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Acute myeloid leukemia risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2], Carlos A Lopez, M.D. [3], Shyam Patel [4]; Grammar Reviewer: Natalie Harpenau, B.S.[5]
Overview[edit | edit source]
Common risk factors in the development of acute myeloid leukemia are advanced age, benzene exposure, prior myelodysplastic syndrome, germline mutations, and other conditions like aplastic anemia.
Risk Factors[edit | edit source]
A number of risk factors for developing acute myeloid leukemia have been identified including:
- Advanced age: This is the most common risk factor for acute leukemia. Elderly patients are more likely to develop myeloid leukemia, due to a longer duration and opportunity for mutations to accumulate in cells. These mutations are more likely to accumulate in hematopoietic stem cells through a process called clonal evolution.[1]
- Benzene[2]: Benzene is a chemical solvent and aromatic hydrocarbon, for which exposure is a significant risk factor for acute leukemia.[2]
- Prior myelodysplastic syndrome: Myelodysplastic syndrome is a disorder characterized by ineffective hematopoiesis, defective maturation of blood cells, and peripheral cytopenias. Antecedent myelodysplastic syndrome is implicated in some forms of acute leukemia, such as acute myeloid leukemia. Myelodysplastic syndrome is a precursor for leukemia, as this disease is characterized by the presence of dysplastic or cancerous cells that do not meet the requirements for a formal diagnosis of leukemia.[3]
- Germline mutations: In general, germline predisposition to acute promyelocytic leukemia is rare. In patients with acute myeloid leukemia, germline mutations in the RUNX1 gene can predispose to the development of the cancer.[4]
- Other conditions: Other causes include myeloproliferative syndromes, aplastic anemia, myelofibrosis, paroxysmal nocturnal hemoglobinuria, polycythemia vera, chemical exposure and several congenital conditions such as Down syndrome, Bloom syndrome, Fanconi anemia, and neurofibromatosis.
References[edit | edit source]
- ↑ Grove CS, Vassiliou GS (2014). "Acute myeloid leukaemia: a paradigm for the clonal evolution of cancer?". Dis Model Mech. 7 (8): 941–51. doi:10.1242/dmm.015974. PMC 4107323. PMID 25056697.
- ↑ 2.0 2.1 McHale CM, Zhang L, Smith MT (2012). "Current understanding of the mechanism of benzene-induced leukemia in humans: implications for risk assessment". Carcinogenesis. 33 (2): 240–52. doi:10.1093/carcin/bgr297. PMC 3271273. PMID 22166497.
- ↑ Malcovati L, Hellström-Lindberg E, Bowen D, Adès L, Cermak J, Del Cañizo C; et al. (2013). "Diagnosis and treatment of primary myelodysplastic syndromes in adults: recommendations from the European LeukemiaNet". Blood. 122 (17): 2943–64. doi:10.1182/blood-2013-03-492884. PMC 3811170. PMID 23980065.
- ↑ Sood R, Kamikubo Y, Liu P (2017). "Role of RUNX1 in hematological malignancies". Blood. 129 (15): 2070–2082. doi:10.1182/blood-2016-10-687830. PMC 5391618. PMID 28179279.
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