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Molecular Pathways |
Authors' Affiliation: Department of Pediatrics, University of California, San Francisco
Requests for reprints: Benjamin S. Braun or Kevin Shannon, HSE 302, Box 0519, Department of Pediatrics, University of California San Francisco, 513 Parnassus Avenue, San Francisco, California 94143. Phone: 415-476-2876; Fax: 415-502-5127; E-mail: braunb{at}peds.ucsf.edu or shannonk{at}peds.ucsf.edu.
Abstract
Ras proteins normally relay growth-promoting signals from many activated cell surface receptors, and they are altered by oncogenic point mutations in
30% of human cancers. Activating KRAS and NRAS mutations are especially common in malignancies of the pancreas, lung, and colon, and in myeloid leukemia. Here, we discuss general strategies for targeting hyperactive Ras signaling in cancer cells with specific reference to myeloid malignancies.
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