hematology and oncology
Acute Myeloid Leukemia (AML)
Classification of AML
Acute myeloid leukemia has a number of subtypes and precursor neoplasms that are distinguished from each other by morphology, immunophenotype, cytochemistry, and genetic abnormalities (see also The 2016 World Health Organization [WHO]Classification of myeloid neoplasms) all of which have important implications for prognosis and treatment. Seven classes are described in the WHO classification, including AML with recurrent genetic abnormalities AML with myelodysplasia-related changes (AML-MRC) Therapy-related AML (t-AML) AML, not otherwise specified (NOS) Myeloid sarcoma Myeloid proliferations related to Down syndrome Blastic plasmacytoid dendritic cell neoplasm Morphologic criteria from the previous French-American-British (FAB) classification system are used for subtypes that are not otherwise specified (NOS). is a subtype of AML with recurrent genetic abnormalities. APL is a particularly important subtype, representing 10 to 15% of all cases of AML, striking a younger age group (median age 31 years) and particular ethnicity (Hispanics). Patients commonly present with a coagulation disorder (eg, Disseminated Intravascular Coagulation (DIC) [DIC]). Therapy-related AML (t-AML)is a subtype of AML caused by prior treatment with certain antineoplastic drugs (eg, alkylating agents,hydroxyurea, and topoisomerase II inhibitors). Most t-AMLs occur 3 to 10 years after initial therapy, with a longer latency for alkylating agents andhydroxyurea(mean latency 5 to 7 years) than for topoisomerase II inhibitors (mean latency 6 months to 3 years). Alkylating agents cause chromosomal deletions and unbalanced translocations.Hydroxyureacauses del(17)p and also inhibitsTP53activation. Topoisomerase II inhibitors lead to balanced chromosomal translocations. Myeloid sarcomais characterized by extramedullary myeloblastic infiltration of skin (leukemia cutis), gingiva, and other mucosal surfaces. 