epidermal growth factor (EGF), the apoptosis inhibitor bcl-2, the cell adhesion molecule E-cadherin, and the multifunctional protein beta-catenin. In addition, genetic instability is commonly seen. Gene amplification and protein overexpression of the growth factor receptors c-erbB2 and K-sam may be prognostic factors for intestinal-type and diffuse-type gastric cancer, respectively. The clinical implications of some of the recent findings for diagnosis and therapy are discussed.
Insights
Gastric cancer exhibits numerous gene alterations, including changes in oncogenes and DNA repair genes. These genetic changes, such as growth factor receptor alterations, may serve as important prognostic factors for gastric cancer subtypes.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gastric cancer is characterized by a rapidly expanding catalog of gene alterations.
- These alterations affect oncogenes, suppressor genes, and DNA repair genes.
- Key molecules like uPA, PAI-1, cyclin E, EGF, bcl-2, E-cadherin, and beta-catenin show altered expression or structure.
Purpose of the Study:
- To review the gene alterations observed in gastric cancer.
- To discuss the clinical implications of these findings for diagnosis and therapy.
- To highlight specific genetic changes as potential prognostic factors.
Main Methods:
- Review of current literature on gene alterations in gastric cancer.
- Analysis of changes in oncogenes, suppressor genes, and DNA repair genes.
- Examination of specific molecular markers and their prognostic relevance.
Main Results:
- Commonly observed genetic instability in gastric cancer.
- Alterations in growth factor receptors c-erbB2 and K-sam are potential prognostic factors for intestinal-type and diffuse-type gastric cancer, respectively.
- Expression changes in uPA, PAI-1, cyclin E, EGF, bcl-2, E-cadherin, and beta-catenin are noted.
Conclusions:
- Gene alterations are prevalent in gastric cancer, impacting various cellular functions.
- Specific genetic alterations, particularly in growth factor receptors, may offer prognostic value.
- Understanding these molecular changes is crucial for advancing gastric cancer diagnosis and therapy.