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Antisense Oligonucleotides to Protein Kinase C-α and C-raf Kinase: Rationale and Clinical Experience in Patients with Solid Tumors

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Book cover Antisense Research and Application

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 131))

Abstract

The mechanisms of action of classical small-molecule cytotoxic chemotherapy are varied, but each depends in part on excessive proliferation of tumor cells relative to that of normal tissue for their therapeutic indices. Small-molecule chemotherapeutic agents have narrow therapeutic indices for a variety of reasons. The most global reason is simply that small molecules do not specifically target cancer cells. However, in addition cytotoxic agents lack target specificity. While designed with specific mechanisms or targets in mind, many small molecules inhibit additional proteins, whether intracellular, membrane associated, or at the cell surface. Historically, the screening process for identifying new anticancer agents has selected agents for their ability to inhibit tumor growth in various animal models rather than with significant consideration for target selectivity.

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© 1998 Springer-Verlag Berlin Heidelberg

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Dorr, F.A., Kisner, D.L. (1998). Antisense Oligonucleotides to Protein Kinase C-α and C-raf Kinase: Rationale and Clinical Experience in Patients with Solid Tumors. In: Crooke, S.T. (eds) Antisense Research and Application. Handbook of Experimental Pharmacology, vol 131. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58785-6_16

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  • DOI: https://doi.org/10.1007/978-3-642-58785-6_16

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-63730-8

  • Online ISBN: 978-3-642-58785-6

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