Acute-onset hypokalemic paralysis with arsenic trioxide therapy in patient with acute promyelocytic leukemia

Acute myeloid leukemia (AML) is characterized by clonal proliferation of myeloid precursors with a reduced capacity to differentiate into mature cellular components.¹ Acute promyeloctic leukemia (APL; previously called AML-M3), a subtype of AML, is further characterized by a balanced translocation t(15;17) (q24.1;q21.1). It is an interesting model in cancer research because it responds to the differentiation and apoptosis induction therapy using arsenic trioxide (ATO) and all-trans retinoic acid (ATRA).²

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