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The identification of activating mutations in the receptor tyrosine kinase c-KIT in acute myelogenous leukemia (AML) coupled with the development of potent c-KIT inhibitors provides an approach for potentially improving survival in a disease where outcomes remain unsatisfactory.1 However, despite the in vitro sensitivity of c-KIT mutant cell lines to c-KIT inhibitors, primary resistance in patients remains a significant concern. Direct interactions between leukemia cells and bone marrow stromal cells in the hematopoietic microenvironment (HM) as well as soluble factors secreted by stromal cells can support leukemic cell proliferation and survival in the presence of cytotoxic and molecularly targeted therapies. Accordingly, defining the mechanisms by which the microenvironment contributes to leukemia growth and therapy resistance is essential for ensuring the success of c-KIT inhibitors, and other new therapies, as they advance from the laboratory to the clinic.

Cytokines secreted by bone marrow stromal cells protect c-KIT mutant AML cells from c-KIT inhibitor-induced apoptosis