This report identifies upregulation of HGF as an autocrine growth pathway in several subsets of AML. Ligand-dependent activation of MET represents a new oncogenic stimulus, and the dynamic regulation of HGF can overcome the effects of MET inhibition. These results suggest that combination treatments may be needed to disrupt this autocrine signaling loop and quell the growth of AML.
- Alex Kentsis
- Casie Reed
- A Thomas Look
