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Glycosylation in Cancer and Oncogenic Transformation

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Glycoproteins and Human Disease

Part of the book series: Medical Intelligence Unit ((MIU.LANDES))

Abstract

Oncogenic transformation in many tissues is associated with altered glycosylation or the appearance of oncofetal glycoforms (Table 6).1,2 The development of colon cancer occurs in several steps including accumulating activation of oncogenes and inactivation of suppressor genes.3 Glycosylation changes arising during carcinogenesis most likely originate as a consequence of malignant transformation and changing growth and differentiation of the cancer cell. However, these glycosylation changes are critical for the biology of the cancer cell and influence their immunogenicity, cell adhesion and other properties. A mutated gene found in colon cancer appears to code for a member of the adhesion molecule family; this supports the idea that extracellular interactions are important in the control of cell growth.4 The regulation of glycosyltransferase gene expression may be linked to the activation of oncogenes. A major challenge is to understand the control of glycosylation during malignant transformation. As discussed in chapter 8, many factors contribute to the biosynthesis of glycans.

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  1. Department of Biochemistry, Research Institute, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada

    Inka Brockhausen Ph.D. & William Kuhns M.S., M.D.

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© 1997 Springer-Verlag Berlin Heidelberg

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Brockhausen, I., Kuhns, W. (1997). Glycosylation in Cancer and Oncogenic Transformation. In: Glycoproteins and Human Disease. Medical Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-21960-7_19

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  • DOI: https://doi.org/10.1007/978-3-662-21960-7_19

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