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Acute myeloid leukemia (AML) cell antigens are a heterogeneous group of surface proteins and receptors overexpressed on malignant myeloblasts and leukemic stem cells. This category includes well-characterized therapeutic targets such as CD33 (a sialic acid-binding lectin), CD123 (the interleukin-3 receptor alpha chain), CD47 (an immune checkpoint), and the FLT3 receptor tyrosine kinase (PubMed: 30206112). These antigens facilitate essential biological processes including pro-survival signaling, proliferation, and evasion of phagocytosis by the innate immune system (NIH: PMC7505671). In clinical practice, these molecules are targeted by a variety of modalities including monoclonal antibodies, antibody-drug conjugates (ADCs) like gemtuzumab ozogamicin, and chimeric antigen receptor (CAR) T-cell therapies. Because many of these antigens are also present on normal hematopoietic stem and progenitor cells, a primary therapeutic challenge is managing off-target myelosuppression (StatPearls: NBK507875). Monitoring these antigens is vital for diagnostic immunophenotyping and the assessment of minimal residual disease (MRD).
Targeting through antibody-drug conjugate (ADC) mediated cytotoxicity, T-cell redirection, blockade of 'don't eat me' signals, and inhibition of receptor tyrosine kinase signaling pathways.
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