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Acute Myelogenous Leukemia

  • Author: Karen Seiter, MD; Chief Editor: Emmanuel C Besa, MD  more...
Updated: Nov 09, 2015


Acute myelogenous leukemia (AML) is a malignant disease of the bone marrow in which hematopoietic precursors are arrested in an early stage of development. Most AML subtypes are distinguished from other related blood disorders by the presence of more than 20% blasts in the bone marrow.

See Chronic Leukemias: 4 Cancers to Differentiate, a Critical Images slideshow, to help detect chronic leukemias and determine the specific type present.

The underlying pathophysiology in AML consists of a maturational arrest of bone marrow cells in the earliest stages of development. (See Pathophysiology.) Several factors have been implicated in the causation of AML, including antecedent hematologic disorders, familial syndromes, environmental exposures, and drug exposures. However, most patients who present with de novo AML have no identifiable risk factor. (See Etiology.)

Patients with AML present with symptoms resulting from bone marrow failure, symptoms resulting from organ infiltration with leukemic cells, or both. The time course is variable. (See Presentation.) The workup for AML includes blood tests, bone marrow aspiration and biopsy (the definitive diagnostic tests), and analysis of genetic abnormalities. (See Workup.)

Current standard chemotherapy regimens cure only a minority of patients with AML. As a result, all patients should be evaluated for entry into well-designed clinical trials. If a clinical trial is not available, the patient can be treated with standard therapy. (See Treatment.) Readmission is frequently required for the management of toxic effects of chemotherapy.



The underlying pathophysiology in AML consists of a maturational arrest of bone marrow cells in the earliest stages of development. The mechanism of this arrest is under study, but in many cases, it involves the activation of abnormal genes through chromosomal translocations and other genetic abnormalities.[1, 2, 3]

This developmental arrest results in 2 disease processes. First, the production of normal blood cells markedly decreases, which results in varying degrees of anemia, thrombocytopenia, and neutropenia. Second, the rapid proliferation of these cells, along with a reduction in their ability to undergo programmed cell death (apoptosis), results in their accumulation in the bone marrow, the blood, and, frequently, the spleen and liver.



Several factors have been implicated in the causation of AML, including antecedent hematologic disorders, familial syndromes, environmental exposures, and drug exposures. However, most patients who present with de novo AML have no identifiable risk factor.

Antecedent hematologic disorders

The most common risk factor for AML is the presence of an antecedent hematologic disorder, the most common of which is myelodysplastic syndrome (MDS). MDS is a bone marrow disease of unknown etiology that occurs most often in older patients and manifests as progressive cytopenias that occur over months to years. Patients with low-risk MDS (eg, refractory anemia with normal cytogenetics findings) generally do not develop AML, whereas patients with high-risk MDS (eg, refractory anemia with excess blasts-type 2) frequently do.

Other antecedent hematologic disorders that predispose patients to AML include aplastic anemia and myelofibrosis.

Congenital disorders

Some congenital disorders that predispose patients to AML include Bloom syndrome, Down syndrome, congenital neutropenia, Fanconi anemia, and neurofibromatosis. Usually, these patients develop AML during childhood; rarely, some may present in young adulthood.

More subtle genetic disorders, including polymorphisms of enzymes that metabolize carcinogens, also predispose patients to AML. For example, polymorphisms of NAD(P)H:quinone oxidoreductase (NQO1), an enzyme that metabolizes benzene derivatives, are associated with an increased risk of AML.[4] Particularly increased risk exists for AML that occurs after chemotherapy for another disease or for de novo AML with an abnormality of chromosomes 5, 7, or both.

Likewise, polymorphisms in glutathione S -transferase are associated with secondary AML after chemotherapy for other malignancies.[5]

Familial syndromes

Germline mutations in the gene AML1 (RUNX1, CBFA2) occur in the familial platelet disorder with predisposition for AML, an autosomal dominant disorder characterized by moderate thrombocytopenia, a defect in platelet function, and propensity to develop AML.[6] Mutation of CEBPA (the gene encoding CCAAT/enhancer binding protein alpha, a granulocytic differentiation factor and member of the bZIP family) was described in a family with 3 members affected by AML.[7]

Holme et al studied 27 families with familial MDS/AML. All of the families were screened for RUNX1, CEBPA, TERC, TERT, GATA2, TET2, and NPM1 mutations. Five of the 27 families had telomerase mutations (3 TERT, 2 TERC), one had a RUNX1 mutation, and four had heterozygous GATA2 mutations.[8]

Gao et al recently reviewed GATA2 mutations associated with familial AML-MDS.[9] GATA2 is a transcription factor crucial for hematopoietic differentiation and lymphatic formation, and germline GATA2 mutations are involved in a rare group of complex syndromes with overlapping clinical features of immune deficiency, lymphedema, and propensity to AML or MDS.

Some hereditary cancer syndromes, such as Li-Fraumeni syndrome, can manifest as leukemia. However, cases of leukemia are less common than the solid tumors that generally characterize these syndromes.

Environmental exposures

Several studies demonstrate a relationship between radiation exposure and leukemia. Early radiologists (before the use of appropriate shielding) were found to have an increased likelihood of developing leukemia. Patients receiving therapeutic irradiation for ankylosing spondylitis were at increased risk of leukemia. Survivors of the atomic bomb explosions in Japan were at a markedly increased risk for the development of leukemia.

Persons who smoke have a small but statistically significant (odds ratio, 1.5) increased risk of developing AML.[10] In several studies, the risk of AML was slightly increased in people who smoked compared with those who did not smoke.

Exposure to benzene is associated with aplastic anemia and pancytopenia. These patients often develop AML. Many of these patients demonstrate M6 morphology.

Previous exposure to chemotherapeutic agents

As more patients with cancer survive their primary malignancy and more patients receive intensive chemotherapy (including bone marrow transplantation [BMT]), the number of patients with AML increases because of exposure to chemotherapeutic agents. For example, the cumulative incidence of acute leukemia in patients with breast cancer who were treated with doxorubicin and cyclophosphamide as adjuvant therapy was 0.2-1.0% at 5 years.[11]

Patients with previous exposure to chemotherapeutic agents can be divided into 2 groups: (1) those with previous exposure to alkylating agents and (2) those with exposure to topoisomerase-II inhibitors.

Patients with a previous exposure to alkylating agents, with or without radiation, often have a myelodysplastic phase before the development of AML. Cytogenetics testing frequently reveals -5 and/or -7 (5q- or monosomy 7).

Patients with a previous exposure to topoisomerase-II inhibitors do not have a myelodysplastic phase. Cytogenetics testing reveals a translocation that involves band 11q23. Less commonly, patients developed leukemia with other balanced translocations, such as inversion 16 or t(15;17).[12]

The typical latency period between drug exposure and acute leukemia is approximately 3-5 years for alkylating agents/radiation exposure, but it is only 9-12 months for topoisomerase inhibitors.



The American Cancer Society estimates that 20,830 new cases of AML (12,730 in men, 8100 in women) will occur in the United States in 2015, accounting for 32% of all leukemia cases in adults 20 years of age and older.[13] AML is more commonly diagnosed in developed countries, and it is more common in whites than in other populations.

The prevalence of AML increases with age. The median age of onset is approximately 70 years. However, AML affects all age groups.

AML is more common in men than in women. The difference is even more apparent in older patients. This is likely because MDS is more common in men, and advanced MDS frequently evolves into AML. Some have proposed that the increased prevalence of AML in men may be related to occupational exposures (see Etiology).



The prognosis relies on several factors. Increasing age is an adverse factor, because older patients more frequently have a previous antecedent hematologic disorder along with comorbid medical conditions that compromise the ability to give full doses of chemotherapy. A previous antecedent hematologic disorder (most commonly, MDS) is associated with a poor outcome to therapy.

A study by Arellano et al found leukopenia at diagnosis had no prognostic significance in patients with AML.[14]

Findings from cytogenetic analysis of the bone marrow constitute one of the most important prognostic factors. Patients with t(8;21), t(15;17), or inversion 16 have the best prognosis, with long-term survival rates of approximately 65%. Patients with normal cytogenetic findings have an intermediate prognosis and have a long-term survival rate of approximately 25%. Patients with poor-risk cytogenetic findings (especially -7, -5) have a poor prognosis, with a long-term survival rate of less than 10%.

Other cytogenetic abnormalities, including +8, 11q23, and miscellaneous, have been reported to be intermediate risk in some series and poor risk in others.

The presence of an FLT3 mutation is associated with a poorer prognosis. Mutations in CEBPA are associated with a longer remission duration and longer overall survival. Mutations in NPM are associated with an increased response to chemotherapy.

A study by Metzeler et al determined that TET2 mutations had an adverse prognostic impact in an otherwise favorable-risk patient subset using the European LeukemiaNet (ELN) molecular-risk classification of patients with primary cytogenetically normal AML.[15]

In adults, treatment results are generally analyzed separately for younger (18-60 y) patients with AML and for older patients (>60 y). With current standard chemotherapy regimens, approximately 30-35% of adults younger than 60 years survive longer than 5 years and are considered cured. Results in older patients are more disappointing, with fewer than 10% of surviving over the long term.

A study by Kayser et al found that therapy-related AML (t-AML) was an adverse prognostic factor for death in complete remission but not relapse and overall survival in younger intensively treated patients.[16] It was also an adverse prognostic factor for relapse but not death in complete remission in older, less intensively treated patients.

A study by Varadarajan et al found that having ever smoked decreased overall survival in patients with AML.[17]

Crysandt and collegeues found that in younger patients with de novo AML, overweight and obesity were risk factors for an impaired response to induction therapy and shorter disease-free and overall survival.[18]  

The American Cancer Society estimates that in 2015, 10,460 deaths from AML will occur in the United States. Of these, 6110 are expected to occur in men and 4350 in women.[13] Death in patients with AML may result from uncontrolled infection or hemorrhage. This may happen even after use of appropriate blood product and antibiotic support.


Patient Education

Patients with AML should be instructed to call their healthcare providers immediately if they are febrile or have signs of bleeding.

For patient education resources, see the Blood and Lymphatic System Center and the Skin, Hair, and Nails Center, as well as Leukemia and Bruises.

Contributor Information and Disclosures

Karen Seiter, MD Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College

Karen Seiter, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Hematology

Disclosure: Received honoraria from Novartis for speaking and teaching; Received consulting fee from Novartis for speaking and teaching; Received honoraria from Celgene for speaking and teaching.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ronald A Sacher, MB, BCh, FRCPC, DTM&H Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, FRCPC, DTM&H is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society on Thrombosis and Haemostasis, Royal College of Physicians and Surgeons of Canada, American Clinical and Climatological Association, International Society of Blood Transfusion

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: GSK Pharmaceuticals,Alexion,Johnson & Johnson Talecris,,Grifols<br/>Received honoraria from all the above companies for speaking and teaching.

Chief Editor

Emmanuel C Besa, MD Professor Emeritus, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American Society of Clinical Oncology, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, New York Academy of Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Clarence Sarkodee Adoo, MD, FACP Consulting Staff, Department of Bone Marrow Transplantation, City of Hope Samaritan BMT Program

Clarence Sarkodee Adoo, MD, FACP is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Society of Hematology, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

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Table 1. Immunophenotyping of AML Cells
Marker Lineage
CD13 Myeloid
CD33 Myeloid
CD34 Early precursor
HLA-DR Positive in most AML, negative in APL
CD11b Mature monocytes
CD14 Monocytes
CD41 Platelet glycoprotein IIb/IIIa complex
CD42a Platelet glycoprotein IX
CD42b Platelet glycoprotein Ib
CD61 Platelet glycoprotein IIIa
Glycophorin A Erythroid
TdT Usually indicates acute lymphocytic leukemia, however, may be positive in M0 or M1
CD11c Myeloid
CD117 (c-kit) Myeloid/stem cell
Table 2. Common Cytogenetic Abnormalities in AML
Abnormality Genes Involved Morphology Response
t(8;21)(q22;q22) AML/ETO M2 Good
inv(16)(p13;q22) CBFb/MYH11 M4eo Good
Normal Multiple Varies Intermediate
-7 Multiple Varies Poor
-5 Multiple Varies Poor
+8 Multiple Varies Intermediate-poor
11q23 MLL Varies Intermediate-poor
Miscellaneous Multiple Varies Intermediate-poor
Multiple complex* Multiple Varies Poor
* Refers to 3-5 different cytogenetic abnormalities, depending on the classification used.
Table 3. Cytogenetic Abnormalities in APL
Translocation Genes Involved All-Trans-Retinoic Acid Response
t(15;17)(q21;q11) PML/RARa Yes
t(11;17)(q23;q11) PLZF/RARa No
t(11;17)(q13;q11) NuMA/RARa Yes
t(5;17)(q31;q11) NPM/RARa Yes
t(17;17) stat5b/RARa Unknown
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