Cancer Health Center

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In the following outline and discussion, the older FAB classifications are noted where appropriate.

• AML with characteristic genetic abnormalities.
  • AML with t(8; 21)(q22;q22); (AML/ETO).
  • AML with inv(16)(p13q22) or t(16;16)(p13; q22); (CBF?/MYH11).
  • Acute promyelocytic leukemia (AML with t(15;17)(q22; q12); (PML/RAR?) and variants).
  • AML with 11q23 (MLL) abnormalities.
• AML with an FLT3 mutation (not in the WHO classification scheme).
• AML with multilineage dysplasia.
• AML and MDS, therapy related.
  • Alkylating agent-related AML and MDS.
  • Topoisomerase II inhibitor-related AML.
• AML not otherwise categorized.
  • Acute myeloblastic leukemia, minimally differentiated (FAB Classification M0).
  • Acute myeloblastic leukemia without maturation (FAB Classification M1).
  • Acute myeloblastic leukemia with maturation (FAB Classification M2).
  • Acute myelomonocytic leukemia (AMML) (FAB Classification M4).
  • Acute monoblastic leukemia and acute monocytic leukemia (FAB classifications M5a and M5b).
  • Acute erythroid leukemias (FAB classifications M6a and M6b).
  • Acute megakaryoblastic leukemia (FAB Classification M7).
    • AML/transient myeloproliferative disorder in Down syndrome.
  • Acute basophilic leukemia.
  • Acute panmyelosis with myelofibrosis.
  • Myeloid sarcoma.
• Acute leukemias of ambiguous lineage.

Acute Myeloid Leukemia (AML) With Characteristic Genetic Abnormalities

This category is characterized by characteristic genetic abnormalities and frequently high rates of remission and favorable prognoses with the notable exception of those with 11q23 abnormalities.[13] The reciprocal translocations t(8; 21), inv(16) or t(16;16), t(15; 17), and translocations involving the 11q23 breakpoint are the most commonly identified genetic abnormalities. These structural chromosome rearrangements result in the formation of fusion genes that encode chimeric proteins that may contribute to the initiation or progression of leukemogenesis. Many of these translocations are detected by reverse transcriptase-polymerase chain reaction (RT-PCR) or fluorescence in situ hybridization (FISH), which has a higher sensitivity than cytogenetics. Other recurring cytogenetic abnormalities are less common and described below in AML not otherwise categorized.

Acute myeloid leukemia with t(8; 21)(q22; q22); (AML/ETO)

AML with the translocation t(8; 21)(q22; q22) (occurring most commonly in FAB classification M2) is one of the most common genetic aberrations in AML and accounts for 5% to 12% of cases of AML and 33% of karyotypically abnormal cases of acute myeloblastic leukemia with maturation.[14] Myeloid sarcomas (chloromas) may be present and may be associated with a bone marrow blast percentage of less than 20%.

Common morphologic features include the following:

• Large blasts with abundant basophilic cytoplasm, often containing numerous azurophilic granules.
• A few blasts in some cases show very large granules (pseudo Chediak-Higashi granules).
• Auer rods, which may be detected in mature neutrophils.
• Smaller blasts, predominantly in the peripheral blood.
• Promyelocytes, myelocytes, and mature neutrophils with variable dysplasia in the bone marrow.
• Abnormal nuclear segmentation (pseudo Pelger-Huet nuclei) and/or cytoplasmic staining abnormalities.
• Increased eosinophil precursors.
• Reduced or absent monocytes.
• Normal erythroblasts and megakaryocytes.