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 Blood, 15 July 2004, Vol. 104, No. 2, pp. 561-564.
Prepublished online as a Blood First Edition Paper on March 25, 2004; DOI 10.1182/blood-2003-11-3801.

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NEOPLASIA
Brief report

Complete remission of TEL-PDGFRB–induced myeloproliferative disease in mice by receptor tyrosine kinase inhibitor SU11657

Jennifer A. Cain, Jay L. Grisolano, A. Douglas Laird, and Michael H. Tomasson

From the Division of Oncology, Departments of Medicine and Genetics, Siteman Cancer Center, Washington University School of Medicine, St Louis, MO; and Preclinical Research and Exploratory Development, SUGEN Inc, South San Francisco, CA.

The TEL-PDGFRB fusion oncogene is associated with chronic myelomonocytic leukemia (CMML) and results in the expression of a constitutively active tyrosine kinase. SU11657 is a multitargeted selective inhibitor of class III/V receptor tyrosine kinases, including the platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) receptors KIT and FLT3. SU11657 inhibited TEL/PDGF{beta}R kinase activity at nanomolar concentrations and inhibited TELPDGFRB-mediated factor-independent growth in myeloblastic 32D cells. Daily oral administration of SU11657 at 40 mg/kg suppressed myeloproliferation and significantly prolonged survival in TELPDGFRB mice treated prior to disease development, as well as in those with large tumor burdens. Our findings suggest that SU11657 or similar agents may have therapeutic potential in humans with hematologic malignancies expressing PDGFR fusion oncogenes. (Blood. 2004;104:561-564)


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