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{{Acute myeloid leukemia}}
{{Acute myeloid leukemia}}


{{CMG}}; {{AE}} {{RT}} {{CLG}}
{{CMG}}; {{AE}} {{RT}}, {{CLG}}, {{shyam}}; {{GRR}} {{Nat}}


==Overview==
==Overview==
 
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==
==Risk Factors==
A number of risk factors for developing acute myeloid leukemia have been identified, including:
A number of risk factors for developing acute myeloid leukemia have been identified including:
 
===Preleukemia===
"Pre-leukemic" blood disorders such as [[myelodysplastic syndrome|myelodysplastic]] or [[myeloproliferative syndrome|myeloproliferative]] syndromes can evolve into acute myeloid leukemia; the exact risk depends on the type of MDS/MPS<ref>{{cite journal | author = Sanz G, Sanz M, Vallespí T, Cañizo M, Torrabadella M, García S, Irriguible D, San Miguel J | title = Two regression models and a scoring system for predicting survival and planning treatment in myelodysplastic syndromes: a multivariate analysis of prognostic factors in 370 patients. | journal = Blood | volume = 74 | issue = 1 | pages = 395–408 | year = 1989 | pmid = 2752119}}</ref>.  Other hematological disorders that can progress to acute myeloid leukemia include:
* [[Aplastic anemia]]
* [[Myelofibrosis]]
* [[Paroxysmal nocturnal hemoglobinuria]]
* [[Polycythemia vera]]
 
===Chemical exposure===
Exposure to [[chemotherapy|anti-cancer chemotherapy]], in particular [[alkylating antineoplastic agent|alkylating agents]], can increase the risk for the subsequent development of acute myeloid leukemia.  The risk is highest about 3–5 years after chemotherapy.<ref>{{cite journal | author = Le Beau M, Albain K, Larson R, Vardiman J, Davis E, Blough R, Golomb H, Rowley J | title = Clinical and cytogenetic correlations in 63 patients with therapy-related myelodysplastic syndromes and acute nonlymphocytic leukemia: further evidence for characteristic abnormalities of chromosomes no. 5 and 7 | journal = J Clin Oncol | volume = 4 | issue = 3 | pages = 325-45 | year = 1986 | pmid = 3950675}}</ref>  Other chemotherapy agents, specifically [[Podophyllotoxin|epipodophyllotoxins]] and [[anthracycline]]s, have also been associated with treatment-related leukemia.  These treatment-related leukemias are often associated with specific chromosomal abnormalities in the leukemic cells.<ref>{{cite journal | author = Thirman M, Gill H, Burnett R, Mbangkollo D, McCabe N, Kobayashi H, Ziemin-van der Poel S, Kaneko Y, Morgan R, Sandberg A | title = Rearrangement of the MLL gene in acute lymphoblastic and acute myeloid leukemias with 11q23 chromosomal translocations | journal = N Engl J Med | volume = 329 | issue = 13 | pages = 909-14 | year = 1993 | pmid = 8361504}}</ref>
 
* [[Ionizing radiation]] exposure can increase the risk of acute myeloid leukemia.  Survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of acute myeloid leukemia,<ref>{{cite journal | author = Bizzozero O, Johnson K, Ciocco A | title = Radiation-related leukemia in Hiroshima and Nagasaki, 1946–1964. I. Distribution, incidence and appearance time | journal = N Engl J Med | volume = 274 | issue = 20 | pages = 1095-101 | year = 1966 | pmid = 5932020}}</ref> as did [[radiologist]]s exposed to high levels of [[X-ray]]s prior to the adoption of modern radiation safety practices.<ref>{{cite journal | author = Yoshinaga S, Mabuchi K, Sigurdson A, Doody M, Ron E | title = Cancer risks among radiologists and radiologic technologists: review of epidemiologic studies | journal = Radiology | volume = 233 | issue = 2 | pages = 313-21 | year = 2004 | pmid = 15375227}}</ref>


* Occupational chemical exposure to [[benzene]] and other [[organic solvent|aromatic organic solvents]] is controversial as a cause of acute myeloid leukemia. Benzene and many of its derivatives are known to be [[carcinogenic]] ''in vitro''.  It is known to cause [[aplastic anemia]] and [[pancytopenia]].  While some studies have suggested a link between occupational exposure to benzene and increased risk of acute myeloid leukemia (M6 type),<ref>{{cite journal | author = Austin H, Delzell E, Cole P | title = Benzene and leukemia. A review of the literature and a risk assessment. | journal = Am J Epidemiol | volume = 127 | issue = 3 | pages = 419-39 | year = 1988 | pmid = 3277397}}</ref> others have suggested that the attributable risk, if any, is slight.<ref>Linet, MS. The Leukemias: Epidemiologic Aspects. Oxford University Press, New York 1985.</ref>
*'''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.<ref name="pmid25056697">{{cite journal| author=Grove CS, Vassiliou GS| title=Acute myeloid leukaemia: a paradigm for the clonal evolution of cancer? | journal=Dis Model Mech | year= 2014 | volume= 7 | issue= 8 | pages= 941-51 | pmid=25056697 | doi=10.1242/dmm.015974 | pmc=4107323 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25056697  }} </ref>
*'''Benzene'''<ref name="pmid22166497">{{cite journal| author=McHale CM, Zhang L, Smith MT| title=Current understanding of the mechanism of benzene-induced leukemia in humans: implications for risk assessment. | journal=Carcinogenesis | year= 2012 | volume= 33 | issue= 2 | pages= 240-52 | pmid=22166497 | doi=10.1093/carcin/bgr297 | pmc=3271273 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22166497 }} </ref>: Benzene is a chemical solvent and aromatic hydrocarbon, for which exposure is a significant risk factor for acute leukemia.<ref name="pmid22166497">{{cite journal| author=McHale CM, Zhang L, Smith MT| title=Current understanding of the mechanism of benzene-induced leukemia in humans: implications for risk assessment. | journal=Carcinogenesis | year= 2012 | volume= 33 | issue= 2 | pages= 240-52 | pmid=22166497 | doi=10.1093/carcin/bgr297 | pmc=3271273 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22166497  }} </ref>
*'''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.<ref name="pmid23980065">{{cite journal| author=Malcovati L, Hellström-Lindberg E, Bowen D, Adès L, Cermak J, Del Cañizo C et al.| title=Diagnosis and treatment of primary myelodysplastic syndromes in adults: recommendations from the European LeukemiaNet. | journal=Blood | year= 2013 | volume= 122 | issue= 17 | pages= 2943-64 | pmid=23980065 | doi=10.1182/blood-2013-03-492884 | pmc=3811170 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23980065  }} </ref>
*'''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.<ref name="pmid28179279">{{cite journal| author=Sood R, Kamikubo Y, Liu P| title=Role of RUNX1 in hematological malignancies. | journal=Blood | year= 2017 | volume= 129 | issue= 15 | pages= 2070-2082 | pmid=28179279 | doi=10.1182/blood-2016-10-687830 | pmc=5391618 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28179279  }} </ref>
*'''Other conditions''': Other causes include [[myeloproliferative syndrome|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]].


===Genetics===
A hereditary risk for acute myeloid leukemia appears to exist. Multiple cases of acute myeloid leukemia developing in a family at a rate higher than predicted by chance alone have been reported.<ref>{{cite book|author=Taylor GM, Birch JM|chapter=The hereditary basis of human leukemia| editor=Henderson ES, Lister TA, Greaves MF| title=Leukemia|edition=6th|location=Philadelphia|publisher= WB Saunders|year= 1996|isbn=0-7216-5381-2|page=210}}</ref><ref>{{cite journal | author = Horwitz M, Goode EL, Jarvik GP | title = Anticipation in familial leukemia | journal = Am. J. Hum. Genet. | volume = 59 | issue = 5 | pages = 990–8 | year = 1996 | pmid = 8900225 | pmc = 1914843 }}</ref><ref>{{cite journal | author = Crittenden LB | title = An interpretation of familial aggregation based on multiple genetic and environmental factors | journal = Ann. N. Y. Acad. Sci. | volume = 91 | issue = 3 | pages = 769–80 | year = 1961 | pmid = 13696504 | doi = 10.1111/j.1749-6632.1961.tb31106.x | bibcode = 1961NYASA..91..769C }}</ref><ref>{{cite journal | author = Horwitz M | title = The genetics of familial leukemia | journal = Leukemia | volume = 11 | issue = 8 | pages = 1347–59 | year = 1997 | pmid = 9264391 | doi = 10.1038/sj.leu.2400707 }}</ref>
Several [[congenital]] conditions may increase the risk of leukemia; the most common is probably [[Down syndrome]], which is associated with a 10 to 18-fold increase in the risk of acute myeloid leukemia.<ref>{{cite journal | author = Evans D, Steward J | title = Down's syndrome and leukaemia | journal = Lancet | volume = 2 | issue = 7790 | pages = 1322 | year = 1972 | pmid = 4117858}}</ref>  Other congenital disorders with such predisposition include:
* [[Bloom syndrome]]
* [[Fanconi anemia]]
* [[Neurofibromatosis]]
* [[Congenital neutropenia]]


==References==
==References==
{{reflist|2}}
{{reflist|2}}
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Latest revision as of 13:03, 11 April 2019

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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

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

A number of risk factors for developing acute myeloid leukemia have been identified including:


References

  1. ↑ 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. ↑ 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.
  3. ↑ 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.
  4. ↑ 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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