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Acute myeloid leukemia (AML) consists of a heterogeneous group of hematologic neoplasms characterized by clonal proliferation of myeloid blasts in the peripheral blood, bone marrow, and extramedullary tissues. Despite advances in our understanding of the molecular biology of AML, its treatment remains challenging and outcomes vary greatly depending on the cytogenetic and molecular features as well as age and comorbidities.

Acute myeloid leukemia is thought to be the culmination of genetic mutations and chromosomal aberrations within myeloid precursors resulting in disrupted differentiation, excessive proliferation, and suppressed apoptosis of neoplastic cells referred to as blasts.

Over the last several decades, improvements in chemotherapeutic regimens and supportive care have resulted in significant but modest progress in treating AML. Better understanding of the biology of AML has resulted in the identification of new therapeutic targets. Despite this, currently, the majority of patients with AML die from the complications of their disease. With better definition of molecular abnormalities and elucidation of the pathogenic events in various AML subtypes and with the development of novel targeted agents, a better outcome for patients with AML may be achievable in the future.


Approximately 13,000 individuals are diagnosed annually in the United States with leukemia. The incidence of AML is 4.3 per 100,000 (1). The median age at presentation is about 65 years. The incidence of AML, as well as myelodysplastic syndrome (MDS), appears to be rising, particularly in individuals over 60 years of age. The incidence of AML is slightly higher in males and in populations of European descent. Acute promyelocytic leukemia (APL), a distinct subtype of AML, has been reported to be more common among populations of Hispanic background (2).

An increased incidence of AML is seen in patients with disorders associated with increased chromatin fragility such as Bloom syndrome, Fanconi anemia, Kostmann syndrome, and Wiskott-Aldrich syndrome or ataxia-telangiectasia. Other syndromes, such as Down (trisomy of chromosome 21), Klinefelter (XXY and variants), and Patau (trisomy of chromosome 13) syndromes, have also been associated with a higher incidence of AML (3).

Therapeutic radiation increases AML risk, particularly if given concomitantly with alkylating agents. Two categories of therapy-related AML have been described. Patients exposed to alkylating agents (eg, cyclophosphamide, melphalan, nitrogen mustard) can develop AML after a latency period of 4 to 8 years, which is often associated with abnormalities of chromosomes 5 and/or 7. Exposure to agents that inhibit the DNA repair enzyme topoisomerase II (eg, etoposide) is also associated with secondary AML with a shorter latency period, usually 1 to 3 years (4). Benzene, smoking, dyes, herbicides, and pesticides have been implicated as potential risk factors for development of AML (5).

Acute myeloid leukemia may also be secondary to transformation of an antecedent myeloid disorder, such as MDS, myeloproliferative neoplasm ...

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