Master Acute Myelogenous Leukemia (AML) with Picmonic for Medicine

Acute myelogenous leukemia (AML) is characterized by an accumulation of immature myeloid forms, also called blasts, caused by acquired oncogenic mutations that impede the normal differentiation process. The accumulation of these immature blast forms suppress normal hematopoiesis and result in bone marrow failure and complications related to anemia, thrombocytopenia, and neutropenia. These neoplasms can occur at all ages but incidence rises throughout life and the median onset is at 60 years of age. There are several different types of AML and can be classified according to the French-American-British (FAB) classifications which divide AMLs into subtypes based on the degree of differentiation and the lineage of the leukemic blasts. The cytoplasm of myeloblasts often contains Auer rods, which are distinctive needle like granules. Auer rods are particularly numerous in the M3 FAB subtype, which is also associated with a (15;17) translocation called acute promyelocytic leukemia. The t(15;17) creates a fusion gene that codes a part of the retinoic acid receptor alpha fused to a protein called PML. This fusion protein can interact with transcriptional repressors causing the inhibition of granulocytic maturation. In addition, this form of AML is commonly associated with bleeding caused by disseminated intravascular coagulation caused by severe thrombocytopenia. A different type of AML, the M5 subtype, is characteristic for gum infiltration which can help differentiate this subtype from others. Treatment of AML depends on the type but can involve chemotherapy or bone marrow transplant. The M3 subtype is unique and responds to pharmacologic doses of all-trans retinoic acid, a form of vitamin A, by binding with the aforementioned fusion protein and antagonizing its inhibitor effect on the transcription of target genes.