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Acute myeloid leukemia
Causes and risk factors

It is unlikely that there is one common etiology for leukemogenesis and most patients who present with de novo AML have no identifiable risk factor. There are, however, some accepted risk factors for acute myeloid leukemia.

Chemical exposure

Increased incidence has been reported in persons with prolonged exposure to benzene and petroleum products. Exposure to benzene is also associated with aplastic anemia and pancytopenia. These patients often develop AML. Chromosomal damage in these subjects is common, many of which demonstrate M6 morphology. The interval between exposure and onset of leukemia is long (up to 10-30 years).

Pesticide exposure also has been linked to some forms of AML. The incidence of AML is beginning to rise in developing countries, as industrialization and pollution increase.

Exposure to hair dyes, smoking, and nonionic radiation may also increase the risk of leukemia.

Antecedent hematological disorders

The most common risk factor is the presence of an antecedent hematological disorders, the most common of which is MDS. Other antecedent hematological disorders include:

• Chronic myeloid leukemia: Most patients with chronic myelogenous leukemia, a myeloproliferative disorder, eventually develop a blast phase indistinguishable from acute myeloid leukemia.

• Myelofibrosis

• Aplastic anemia

• Paroxysmal nocturnal hemoglobinuria

• Polycythemia vera

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Prior chemotherapy & radiotherapy

This has become more common as more patients with cancer survive their primary malignancy and more patients receive intensive chemotherapy (including bone marrow transplantation [BMT].

Alkylating agents

Use of alkylating agents, such as cyclophosphamide (Cytoxan, Neosar) and melphalan (Alkeran), in the treatment of lymphomas, myelomas, and breast and ovarian cancers has been associated with the development of AML, usually within 3-5 years of exposure and often preceded by a myelodysplastic phase. Cytogenetic abnormalities, particularly monosomy 5, 7, 11, and 17, are common.

Radiotherapy

Concurrent radiation exposure slightly increases the risk of leukemogenesis posed by alkylating agents.

Topoisomerase II

• Topoisomerase II inhibitors (etoposide [VePesid], teniposide [Vumon]

• Doxorubicin and its derivatives, and mitoxantrone [Novantrone])

These agents, in contrast to alkylators, are associated with a short latency period (9-12 months) without antecedent myelodysplasia and with cytogenetic abnormalities involving chromosome 11q23 or 21q22 in the malignant clone.

Genetic disorders

An increased incidence of AML is seen in patients with:

• Fanconi’s anemia
• Ataxia-telangiectasia
• Down syndrome

• Bloom syndrome

• Wiskott-Aldrich syndrome

Familial syndromes

Familial syndromes are rare such as those of familial erythroleukemia (a subtype of AML). Some hereditary cancer syndromes, such as Li-Fraumeni syndrome, can manifest as leukemia.

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