Molecular Mechanisms of Carcinogenesis in Gastric Cancer

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Molecular Staging of Cancer

Part of the book series: Recent Results in Cancer Research ((RECENTCANCER,volume 162))

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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.

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Höfler, H., Becker, KF. (2003). Molecular Mechanisms of Carcinogenesis in Gastric Cancer. In: Allgayer, H., Heiss, M.M., Schildberg, F.W. (eds) Molecular Staging of Cancer. Recent Results in Cancer Research, vol 162. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59349-9_5

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  • DOI: https://doi.org/10.1007/978-3-642-59349-9_5

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-63945-6

  • Online ISBN: 978-3-642-59349-9

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