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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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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.

AML with maturation (FAB classification M2) is the most common morphologic type correlating with t(8; 21). Rarely, AML with this translocation presents with a bone marrow blast percentage less than 20%.[13]

The translocation t(8; 21)(q22; q22) involves the AML1 gene, also known as RUNX1, which encodes core binding factor-alpha (CBF-alpha), and the ETO (eight-twenty-one) gene.[13,15] The AML1/ETO fusion transcript is consistently detected in patients with t(8; 21) AML. This type of AML is usually associated with a good response to chemotherapy and a high complete remission rate with long-term survival when treated with high-dose cytarabine in the postremission phase as in the Cancer and Leukemia Group B (CLB-9022 and CLB-8525) trials.[16,17,18,19] Additional chromosome abnormalities are common, e.g., loss of a sex chromosome and del(9)(q22). Expression of the neural cell adhesion molecule CD56 appears to be an adverse prognostic indicator.[20,21]

Acute myeloid leukemia with inv(16)(p13; q22) or t(16; 16)(p13; q22); (CBFβ/MYH11)

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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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