AML
Our results show a widespread dependence of AML cells on autocrine activation of MET, as well as the key role of compensatory upregulation of HGF expression in maintaining leukemogenic signaling by this receptor.
Our results show a widespread dependence of <span class="disease" id="22683780-8-44-47">AML</span> cells on autocrine activation of MET, as well as the key role of compensatory upregulation of <span class="gene" id="22683780-8-142-145">HGF</span> expression in maintaining leukemogenic signaling by this receptor.