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Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cell production. [1] Symptoms may include feeling tired, shortness of breath, easy bruising and bleeding, and increased risk of infection. [1]
Acute myeloid leukemia is a very heterogeneous disease, composed of a variety of translocations and mutations. However, one tenth of all acute myeloid leukemia cases diagnosed have the AML1-ETO fusion oncoprotein due to the t(8;21) translocation. AML1 or RUNX1 is a DNA-binding transcription factor located at the 21q22.
The underlying pathophysiology of acute myeloid leukemia consist of maturational arrest of the bone marrow cell during the early stages of development. A myeloblast is an immature precursor cell that will change into a monocyte, healthy white blood cell. In AML, Myeloblast do not mature but grow and multiply with regulation.
Acute monocytic leukemia (AMoL, or AML-M5) [2] is a type of acute myeloid leukemia. In AML-M5 >80% of the leukemic cells are of monocytic lineage. [3] This cancer is characterized by a dominance of monocytes in the bone marrow. There is an overproduction of monocytes that the body does not need in the periphery.
For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia. [46] Mutation in SPRED1 gene has been associated with a predisposition to childhood leukemia. [54]
Acute promyelocytic leukemia was first characterized in 1957 [4] [5] by French and Norwegian physicians as a hyperacute fatal illness, [3] with a median survival time of less than a week. [6] Today, prognoses have drastically improved; 10-year survival rates are estimated to be approximately 80-90% according to one study.
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