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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]
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 myeloid leukemia (AML) is a type of cancer affecting blood cells that eventually develop into non-lymphocyte white blood cells. The disease originates from the bone marrow, the soft inner portion of select bones where blood stem cells develop into either lymphocyte or in this particular condition, myeloid cells.
ADE is a chemotherapy regimen most often used as an induction or consolidation regimen in acute myelogenous leukemia, especially in poor-risk patients or those refractory to the standard first-line induction with standard "7+3" regimen or who are relapsed after the standard chemotherapy. ADE regimen consists of three drugs:
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.
Acute megakaryoblastic leukemia (AMKL) is life-threatening leukemia in which malignant megakaryoblasts proliferate abnormally and injure various tissues. Megakaryoblasts are the most immature precursor cells in a platelet-forming lineage; they mature to promegakaryocytes and, ultimately, megakaryocytes which cells shed membrane-enclosed particles, i.e. platelets, into the circulation.
Acute promyelocytic leukemia is characterized by a chromosomal translocation involving the retinoic acid receptor alpha (RARA) gene on chromosome 17. [3] In 95% of cases of APL, the RARA gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, a translocation denoted as t(15;17)(q22;q21). [3]
Chemotherapy has strong side effects such as typhlitis, gastrointestinal distress, anemia, fatigue, hair loss, nausea and vomiting, etc. Thus, the different dose and times of chemotherapy for different individuals is important. If the patients enter fully remission, the consolidation with stem cell transplantation is highly recommended.