ABSTRACT
Acute myeloid leukemia (AML) is a clonal proliferation of immature hematopoietic precursors involving primarily the bone marrow (BM) and blood [1]. The classification of acute leukemia is based on morphologic, immunophenotypic, cytogenetic, molecular, and clinical data. Generally, acute leukemias are divided into acute lymphoblastic leukemia (ALL) and AML, with a subset of leukemias displaying features of both types (mixed phenotype acute leukemia; MPAL). AML represents a heterogeneous group of disorders with variable clinical presentation, cellular morphology, immunophenotype, chromosomal and molecular changes, therapeutic response, and overall prognosis. Generally, AML can be defined as a clonal malignancy of transformed multipotent hematopoietic progenitor cells leading to accumulation of immature cells in the BM that replace normal elements causing cytopenias and their complications (e.g., fatigue due to anemia, infections due to granulocytopenia, and bleeding due to thrombocytopenia). AMLs can be broadly categorized into: (1) primary (de novo) AML; (2) secondary AML arising from an antecedent myeloid malignancy such as myelodysplastic syndrome (MDS), myeloproliferative neoplasm (MPN) or mixed MDS/MPN; and (3) therapy-related AML (tAML) arising as a complication of prior toxic therapy (due to treatment with DNA-damaging agents or radiotherapy). The diagnosis and prognosis are most accurately provided by pretreatment assessment of the morphology, immunophenotype, and most importantly, underlying chromosomal and/or molecular aberrations (Figure 37.1). The World Health Organization (WHO) classifies AML based on genetic, immunophenotypic, and clinical characteristics into (1) AML with recurrent genetic abnormalities, (2) AML, not otherwise specified (AML, NOS), (3) AML with myelodysplasia-related changes (AML-MRC), and (4) therapy-related myeloid neoplasm (Table 37.1). AML, NOS is subdivided further based on morphologic criteria similar to prior FAB (French-American-British) classification (see Chapter 38).
