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. Author manuscript; available in PMC: 2023 Jul 1.
Published in final edited form as: Exp Hematol. 2022 Apr 10;111:13–24. doi: 10.1016/j.exphem.2022.04.001

Figure 1:

Figure 1:

Mechanisms of Resistance to tyrosine kinase inhibitors in FLT3 mutated AML. A. Altered signaling in previously untreated newly diagnosed or relapsed AML with mutated FLT3. B. Decreased FLT3 mediated signaling and induction of apoptosis with tyrosine kinase inhibitor treatment in sensitive cells carrying FLT3 mutations. C. Mutations associated with resistance in relapsed refractory FLT3 mutated AML treated with tyrosine kinase inhibitors. Star indicates reported mutations. D. Altered cellular regulatory processes that allow for improved survival in treatment resistant cell lines or relapsed or refractory AML samples. Increased survival can be mediated through upregulation of alternative cell surface receptors or ligand-mediated signaling (1), expression of anti-apoptotic proteins (2), and STAT5 activation by mutated FLT3 in the endoplasmic reticulum (ER) (3).