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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 myelogenous leukemia (AML) occurs far more commonly in adults than in children, and more commonly in men than women. It is treated with chemotherapy. The five-year survival rate is 20%. [19] Subtypes of AML include acute promyelocytic leukemia, acute myeloblastic leukemia, and acute megakaryoblastic leukemia.
In a phase 3 study of azacitidine and venetoclax in untreated acute myeloid leukemia not eligible for standard induction chemotherapy, the addition of venetoclax to azacitidine resulted in an improvement in median overall survival (14.7 months versus 9.6 months) and improved complete remission rates. [19]
The 5-year event free survival, disease-free survival, and overall survival rate in the phase 3 clinical study in DS-AMKL were 79, 89, 84 percent, respectively. [13] Other studies that use a treatment regimen similar to that used in the phase 3 clinical study report overall survival rates of ~80% [ 7 ] and long-term survivals of 74-91%. [ 9 ]
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