Core binding factor acute myeloid leukemia
Última actualización 8 Sept 2020
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Core binding factor acute myeloid leukemia (CBF-AML) is one form of a cancer of the blood-forming tissue (bone marrow) called acute myeloid leukemia. In normal bone marrow, early blood cells called hematopoietic stem cells develop into several types of blood cells: white blood cells (leukocytes) that protect the body from infection, red blood cells (erythrocytes) that carry oxygen, and platelets (thrombocytes) that are involved in blood clotting. In acute myeloid leukemia, the bone marrow makes large numbers of abnormal, immature white blood cells called myeloid blasts. Instead of developing into normal white blood cells, the myeloid blasts develop into cancerous leukemia cells. The large number of abnormal cells in the bone marrow interferes with the production of functional white blood cells, red blood cells, and platelets.
Descripción
Core binding factor acute myeloid leukemia (CBF-AML) is one form of a cancer of the blood-forming tissue (bone marrow) called acute myeloid leukemia. In normal bone marrow, early blood cells called hematopoietic stem cells develop into several types of blood cells: white blood cells (leukocytes) that protect the body from infection, red blood cells (erythrocytes) that carry oxygen, and platelets (thrombocytes) that are involved in blood clotting. In acute myeloid leukemia, the bone marrow makes large numbers of abnormal, immature white blood cells called myeloid blasts. Instead of developing into normal white blood cells, the myeloid blasts develop into cancerous leukemia cells. The large number of abnormal cells in the bone marrow interferes with the production of functional white blood cells, red blood cells, and platelets.
People with CBF-AML have a shortage of all types of mature blood cells: a shortage of white blood cells (leukopenia) leads to increased susceptibility to infections, a low number of red blood cells (anaemia) causes fatigue and weakness, and a reduction in the amount of platelets (thrombocytopenia) can result in easy bruising and abnormal bleeding. Other symptoms of CBF-AML may include fever and weight loss.
While acute myeloid leukemia is generally a disease of older adults, CBF-AML often begins in young adulthood and can occur in childhood. Compared to other forms of acute myeloid leukemia, CBF-AML has a relatively good prognosis: about 90 percent of individuals with CBF-AML recover from their disease following treatment, compared with 25 to 40 percent of those with other forms of acute myeloid leukemia. However, the disease recurs in approximately half of them after successful treatment of the initial occurrence.
Patrones de herencia
The source lists the following possible inheritance patterns: Not inherited. More than one pattern can apply in different cases.
Related genes
Otros nombres
CBF acute myeloid leukemia
CBF-AML
Core-binding factor AML
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Lecturas adicionales y referencias
- Core binding factor acute myeloid leukemia; MedlinePlus, National Library of Medicine.
- Goyama S, Mulloy JC. Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects. Int J Hematol. 2011 Aug;94(2):126-133. doi: 10.1007/s12185-011-0858-z. Epub 2011 May 3.
- Kuykendall A, Duployez N, Boissel N, Lancet JE, Welch JS. Acute Myeloid Leukemia: The Good, the Bad, and the Ugly. Am Soc Clin Oncol Educ Book. 2018 May 23;38:555-573. doi: 10.1200/EDBK_199519.
- Lam K, Zhang DE. RUNX1 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis. Front Biosci (Landmark Ed). 2012 Jan 1;17(3):1120-39. doi: 10.2741/3977.
- Marcucci G, Haferlach T, Dohner H. Molecular genetics of adult acute myeloid leukemia: prognostic and therapeutic implications. J Clin Oncol. 2011 Feb 10;29(5):475-86. doi: 10.1200/JCO.2010.30.2554. Epub 2011 Jan 10.
- Paschka P, Dohner K. Core-binding factor acute myeloid leukemia: can we improve on HiDAC consolidation? Hematology Am Soc Hematol Educ Program. 2013;2013:209-19. doi: 10.1182/asheducation-2013.1.209.
- Sangle NA, Perkins SL. Core-binding factor acute myeloid leukemia. Arch Pathol Lab Med. 2011 Nov;135(11):1504-9. doi: 10.5858/arpa.2010-0482-RS.
- Welch JS, Ley TJ, Link DC, Miller CA, Larson DE, Koboldt DC, Wartman LD, Lamprecht TL, Liu F, Xia J, Kandoth C, Fulton RS, McLellan MD, Dooling DJ, Wallis JW, Chen K, Harris CC, Schmidt HK, Kalicki-Veizer JM, Lu C, Zhang Q, Lin L, O'Laughlin MD, McMichael JF, Delehaunty KD, Fulton LA, Magrini VJ, McGrath SD, Demeter RT, Vickery TL, Hundal J, Cook LL, Swift GW, Reed JP, Alldredge PA, Wylie TN, Walker JR, Watson MA, Heath SE, Shannon WD, Varghese N, Nagarajan R, Payton JE, Baty JD, Kulkarni S, Klco JM, Tomasson MH, Westervelt P, Walter MJ, Graubert TA, DiPersio JF, Ding L, Mardis ER, Wilson RK. The origin and evolution of mutations in acute myeloid leukemia. Cell. 2012 Jul 20;150(2):264-78. doi: 10.1016/j.cell.2012.06.023.
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