Acute myeloid leukemia risk factors: Difference between revisions
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===Genetics=== | ===Genetics=== | ||
A hereditary risk for AML appears to exist. Multiple cases of AML 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> | A hereditary risk for AML appears to exist. Multiple cases of AML 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 AML.<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: | 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 AML.<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]] | * [[Bloom syndrome]] | ||
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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]
Overview
Risk Factors
A number of risk factors for developing AML have been identified, including:
Preleukemia
"Pre-leukemic" blood disorders such as myelodysplastic or myeloproliferative syndromes can evolve into AML; the exact risk depends on the type of MDS/MPS[1]. Other hematological disorders that can progress to AML include:
Chemical exposure
Exposure to anti-cancer chemotherapy, in particular alkylating agents, can increase the risk for the subsequent development of AML. The risk is highest about 3–5 years after chemotherapy.[2] Other chemotherapy agents, specifically epipodophyllotoxins and anthracyclines, have also been associated with treatment-related leukemia. These treatment-related leukemias are often associated with specific chromosomal abnormalities in the leukemic cells.[3]
- Ionizing radiation exposure can increase the risk of AML. Survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of AML,[4] as did radiologists exposed to high levels of X-rays prior to the adoption of modern radiation safety practices.[5]
- Occupational chemical exposure to benzene and other aromatic organic solvents is controversial as a cause of AML. 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 AML (M6 type),[6] others have suggested that the attributable risk, if any, is slight.[7]
Genetics
A hereditary risk for AML appears to exist. Multiple cases of AML developing in a family at a rate higher than predicted by chance alone have been reported.[8][9][10][11] 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 AML.[12] Other congenital disorders with such predisposition include:
References
- ↑ Sanz G, Sanz M, Vallespí T, Cañizo M, Torrabadella M, García S, Irriguible D, San Miguel J (1989). "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". Blood. 74 (1): 395–408. PMID 2752119.
- ↑ Le Beau M, Albain K, Larson R, Vardiman J, Davis E, Blough R, Golomb H, Rowley J (1986). "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". J Clin Oncol. 4 (3): 325–45. PMID 3950675.
- ↑ Thirman M, Gill H, Burnett R, Mbangkollo D, McCabe N, Kobayashi H, Ziemin-van der Poel S, Kaneko Y, Morgan R, Sandberg A (1993). "Rearrangement of the MLL gene in acute lymphoblastic and acute myeloid leukemias with 11q23 chromosomal translocations". N Engl J Med. 329 (13): 909–14. PMID 8361504.
- ↑ Bizzozero O, Johnson K, Ciocco A (1966). "Radiation-related leukemia in Hiroshima and Nagasaki, 1946–1964. I. Distribution, incidence and appearance time". N Engl J Med. 274 (20): 1095–101. PMID 5932020.
- ↑ Yoshinaga S, Mabuchi K, Sigurdson A, Doody M, Ron E (2004). "Cancer risks among radiologists and radiologic technologists: review of epidemiologic studies". Radiology. 233 (2): 313–21. PMID 15375227.
- ↑ Austin H, Delzell E, Cole P (1988). "Benzene and leukemia. A review of the literature and a risk assessment". Am J Epidemiol. 127 (3): 419–39. PMID 3277397.
- ↑ Linet, MS. The Leukemias: Epidemiologic Aspects. Oxford University Press, New York 1985.
- ↑ Taylor GM, Birch JM (1996). "The hereditary basis of human leukemia". In Henderson ES, Lister TA, Greaves MF. Leukemia (6th ed.). Philadelphia: WB Saunders. p. 210. ISBN 0-7216-5381-2.
- ↑ Horwitz M, Goode EL, Jarvik GP (1996). "Anticipation in familial leukemia". Am. J. Hum. Genet. 59 (5): 990–8. PMC 1914843. PMID 8900225.
- ↑ Crittenden LB (1961). "An interpretation of familial aggregation based on multiple genetic and environmental factors". Ann. N. Y. Acad. Sci. 91 (3): 769–80. Bibcode:1961NYASA..91..769C. doi:10.1111/j.1749-6632.1961.tb31106.x. PMID 13696504.
- ↑ Horwitz M (1997). "The genetics of familial leukemia". Leukemia. 11 (8): 1347–59. doi:10.1038/sj.leu.2400707. PMID 9264391.
- ↑ Evans D, Steward J (1972). "Down's syndrome and leukaemia". Lancet. 2 (7790): 1322. PMID 4117858.