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. Therefore the number of circulating myeloblasts are typically increased on peripheral smear.
These neoplasms can occur at all ages but incidence rises throughout life and the median onset is at 60 years of age.
The M3 FAB subtype is associated with a (15;17) translocation called acute promyelocytic leukemia (APML or APL). The t(15;17) creates a fusion gene that encodes a part of the retinoic acid receptor alpha fused to a protein called PML. This fusion protein can interact with transcriptional repressors which result in the inhibition of granulocytic maturation.
The cytoplasm of myeloblasts often contains Auer rods, which are distinctive needle-like granules. Auer rods are particularly numerous in the M3 FAB subtype and identification of these rods on histology can help with disease diagnosis.
In addition, this form of AML is commonly associated with bleeding caused by disseminated intravascular coagulation (DIC) caused by severe thrombocytopenia.
Of note, the M5 subtype (Acute Monocytic Leukemia) is characteristic for gum infiltration, which can help differentiate this subtype from others.
Translocation guides therapy because these tumors respond to pharmacologic doses of all trans retinoic acid (a form of vitamin A) by binding with the fusion protein and antagonizing its inhibitor effect on the transcription of target genes. The M3 subtype of AML, otherwise known as APL, is the one that is responsive mainly to this treatment.
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