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Childhood Acute Myeloid Leukemia/Other Myeloid Malignancies Treatment (PDQ®): Treatment - Health Professional Information [NCI] - Classification of Pediatric Myeloid Malignancies

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Other extremely rare subtypes of AML include acute eosinophilic leukemia and acute basophilic leukemia.

Fifty percent to 60% of children with AML can be classified as having M1, M2, M3, M6, or M7 subtypes; approximately 40% have M4 or M5 subtypes. About 80% of children younger than 2 years with AML have an M4 or M5 subtype. The response to cytotoxic chemotherapy among children with the different subtypes of AML is relatively similar. One exception is FAB subtype M3, for which all-trans retinoic acid plus chemotherapy achieves remission and cure in approximately 70% to 80% of affected children.

World Health Organization (WHO) Classification System

In 2002, the WHO proposed a new classification system that incorporated diagnostic cytogenetic information and more reliably correlated with outcome. In this classification, patients with t(8;21), inv(16), t(15;17), and those with MLL translocations, which collectively constituted nearly half of the cases of childhood AML, were classified as "AML with recurrent cytogenetic abnormalities." This classification system also decreased the bone marrow percentage of leukemic blast requirement for the diagnosis of AML from 30% to 20%; an additional clarification was made so that patients with recurrent cytogenetic abnormalities did not need to meet the minimum blast requirement to be considered AML.[9,10,11] In 2008, WHO expanded the number of cytogenetic abnormalities linked to AML classification, and for the first time included specific gene mutations (CEBPA and NPM mutations) in its classification system.[12] (Refer to the WHO classification of myeloid leukemias section of this summary for more information.) Such a genetically based classification system links AML class with outcome and provides significant biologic and prognostic information. With new emerging technologies aimed at genetic, epigenetic, proteomic, and immunophenotypic classification, AML classification will likely evolve and provide informative prognostic and biologic guidelines to clinicians and researchers.

WHO classification of AML

  • AML with recurrent genetic abnormalities:
    • AML with t(8;21)(q22;q22), RUNX1-RUNX1T1(CBFA/ETO).
    • AML with inv(16)(p13;q22) or t(16;16)(p13;q22), CBFB-MYH11.
    • APL with t(15;17)(q22;q11-12), PML-RARA.
    • AML with t(9;11)(p22;q23), MLLT3-MLL.
    • AML with t(6;9)(p23;q34), DEK-NUP214.
    • AML with inv(3)(q21;q26.2) or t(3;3)(q21;q26.2), RPN1-EVI1.
    • AML (megakaryoblastic) with t(1;22)(p13;q13), RBM15-MKL1.
    • AML with mutated NPM1.
    • AML with mutated CEBPA.
  • AML with myelodysplasia-related features.
  • Therapy-related myeloid neoplasms.
  • AML, not otherwise specified:
    • AML with minimal differentiation.
    • AML without maturation.
    • AML with maturation.
    • Acute myelomonocytic leukemia.
    • Acute monoblastic and monocytic leukemia.
    • Acute erythroid leukemia.
    • Acute megakaryoblastic leukemia.
    • Acute basophilic leukemia.
    • Acute panmyelosis with myelofibrosis.
  • Myeloid sarcoma.
  • Myeloid proliferations related to Down syndrome:
    • Transient abnormal myelopoiesis.
    • Myeloid leukemia associated with Down syndrome.
  • Blastic plasmacytoid dendritic cell neoplasm.
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