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Detection of ras Gene Mutations Using Oligonucleotide Ligation Technology

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Tumor Marker Protocols

Part of the book series: Methods in Molecular Medicine™ ((MIMM,volume 14))

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Abstract

The human ras genes (H-, K-, and N-rus) are members of a superfamily of low-mol-wt GTP-binding proteins that function as G proteins in signal transduction pathways controlling cell proliferation and differentiation (1,2). Ras genes acquire oncogenic potential primarily as a result of point, missense mutations in codons 12, 13, or 61, producing single amino-acid substitutions that alter the ability of the protein to bind or hydrolyze GTP. The net consequence of somatic ras missense mutations is to lock the protein in a GTP-bound, active conformation, thus perturbing cellular physiology and contributing to tumorigenesis. Different tumor types show specificity of ras oncogene activation. For example, activated H-ras occurs most often in bladder cancers (3,4); K-ras mutations are found predominantly in pancreatic (90% cases), colon (40–50% cases) and lung carcinomas (57), and N-ras mutations are most often associated with hematopoietic malignancies, particularly myeloid leukemias (8,9).

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© 1998 Humana Press Inc, Totowa, NJ

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Eggerding, F.A. (1998). Detection of ras Gene Mutations Using Oligonucleotide Ligation Technology. In: Hanausek, M., Walaszek, Z. (eds) Tumor Marker Protocols. Methods in Molecular Medicine™, vol 14. Springer, Totowa, NJ. https://doi.org/10.1385/0-89603-380-5:341

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  • DOI: https://doi.org/10.1385/0-89603-380-5:341

  • Publisher Name: Springer, Totowa, NJ

  • Print ISBN: 978-0-89603-380-1

  • Online ISBN: 978-1-59259-598-3

  • eBook Packages: Springer Protocols

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