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Myeloid leukemia cells are malignant hematopoietic cells of the myeloid lineage, primarily found in the bone marrow and peripheral blood of patients with leukemia [1,2]. These cells, often referred to as blasts in acute forms, exhibit a block in differentiation and uncontrolled proliferation, which suppresses normal hematopoiesis and leads to bone marrow failure [2,3]. They are the hallmark of diseases such as Acute Myeloid Leukemia (AML) and Chronic Myeloid Leukemia (CML) [1,2]. While not a single molecular target, these cells harbor numerous specific therapeutic targets such as FLT3, IDH1/2, and BCR-ABL1, which are exploited by modern targeted therapies [4,5]. Current treatment strategies aim to eradicate these cells through cytotoxic chemotherapy, targeted small molecule inhibitors, or antibody-drug conjugates that recognize specific surface antigens like CD33 [3,5]. Because 'Myeloid leukemia cells' refers to a heterogeneous population of diseased cells rather than a specific protein or gene, it is classified as a disease-state cell type rather than a singular therapeutic molecular target [1,4].
Drugs targeting these cells work via diverse mechanisms including DNA synthesis inhibition, induction of apoptosis through BCL-2 inhibition, and targeted inhibition of oncogenic proteins such as FLT3, IDH1/2, or BCR-ABL1 to restore differentiation and eliminate malignant clones.
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