Leukemia, Acute Myeloid



  • Acute myeloid leukemia (AML) is characterized by proliferation of abnormal immature myeloid progenitors (blasts) with reduced capacity to differentiate leading to bone marrow failure and a variety of systemic symptoms.
  • Historically, the French–American–British (FAB) classification system divided AML based on the cell morphology with the addition of cytogenetics (subtypes M0 to M7).
  • The World Health Organization (WHO) classification attempts to provide more meaningful prognostic information.
    • AML with characteristic genetic abnormalities: translocation t(8;21), t(15;17), and inversion in chromosome 16 inv(16)
    • AML with multilineage dysplasia: presence of a prior myelodysplastic syndrome (MDS) or myeloproliferative neoplasm (MPN) that transformed into AML
    • AML and MDS, therapy related
    • AML not otherwise categorized
    • Acute leukemias of ambiguous lineage (biphenotypic acute leukemia)


  • ~19,940 cases estimated in 2020, making it the most common type of leukemia in adults
  • Predominant sex: male ≥ female

The incidence of AML increases with age, and median age is 67 years.

Etiology and Pathophysiology

Precise causes unknown, but some risk factors have been identified (see “Risk Factors”).


  • Three risk groups
    • Good risk: inv(16), t(8;21), t(15;17)
    • Standard risk: normal karyotype
    • Poor risk: monosomy 5 and 7 (typically secondary AML), deletion 5q, abnormalities of 11q23, or complex karyotype
  • FLT3 gene mutations, especially internal tandem duplications (FLT3-ITD), have been associated with poor survival in AML. These and growing list of (onco)gene (e.g., NPM1, IDH1/2, DNMT3A, and P53) mutations have been studied to further risk-stratify patients (1).

Risk Factors

  • Genetic predisposition (e.g., Down syndrome); Bloom syndrome (~25% develop AML), Fanconi anemia (52%), neurofibromatosis, Li-Fraumeni syndrome, Wiskott-Aldrich syndrome, Kostmann syndrome, and Diamond-Blackfan anemia
  • Radiation exposure
  • Immunodeficiency states
  • Chemical and drug exposure (nitrogen mustard and alkylating agents; benzene)
  • MDS
  • Cigarette smoking

General Prevention

None currently identified, but treatment of high-risk MDS with hypomethylating agents (5-azacitidine [Vidaza]) has been shown to prolong time to transformation from MDS into AML

Commonly Associated Conditions

  • Disseminated intravascular coagulopathy (DIC) especially in acute promyelocytic leukemia (APL) but may be seen in any AML
  • Leukostasis (high blast number and increased adhesive ability of blasts)
  • Tumor lysis syndrome (TLS): spontaneous or in response to chemotherapy

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