Journal
ONCOGENE
Volume 21, Issue 21, Pages 3314-3333Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1205317
Keywords
leukemia; lymphoma; protein tyrosine kinase; signal transduction; translocation
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Tyrosine kinase oncogenes are formed as a result of mutations that induce constitutive kinase activity. Many of these tyrosine kinase oncogenes that are derived from genes, such as c-Abl, c-Fes, FIt3, c-Fms, c-Kit and PDGFRbeta, that are normally involved in the regulation of hematopoiesis or hematopoietic cell function. Despite differences in structure, normal function, and subcellular location, many of the tyrosine kinase oncogenes signal through the same pathways, and typically enhance proliferation and prolong viability. They represent excellent potential drug targets, and it is likely that additional mutations will be identified in other kinases, their immediate downstream targets, or in proteins regulating their function.
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