¹Department of Adult Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts, MA 02115, USA

²Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

Correspondence to: J D Griffin, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. E-mail: james_griffin@dfci.harvard.edu

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, Flt3, c-Fms, c-Kit and PDGFR, 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.

Oncogene (2002) 21, 3314-3333 DOI: 10.1038/sj/onc/1205317

leukemia; lymphoma; protein tyrosine kinase; signal transduction; translocation