Introduction: Acute Myeloid Leukemia is a heterogeneous hematological malignancy characterized by the uncontrolled proliferation of abnormal myeloid cells. Besides several other genetic abnormalities developed in AML, FLT3 mutations are significant due to their worse prognostic impacts and therapeutic resistance. As a result, these mutations enable AML cells to develop mechanisms for evading immune surveillance.
Areas Covered: This review discusses the ways of immune escape of FLT3-mutated AML cells. A literature search was conducted on PubMed, Scopus, and Web of Science databases, covering articles published between 2010 and 2024 with related keywords. The discussion covers AML cells' downregulation of immune recognition markers, expression of immune checkpoint proteins, and establishment of an immunosuppressive tumor microenvironment. Specific attention is given to small extracellular vesicles and their participation in immune escape. The focus is on exosome-mediated pathways and possible combination therapies.
Expert Opinion: FLT3 mutations in AML represent a formidable therapeutic challenge due to their crucial role in immune evasion. Exosomes are major players in these processes. Combination therapies targeting the exosome pathway could significantly improve these patients' immune recognition and overall outcomes. Understanding the underlying mechanisms, including targeted therapies, will be required to transcend existing therapeutic limitations and push newer strategies in treatment.
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