Adapted from Leather HL Bickert B Acute Leukemias In DiPiro JTP Talbert RLr Yee GC et a I [eds Pharmacotherapy A Pathophysiologic Approach 6th ed New York McGraw Hill 2005 248525R

Table 95-4 WHO Classification of AML

AML with recurrent genetic abnormalities: AML with t(8;21)(q22;q22), (AML1/ETO)

AML with abnormal bone marrow eosinophils and inv(16)(p13q22) or t(16;16)(p13;q22), (CBFß/ MYH11)

Acute promyelocytic leukemia with t(15;17)(q22;q12), (PML/RARa) and variants AML with 11q23 (MLL) abnormalities AML with multilineage dysplasia Following MDS or MDS/MPD

Without antecedent MDS or MDS/MPD, but with dysplasia in at least 50% of cells in 2 or more myeloid lineages

AML and MDSs, therapy related Alkylating agent/radiation-related type

Topoisomerase II inhibitor-related type (some may be lymphoid) Others

AML, not otherwise categorized Classify as:

AML, minimally differentiated

AML without maturation

AML with maturation

Acute myelomonocytic leukemia

Acute monoblastic/acute monocytic leukemia

Acute erythroid leukemia (erythroid/myeloid and pure erythroleukemia)

Acute megakaryoblastic leukemia

Acute basophilic leukemia

Acute panmyelosis with myelofibrosis

Myeloid sarcoma

AML, acute myeloid leukemia; MDS, myelodysplastic syndrome; MPD, myeloproliferative disorders. Adapted from Ref. 6.

Classification methods for leukemia have evolved from simple schemes that were largely phenotypic and considered only age, gender, WBC, and blast morphology to now-complex methods that include biological features such as cell-surface receptors, DNA content (ploidy; more or less then normal chromosomal DNA content), and a variety of cytogenetic abnormalities.

Markers on the cell surface or membrane of the lymphoblast can be used to classify ALL. Among the early classification system was the FAB scheme, which was based purely on morphology and apparent degree of cellular differentiation. This system is no longer used, and the current classification of acute leukemias is based on features that can be identified only by immunological and molecular analyses. Markers on the cell surface or membranes of the leukemic cell (lymphoblasts) are now more regularly used to classify ALL and to assign prognosis and, in turn, treatment.

Immunophenotyping by flow cytometry has taken on an increasingly important role in the diagnosis of leukemia. Owing to the ease of application, sensitivity, and quantifiable results, flow cytometry is the preferred method for leukemic lineage as well as prognostic assignment.8 This approach takes advantage of the development of monoclonal antibodies (MABs) to many cell-surface antigens that are differentially expressed during hematopoietic differentiation. The antigens are referred to as antibody cluster determinants (CDs) that define cells at various stages of development and can easily separate ALL from AML and T-cell from preB-cell ALL.5,11 The combined approach of flow cytometric identification and cytogenetic DNA content, much of which is also revealed by flow cytometry and fluorescent in-situ hybridization (FISH; microscopic, fluorescence identification of chromosomal features) has facilitated diagnosis and delineation of specific treatments for the major subtypes of the acute leukemias. Common immunophenotypic markers seen in AML and ALL are provided in Table 95-5.

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