Classification of acute myeloid leukemia
- Charles A Schiffer, MD
Charles A Schiffer, MD
- Professor of Medicine and Oncology
- Barbara Ann Karmanos Cancer Institute
- Wayne State University School of Medicine
- Sandeep Gurbuxani, MBBS, PhD
Sandeep Gurbuxani, MBBS, PhD
- Assistant Professor, Section of Hematopathology, Department of Pathology
- University of Chicago
Acute myeloid leukemia (AML) consists of a group of relatively well-defined hematopoietic neoplasms involving precursor cells committed to the myeloid line of cellular development (ie, those giving rise to granulocytic, monocytic, erythroid, or megakaryocytic elements) (table 1). AML has also been called acute myelogenous leukemia and acute non-lymphocytic leukemia.
AML is characterized by a clonal proliferation of myeloid precursors with a reduced capacity to differentiate into more mature cellular elements. As a result, there is an accumulation of leukemic blasts or immature forms in the bone marrow, peripheral blood, and occasionally in other tissues, with a variable reduction in the production of normal red blood cells, platelets, and mature granulocytes. The increased production of malignant cells, along with a reduction in these mature elements, results in a variety of systemic consequences including anemia, bleeding, and an increased risk of infection. (See "Clinical manifestations, pathologic features, and diagnosis of acute myeloid leukemia" and "Pathogenesis of acute myeloid leukemia".)
Following diagnosis, AML is classified using the World Health Organization (WHO) classification system based upon a combination of morphology, immunophenotype, genetics, and clinical features [1-3]. The classification attempts to identify biologic entities in the hopes that future work will elucidate molecular pathways that might be amenable to targeted therapies.
There are six main groups of AML recognized in this classification system [1,3-5]:
●AML with recurrent genetic abnormalities
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- AML WITH RECURRENT GENETIC ABNORMALITIES
- Defined structural abnormalities
- - AML with t(8;21)(q22;q22); RUNX1-RUNX1T1
- - AML with inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB-MYH11
- - APL with PML-RARA
- - AML with t(9;11)(p21.3;q23.3); MLLT3-KMT2A
- - AML with t(6;9)(p23;q34.1); DEK-NUP214
- - AML with inv(3)(q21.3q26.2) or t(3;3)(q21.3;q26.2); GATA2,MECOM
- - AML (megakaryoblastic) with t(1;22)(p13.3;q13.3); RBM15-MKL1
- - AML with BCR-ABL1
- AML with gene mutations
- - AML with mutated NPM1
- - AML with biallelic mutations of CEBPA
- - AML with mutated RUNX1
- AML WITH MDS-RELATED FEATURES
- THERAPY-RELATED AML
- AML NOT OTHERWISE SPECIFIED
- AML with minimal differentiation (FAB M0)
- AML without maturation (FAB M1)
- AML with maturation (FAB M2)
- Acute myelomonocytic leukemia (FAB M4)
- Acute monoblastic and monocytic leukemia (FAB M5)
- Pure erythroid leukemia (FAB M6)
- Acute megakaryoblastic leukemia (FAB M7)
- Acute basophilic leukemia
- Acute panmyelosis with myelofibrosis
- MYELOID SARCOMA
- MYELOID PROLIFERATIONS RELATED TO DOWN SYNDROME