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From NCI's PDQ on AML

The risk factors for developing childhood AML, childhood CML, JMML, TMD, and MDS are similar.

Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn’t mean that you will not get cancer. People who think they may be at risk should discuss this with their doctor. Possible risk factors for childhood AML, childhood CML, JMML, TMD, and MDS include the following:

* Having a brother or sister, especially a twin, with leukemia.
* Being Hispanic.
* Being exposed to cigarette smoke or alcohol before birth.
* Having a history of MDS (also called preleukemia) or aplastic anemia.
* Past treatment with chemotherapy or radiation therapy.
* Being exposed to ionizing radiation or chemicals such as benzene.
* Having certain genetic disorders, such as Down syndrome, Fanconi anemia, neurofibromatosis type 1, or Noonan syndrome.

There are genetic risks associated with the development of AML. There is a high concordance rate of AML in identical twins, which is believed to be in large part a result of shared circulation and the inability of one twin to reject leukemic cells from the other twin during fetal development.[1-3] There is an estimated twofold to fourfold risk of fraternal twins both developing leukemia up to about age 6 years, after which the risk is not significantly greater than that of the general population.[4,5] The development of AML has also been associated with a variety of predisposition syndromes that result from chromosomal imbalances or instabilities, defects in DNA repair, altered cytokine receptor or signal transduction pathway activation, as well as altered protein synthesis. (Refer to the following list of inherited and acquired genetic syndromes associated with myeloid malignancies.)

Inherited and Acquired Genetic Syndromes Associated with Myeloid Malignancies

  • Inherited syndromes
    • Chromosomal imbalances:
      • Down syndrome.
      • Familial monosomy 7 syndrome.
    • Chromosomal instability syndromes:
      • Fanconi anemia.
      • Dyskeratosis congenita.
      • Bloom syndrome.


    • Syndromes of growth and cell survival signaling pathway defects:
      • Neurofibromatosis type 1 (particularly JMML
        development).
      • Noonan syndrome (particularly JMML development).
      • Severe congenital neutropenia (Kostmann syndrome).
      • Diamond-Blackfan anemia.
      • Familial platelet disorder with a propensity to develop AML.
      • Congenital amegakaryocytic thrombocytopenia.

  • Acquired syndromes

    • Severe aplastic anemia.

    • Paroxysmal nocturnal hemoglobinuria.

    • Amegakaryocytic thrombocytopenia.


    • Acquired monosomy 7.

References

  1. Zuelzer WW, Cox DE: Genetic aspects of leukemia. Semin Hematol 6 (3): 228-49, 1969.
    [PUBMED Abstract]


  2. Miller RW: Persons with exceptionally high risk of leukemia. Cancer Res 27 (12): 2420-3, 1967.
    [PUBMED Abstract]


  3. Inskip PD, Harvey EB, Boice JD Jr, et al.: Incidence of childhood cancer in twins. Cancer Causes Control 2 (5): 315-24, 1991.
    [PUBMED Abstract]


  4. Kurita S, Kamei Y, Ota K: Genetic studies on familial leukemia. Cancer 34 (4): 1098-101, 1974.
    [PUBMED Abstract]


  5. Greaves M: Pre-natal origins of childhood leukemia. Rev Clin Exp Hematol 7 (3): 233-45, 2003.
    [PUBMED Abstract]






 
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