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Adult Acute Myeloid Leukemia Treatment (PDQ®): Treatment - Health Professional Information [NCI] - Classification of Adult Acute Myeloid Leukemia

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Topoisomerase II inhibitor-related acute myeloid leukemia

This type of AML occurs in patients treated with topoisomerase II inhibitors. The agents implicated are the epipodophyllotoxins etoposide and teniposide and the anthracyclines doxorubicin and 4-epi-doxorubicin.[49] The mean latency period from the time of institution of the causative therapy to the development of AML is approximately 2 years.[55] Morphologically, there is a significant monocytic component. Most cases are categorized as acute monoblastic or myelomonocytic leukemia. Other morphologies reported include acute promyelocytic leukemia, myelodysplastic syndromes, and acute megakaryoblastic leukemia.[49]

As with alkylating agent/radiation-related acute leukemias and myelodysplastic syndromes, the cytogenetic abnormalities are often complex.[50,52,53,54] The predominant cytogenetic finding involves chromosome 11q23 and the MLL gene.[50,56] Current data are insufficient to predict survival times.

Acute Myeloid Leukemia Not Otherwise Categorized

Cases of AML that do not fulfill the criteria for AML with recurrent genetic abnormalities, AML with multilineage dysplasia, or AML and MDS, therapy-related, fall within this category. Classification within this category is based on leukemic cell features of morphology, cytochemistry, and maturation.[57]

Acute myeloblastic leukemia, minimally differentiated (FAB Classification M0)

This AML shows no evidence of myeloid differentiation by morphology and light microscopy cytochemistry.[58] The myeloid nature of the blasts is demonstrated by immunophenotyping and/or ultrastructural studies.[57] Immunophenotyping studies must be performed to distinguish this acute leukemia from acute lymphoblastic leukemia (ALL).[57] Cases of AML, minimally differentiated, comprise approximately 5% of cases of AML. Patients with this AML typically present with evidence of marrow failure, thrombocytopenia, and neutropenia.[58]

Morphologic and cytochemical features include the following:

  • Medium-sized blasts with dispersed nuclear chromatin.
  • Agranular cytoplasm.
  • Occasionally small blasts that resemble lymphoblasts.
  • Cytochemistry negative for myeloperoxidase (MPO), Sudan Black B (SBB), and naphthol ASD chloroacetate esterase (<3% positive blasts).
  • Cytochemistry negative for alpha naphthyl acetate and butyrate esterases.
  • Markedly hypercellular marrow.

Immunophenotyping reveals blast cells that express one or more panmyeloid antigens (CD13, CD33, and CD117) and are negative for B and T lymphoid-restricted antigens. Most cases express primitive hematopoietic-associated antigens (CD34, CD38, and HLA-DR). The differential diagnosis includes ALL, acute megakaryoblastic leukemia, biphenotypic/mixed lineage acute leukemia, and, rarely, the leukemic phase of large cell lymphoma. Immunophenotyping studies are required to distinguish these disorders.[57]

Although no specific chromosomal abnormalities have been found in AML, minimally differentiated point mutations of the AML1 gene have been observed in approximately 25% of cases. This mutation appears to correlate clinically with a higher white blood cell count and greater marrow blast involvement.[57,59] Mutation of FLT3, a receptor tyrosine kinase gene, occurs in approximately 25% of cases and has been associated with short survival.[40,59] The median OS is approximately 10 months.[60]

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WebMD Public Information from the National Cancer Institute

Last Updated: February 25, 2014
This information is not intended to replace the advice of a doctor. Healthwise disclaims any liability for the decisions you make based on this information.
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