Practice Essentials

Acute myelogenous leukemia (AML) is a malignant disease of the bone marrow in which
hematopoietic precursors are arrested in an early stage of development. Most AML subtypes are
distinguished from other related blood disorders by the presence of more than 20% blasts in the
bone marrow.

See Chronic Leukemias: 4 Cancers to Differentiate, a Critical Images slideshow, to help detect
chronic leukemias and determine the specific type present.

The underlying pathophysiology in AML consists of a maturational arrest of bone marrow cells
in the earliest stages of development. (See Pathophysiology.) Several factors have been
implicated in the causation of AML, including antecedent hematologic disorders, familial
syndromes, environmental exposures, and drug exposures. However, most patients who present
with de novo AML have no identifiable risk factor. (See Etiology.)

Patients with AML present with symptoms resulting from bone marrow failure, symptoms
resulting from organ infiltration with leukemic cells, or both. The time course is variable. (See
Presentation.) The workup for AML includes blood tests, bone marrow aspiration and biopsy
(the definitive diagnostic tests), and analysis of genetic abnormalities. (See Workup.)

Current standard chemotherapy regimens cure only a minority of patients with AML. As a result,
all patients should be evaluated for entry into well-designed clinical trials. If a clinical trial is not
available, the patient can be treated with standard therapy. (See Treatment.) Readmission is
frequently required for the management of toxic effects of chemotherapy.

Pathophysiology
The underlying pathophysiology in AML consists of a maturational arrest of bone marrow cells
in the earliest stages of development. The mechanism of this arrest is under study, but in many
cases, it involves the activation of abnormal genes through chromosomal translocations and other
genetic abnormalities. [1, 2, 3]

This developmental arrest results in 2 disease processes. First, the production of normal blood
cells markedly decreases, which results in varying degrees of anemia, thrombocytopenia, and
neutropenia. Second, the rapid proliferation of these cells, along with a reduction in their ability
to undergo programmed cell death (apoptosis), results in their accumulation in the bone marrow,
the blood, and, frequently, the spleen and liver.

Etiology
Several factors have been implicated in the causation of AML, including antecedent hematologic
disorders, familial syndromes, environmental exposures, and drug exposures. However, most
patients who present with de novo AML have no identifiable risk factor.
Antecedent hematologic disorders

The most common risk factor for AML is the presence of an antecedent hematologic disorder,
the most common of which is myelodysplastic syndrome (MDS). MDS is a bone marrow disease
of unknown etiology that occurs most often in older patients and manifests as progressive
cytopenias that occur over months to years. Patients with low-risk MDS (eg, refractory anemia
with normal cytogenetics findings) generally do not develop AML, whereas patients with high-
risk MDS (eg, refractory anemia with excess blasts-type 2) frequently do.

Other antecedent hematologic disorders that predispose patients to AML include aplastic anemia
and myelofibrosis.

Congenital disorders

Some congenital disorders that predispose patients to AML include Bloom syndrome, Down
syndrome, congenital neutropenia, Fanconi anemia, and neurofibromatosis. Usually, these
patients develop AML during childhood; rarely, some may present in young adulthood.

More subtle genetic disorders, including polymorphisms of enzymes that metabolize

carcinogens, also predispose patients to AML. For example, polymorphisms of
NAD(P)H:quinone oxidoreductase (NQO1), an enzyme that metabolizes benzene derivatives, are
associated with an increased risk of AML. [4] Particularly increased risk exists for AML that
occurs after chemotherapy for another disease or for de novo AML with an abnormality of
chromosomes 5, 7, or both.

Likewise, polymorphisms in glutathione S -transferase are associated with secondary AML after
chemotherapy for other malignancies. [5]

Familial syndromes

Germline mutations in the gene AML1 (RUNX1, CBFA2) occur in the familial platelet disorder
with predisposition for AML, an autosomal dominant disorder characterized by moderate
thrombocytopenia, a defect in platelet function, and propensity to develop AML. [6] Mutation of
CEBPA (the gene encoding CCAAT/enhancer binding protein alpha, a granulocytic
differentiation factor and member of the bZIP family) was described in a family with 3 members
affected by AML. [7]

Holme et al studied 27 families with familial MDS/AML. All of the families were screened for
RUNX1, CEBPA, TERC, TERT, GATA2, TET2, and NPM1 mutations. Five of the 27 families had
telomerase mutations (3 TERT, 2 TERC), one had a RUNX1 mutation, and four had heterozygous
GATA2 mutations. [8]

Gao et al recently reviewed GATA2 mutations associated with familial AML-MDS. [9] GATA2 is
a transcription factor crucial for hematopoietic differentiation and lymphatic formation, and
germline GATA2 mutations are involved in a rare group of complex syndromes with
overlapping clinical features of immune deficiency, lymphedema, and propensity to AML or
MDS.

Some hereditary cancer syndromes, such as Li-Fraumeni syndrome, can manifest as leukemia.
However, cases of leukemia are less common than the solid tumors that generally characterize
these syndromes.

Environmental exposures

Several studies demonstrate a relationship between radiation exposure and leukemia. Early
radiologists (before the use of appropriate shielding) were found to have an increased likelihood
of developing leukemia. Patients receiving therapeutic irradiation for ankylosing spondylitis
were at increased risk of leukemia. Survivors of the atomic bomb explosions in Japan were at a
markedly increased risk for the development of leukemia.

Persons who smoke have a small but statistically significant (odds ratio, 1.5) increased risk of
developing AML. [10] In several studies, the risk of AML was slightly increased in people who
smoked compared with those who did not smoke.

Exposure to benzene is associated with aplastic anemia and pancytopenia. These patients often
develop AML. Many of these patients demonstrate M6 morphology. Exposure to soot, creosote,
inks, dyes and tanning solutions and coal dust have also been associated with AML. [80]

Previous exposure to chemotherapeutic agents

As more patients with cancer survive their primary malignancy and more patients receive
intensive chemotherapy (including bone marrow transplantation [BMT]), the number of patients
with AML increases because of exposure to chemotherapeutic agents. For example, the
cumulative incidence of acute leukemia in patients with breast cancer who were treated with
doxorubicin and cyclophosphamide as adjuvant therapy was 0.2-1.0% at 5 years. [11]

Patients with previous exposure to chemotherapeutic agents can be divided into 2 groups: (1)
those with previous exposure to alkylating agents and (2) those with exposure to topoisomerase-
II inhibitors.

Patients with a previous exposure to alkylating agents, with or without radiation, often have a
myelodysplastic phase before the development of AML. Cytogenetics testing frequently reveals -
5 and/or -7 (5q- or monosomy 7).

Patients with a previous exposure to topoisomerase-II inhibitors do not have a myelodysplastic

phase. Cytogenetics testing reveals a translocation that involves band 11q23. Less commonly,
patients developed leukemia with other balanced translocations, such as inversion 16 or t(15;17).
[12]

The typical latency period between drug exposure and acute leukemia is approximately 3-5 years
for alkylating agents/radiation exposure, but it is only 9-12 months for topoisomerase inhibitors.
Epidemiology
The American Cancer Society estimates that 19,950 new cases of AML (11,130 in men, 8820 in
women) will occur in the United States in 2016, accounting for 31% of all leukemia cases in
adults 20 years of age and older. [13] AML is more commonly diagnosed in developed countries,
and it is more common in whites than in other populations.

The prevalence of AML increases with age. The median age of onset is approximately 70 years.
However, AML affects all age groups.

AML is more common in men than in women. The difference is even more apparent in older
patients. This is likely because MDS is more common in men, and advanced MDS frequently
evolves into AML. Some have proposed that the increased prevalence of AML in men may be
related to occupational exposures (see Etiology).

Prognosis
The prognosis relies on several factors. Increasing age is an adverse factor, because older
patients more frequently have a previous antecedent hematologic disorder along with comorbid
medical conditions that compromise the ability to give full doses of chemotherapy. A previous
antecedent hematologic disorder (most commonly, MDS) is associated with a poor outcome to
therapy.

A study by Arellano et al found leukopenia at diagnosis had no prognostic significance in

patients with AML. [14]

Findings from cytogenetic analysis of the bone marrow constitute one of the most important
prognostic factors. Patients with t(8;21), t(15;17), or inversion 16 have the best prognosis, with
long-term survival rates of approximately 65%. Patients with normal cytogenetic findings have
an intermediate prognosis and have a long-term survival rate of approximately 25%. Patients
with poor-risk cytogenetic findings (especially -7, -5) have a poor prognosis, with a long-term
survival rate of less than 10%.

Other cytogenetic abnormalities, including +8, 11q23, and miscellaneous, have been reported to
be intermediate risk in some series and poor risk in others.

The presence of an FLT3 mutation is associated with a poorer prognosis. Mutations in CEBPA
are associated with a longer remission duration and longer overall survival. Mutations in NPM
are associated with an increased response to chemotherapy.

A study by Metzeler et al determined that TET2 mutations had an adverse prognostic impact in
an otherwise favorable-risk patient subset using the European LeukemiaNet (ELN) molecular-
risk classification of patients with primary cytogenetically normal AML. [15]
In adults, treatment results are generally analyzed separately for younger (18-60 y) patients with
AML and for older patients (>60 y). With current standard chemotherapy regimens,
approximately 30-35% of adults younger than 60 years survive longer than 5 years and are
considered cured. Results in older patients are more disappointing, with fewer than 10% of
surviving over the long term.

A study by Kayser et al found that therapy-related AML (t-AML) was an adverse prognostic
factor for death in complete remission but not relapse and overall survival in younger intensively
treated patients. [16] It was also an adverse prognostic factor for relapse but not death in complete
remission in older, less intensively treated patients.

A study by Varadarajan et al found that having ever smoked decreased overall survival in
patients with AML. [17]

Crysandt and collegeues found that in younger patients with de novo AML, overweight and
obesity were risk factors for an impaired response to induction therapy and shorter disease-free
and overall survival. [18]

The American Cancer Society estimates that in 2015, 10,460 deaths from AML will occur in the
United States. Of these, 6110 are expected to occur in men and 4350 in women. [13] Death in
patients with AML may result from uncontrolled infection or hemorrhage. This may happen even
after use of appropriate blood product and antibiotic support.

Patient Education
Patients with AML should be instructed to call their healthcare providers immediately if they are
febrile or have signs of bleeding.

For patient education resources, see the Blood and Lymphatic System Center and the Skin, Hair,
and Nails Center, as well as Leukemia and Bruises.

1. Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, et al. The 2016
revision to the World Health Organization classification of myeloid neoplasms and acute
leukemia. Blood. 2016 May 19. 127 (20):2391-405. [Medline]. [Full Text].
2. Smith MT, Skibola CF, Allan JM, Morgan GJ. Causal models of leukaemia and
lymphoma. IARC Sci Publ. 2004. 373-92. [Medline].
3. Ghiaur G, Wroblewski M, Loges S. Acute Myelogenous Leukemia and its
Microenvironment: A Molecular Conversation. Semin Hematol. 2015 Jul. 52 (3):200-6.
[Medline].
4. Larson RA, Wang Y, Banerjee M, Wiemels J, Hartford C, Le Beau MM, et al. Prevalence
of the inactivating 609C-->T polymorphism in the NAD(P)H:quinone oxidoreductase
(NQO1) gene in patients with primary and therapy-related myeloid leukemia. Blood.
1999 Jul 15. 94(2):803-7. [Medline]. [Full Text].
5. Allan JM, Wild CP, Rollinson S, Willett EV, Moorman AV, Dovey GJ, et al.
Polymorphism in glutathione S-transferase P1 is associated with susceptibility to
 chemotherapy-induced leukemia. Proc Natl Acad Sci U S A. 2001 Sep 25. 98(20):11592-
7. [Medline]. [Full Text].
6. Song WJ, Sullivan MG, Legare RD, Hutchings S, Tan X, Kufrin D, et al.
Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to
develop acute myelogenous leukaemia. Nat Genet. 1999 Oct. 23(2):166-75. [Medline].
7. Smith ML, Cavenagh JD, Lister TA, Fitzgibbon J. Mutation of CEBPA in familial acute
myeloid leukemia. N Engl J Med. 2004 Dec 2. 351(23):2403-7. [Medline]. [Full Text].
8. Holme H, Hossain U, Kirwan M, Walne A, Vulliamy T, Dokal I. Marked genetic
heterogeneity in familial myelodysplasia/acute myeloid leukaemia. Br J Haematol. 2012
Jul. 158(2):242-8. [Medline].
9. Gao J, Gentzler RD, Timms AE, Horwitz MS, Frankfurt O, Altman JK. Heritable
GATA2 mutations associated with familial AML-MDS: a case report and review of
literature. J Hematol Oncol. 2014 Apr 22. 7(1):36. [Medline].
10. Brownson RC, Chang JC, Davis JR. Cigarette smoking and risk of adult leukemia. Am J
Epidemiol. 1991 Nov 1. 134(9):938-41. [Medline].
11. Smith RE, Bryant J, DeCillis A, Anderson S. Acute myeloid leukemia and
myelodysplastic syndrome after doxorubicin-cyclophosphamide adjuvant therapy for
operable breast cancer: the National Surgical Adjuvant Breast and Bowel Project
Experience. J Clin Oncol. 2003 Apr 1. 21(7):1195-204. [Medline]. [Full Text].
12. Andersen MK, Larson RA, Mauritzson N, Schnittger S, Jhanwar SC, Pedersen-Bjergaard
J. Balanced chromosome abnormalities inv(16) and t(15;17) in therapy-related
myelodysplastic syndromes and acute leukemia: report from an international workshop.
Genes Chromosomes Cancer. 2002 Apr. 33(4):395-400. [Medline].
13. Cancer Facts & Figures 2016. American Cancer Society. Available at
http://www.cancer.org/acs/groups/content/@research/documents/document/acspc-
047079.pdf. Accessed: September 29, 2016.
14. Arellano M, Bernal-Mizrachi L, Pan L, et al. Prognostic significance of leukopenia at the
time of diagnosis in acute myeloid leukemia. Clin Lymphoma Myeloma Leuk. 2011 Oct.
11(5):427-32. [Medline].
15. Metzeler KH, Maharry K, Radmacher MD, et al. TET2 Mutations Improve the New
European LeukemiaNet Risk Classification of Acute Myeloid Leukemia: A Cancer and
Leukemia Group B Study. J Clin Oncol. 2011 Apr 1. 29(10):1373-81. [Medline].
16. Kayser S, Dohner K, Krauter J, et al. The impact of therapy-related acute myeloid
leukemia (AML) on outcome in 2853 adult patients with newly diagnosed AML. Blood.
2011 Feb 17. 117(7):2137-45. [Medline].
17. Varadarajan R, Licht AS, Hyland AJ, et al. Smoking adversely affects survival in acute
myeloid leukemia patients. Int J Cancer. 2012 Mar 15. 130(6):1451-8. [Medline]. [Full
Text].
18. Crysandt M, Kramer M, Ehninger G, Bornhuser M, Berdel WE, et al. A high BMI is a
risk factor in younger patients with de novo acute myelogenous leukemia. Eur J
Haematol. 2015 Aug 16. [Medline].
19. [Guideline] NCCN Clinical Practice Guidelines in Oncology. Acute Myeloid Leukemia:
Version 1.2016. National Comprehensive Cancer Network. Available at
http://www.nccn.org/professionals/physician_gls/f_guidelines.asp. June 29, 2016;
Accessed: September 22, 2016.
20. Breems DA, Van Putten WL, De Greef GE, Van Zelderen-Bhola SL, Gerssen-Schoorl
KB, Mellink CH, et al. Monosomal karyotype in acute myeloid leukemia: a better
indicator of poor prognosis than a complex karyotype. J Clin Oncol. 2008 Oct 10.
26(29):4791-7. [Medline].
21. Voutiadou G, Papaioannou G, Gaitatzi M, Lalayanni C, Syrigou A, Vadikoliou C, et al.
Monosomal karyotype in acute myeloid leukemia defines a distinct subgroup within the
adverse cytogenetic risk category. Cancer Genet. 2013 Jan-Feb. 206(1-2):32-6.
[Medline].
22. Haferlach C, Alpermann T, Schnittger S, Kern W, Chromik J, Schmid C, et al. Prognostic
value of monosomal karyotype in comparison to complex aberrant karyotype in acute
myeloid leukemia: a study on 824 cases with aberrant karyotype. Blood. 2012 Mar 1.
119(9):2122-5. [Medline].
23. Griswold IJ, Shen LJ, La Rose P, Demehri S, Heinrich MC, Braziel RM, et al. Effects of
MLN518, a dual FLT3 and KIT inhibitor, on normal and malignant hematopoiesis.
Blood. 2004 Nov 1. 104(9):2912-8. [Medline]. [Full Text].
24. Falini B, Mecucci C, Tiacci E, Alcalay M, Rosati R, Pasqualucci L, et al. Cytoplasmic
nucleophosmin in acute myelogenous leukemia with a normal karyotype. N Engl J Med.
2005 Jan 20. 352(3):254-66. [Medline]. [Full Text].
25. Thiede C, Steudel C, Mohr B, Schaich M, Schkel U, Platzbecker U, et al. Analysis of
FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association
with FAB subtypes and identification of subgroups with poor prognosis. Blood. 2002 Jun
15. 99(12):4326-35. [Medline]. [Full Text].
26. Frhling S, Schlenk RF, Stolze I, Bihlmayr J, Benner A, Kreitmeier S, et al. CEBPA
mutations in younger adults with acute myeloid leukemia and normal cytogenetics:
prognostic relevance and analysis of cooperating mutations. J Clin Oncol. 2004 Feb 15.
22(4):624-33. [Medline]. [Full Text].
27. Schwind S, Marcucci G, Maharry K, Radmacher MD, Mrzek K, Holland KB, et al.
BAALC and ERG expression levels are associated with outcome and distinct gene and
microRNA expression profiles in older patients with de novo cytogenetically normal
acute myeloid leukemia: a Cancer and Leukemia Group B study. Blood. 2010 Dec 16.
116(25):5660-9. [Medline]. [Full Text].
28. Ley TJ, Ding L, Walter MJ, McLellan MD, et al. DNMT3A mutations in acute myeloid
leukemia. N Engl J Med. 2010 Dec 16. 363(25):2424-33. [Medline].
29. Schwind S, Maharry K, Radmacher MD, Mrzek K, Holland KB, Margeson D, et al.
Prognostic significance of expression of a single microRNA, miR-181a, in
cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study.
J Clin Oncol. 2010 Dec 20. 28(36):5257-64. [Medline]. [Full Text].
30. Conway O'Brien E, Prideaux S, Chevassut T. The epigenetic landscape of acute myeloid
leukemia. Adv Hematol. 2014. 2014:103175. [Medline]. [Full Text].
31. Marcucci G, Yan P, Maharry K, Frankhouser D, Nicolet D, Metzeler KH, et al.
Epigenetics meets genetics in acute myeloid leukemia: clinical impact of a novel seven-
gene score. J Clin Oncol. 2014 Feb 20. 32(6):548-56. [Medline]. [Full Text].
32. Marcucci G, Maharry K, Wu YZ, Radmacher MD, Mrzek K, Margeson D, et al. IDH1
and IDH2 gene mutations identify novel molecular subsets within de novo
cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study.
J Clin Oncol. 2010 May 10. 28(14):2348-55. [Medline]. [Full Text].
33. Schechter T, Gassas A, Chen H, Pollard J, Meshinchi S, Zaidman I, et al. The outcome of
allogeneic hematopoietic cell transplantation for children with FMS-like tyrosine kinase 3
internal tandem duplication-positive acute myelogenous leukemia. Biol Blood Marrow
Transplant. 2015 Jan. 21 (1):172-5. [Medline].
34. DiNardo CD, Cortes JE. New treatment for acute myelogenous leukemia. Expert Opin
Pharmacother. 2015 Jan. 16 (1):95-106. [Medline].
35. Fernandez HF, Sun Z, Yao X, Litzow MR, Luger SM, Paietta EM, et al. Anthracycline
dose intensification in acute myeloid leukemia. N Engl J Med. 2009 Sep 24.
361(13):1249-59. [Medline].
36. Lwenberg B, Ossenkoppele GJ, van Putten W, Schouten HC, Graux C, Ferrant A, et al.
High-dose daunorubicin in older patients with acute myeloid leukemia. N Engl J Med.
2009 Sep 24. 361(13):1235-48. [Medline].
37. Lowenberg B, Pabst T, Vellenga E, et al. Cytarabine dose for acute myeloid leukemia. N
Engl J Med. 2011 Mar 17. 364(11):1027-36. [Medline].
38. Mayer RJ, Davis RB, Schiffer CA, Berg DT, Powell BL, Schulman P, et al. Intensive
postremission chemotherapy in adults with acute myeloid leukemia. Cancer and
Leukemia Group B. N Engl J Med. 1994 Oct 6. 331(14):896-903. [Medline]. [Full Text].
39. Lwenberg B, Verdonck LJ, Dekker AW, Willemze R, Zwaan FE, de Planque M, et al.
Autologous bone marrow transplantation in acute myeloid leukemia in first remission:
results of a Dutch prospective study. J Clin Oncol. 1990 Feb. 8(2):287-94. [Medline].
40. Grimwade D, Walker H, Oliver F, Wheatley K, Harrison C, Harrison G, et al. The
importance of diagnostic cytogenetics on outcome in AML: analysis of 1,612 patients
entered into the MRC AML 10 trial. The Medical Research Council Adult and Children's
Leukaemia Working Parties. Blood. 1998 Oct 1. 92(7):2322-33. [Medline]. [Full Text].
41. Zittoun RA, Mandelli F, Willemze R, de Witte T, Labar B, Resegotti L, et al. Autologous
or allogeneic bone marrow transplantation compared with intensive chemotherapy in
acute myelogenous leukemia. European Organization for Research and Treatment of
Cancer (EORTC) and the Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto
(GIMEMA) Leukemia Cooperative Groups. N Engl J Med. 1995 Jan 26. 332(4):217-23.
[Medline]. [Full Text].
42. Harousseau JL, Cahn JY, Pignon B, Witz F, Milpied N, Delain M, et al. Comparison of
autologous bone marrow transplantation and intensive chemotherapy as postremission
therapy in adult acute myeloid leukemia. The Groupe Ouest Est Leucmies Aigus
Myloblastiques (GOELAM). Blood. 1997 Oct 15. 90(8):2978-86. [Medline]. [Full
Text].
43. Powell BL, Moser B, Stock W, et al. Effect of consolidation with arsenic trioxide
(As2O3) on event-free survival (EFS) and overall survival (OS) among patients with
newly diagnosed acute promyelocytic leukemia (APL): North American Intergroup
Protocol C9710. J Clin Oncol. 2007. 25 (18S June 20 supp):2.
44. Menzin J, Lang K, Earle CC, Kerney D, Mallick R. The outcomes and costs of acute
myeloid leukemia among the elderly. Arch Intern Med. 2002 Jul 22. 162(14):1597-603.
[Medline]. [Full Text].
45. Lwenberg B, Zittoun R, Kerkhofs H, Jehn U, Abels J, Debusscher L, et al. On the value
of intensive remission-induction chemotherapy in elderly patients of 65+ years with acute
myeloid leukemia: a randomized phase III study of the European Organization for
 Research and Treatment of Cancer Leukemia Group. J Clin Oncol. 1989 Sep. 7(9):1268-
74. [Medline].
46. Kantarjian H, O'brien S, Cortes J, Giles F, Faderl S, Jabbour E, et al. Results of intensive
chemotherapy in 998 patients age 65 years or older with acute myeloid leukemia or high-
risk myelodysplastic syndrome: predictive prognostic models for outcome. Cancer. 2006
Mar 1. 106(5):1090-8. [Medline]. [Full Text].
47. Burnett AK, Milligan D, Prentice AG, Goldstone AH, McMullin MF, Hills RK, et al. A
comparison of low-dose cytarabine and hydroxyurea with or without all-trans retinoic
acid for acute myeloid leukemia and high-risk myelodysplastic syndrome in patients not
considered fit for intensive treatment. Cancer. 2007 Mar 15. 109(6):1114-24. [Medline].
[Full Text].
48. Burnett AK, Milligan D, Prentice AG, et al. A comparison of low-dose cytarabine and
hydroxyurea with or without all-trans retinoic acid for acute myeloid leukemia and high-
risk myelodysplastic syndrome in patients not considered fit for intensive treatment.
Cancer. 2007 Mar 15. 109(6):1114-24. [Medline].
49. Burnett AK, Hills RK, Hunter AE, Milligan D, Kell WJ, Wheatley K, et al. The addition
of gemtuzumab ozogamicin to low-dose Ara-C improves remission rate but does not
significantly prolong survival in older patients with acute myeloid leukaemia: results
from the LRF AML14 and NCRI AML16 pick-a-winner comparison. Leukemia. 2013
Jan. 27(1):75-81. [Medline].
50. Itzykson R, Thepot S, Beyne-Rauzy O, et al. 52nd ASH Annual Meeting and Exposition.
Prolonged Survival without Complete Remission (CR) In AML Patients (Pts) Treated
with Azacitidine (AZA). Oral and Poster Abstracts. Poster Board II-63. American Society
of Hematology. Available at
http://ash.confex.com/ash/2010/webprogram/Paper30951.html. Accessed: March 28,
2011.
51. Ansstas G, Touma W, Adeimy C, et al. 52nd ASH Annual Meeting and Exposition.
Decitabine for Older AML Patients: An Effective Therapy Associated with Short
Hospitalization and No Invasive Fungal Infection. Oral and Poster Abstracts. Poster
Board I-43. American Society of Hematology. Available at
http://ash.confex.com/ash/2010/webprogram/Paper34114.html. Accessed: March 28,
2011.
52. Kantarjian HM, Thomas XG, Dmoszynska A, Wierzbowska A, Mazur G, Mayer J.
Multicenter, randomized, open-label, phase III trial of decitabine versus patient choice,
with physician advice, of either supportive care or low-dose cytarabine for the treatment
of older patients with newly diagnosed acute myeloid leukemia. J Clin Oncol. 2012 Jul
20. 30(21):2670-7. [Medline].
53. Faderl S, Verstovsek S, Cortes J, Ravandi F, Beran M, Garcia-Manero G, et al.
Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia
(AML) in patients 50 years of age or older. Blood. 2006 Jul 1. 108(1):45-51. [Medline].
[Full Text].
54. de Lima M, Anagnostopoulos A, Munsell M, Shahjahan M, Ueno N, Ippoliti C, et al.
Nonablative versus reduced-intensity conditioning regimens in the treatment of acute
myeloid leukemia and high-risk myelodysplastic syndrome: dose is relevant for long-
term disease control after allogeneic hematopoietic stem cell transplantation. Blood. 2004
Aug 1. 104(3):865-72. [Medline]. [Full Text].
55. Slavin S, Nagler A, Shapira MY, Aker M, Gabriel C, Or R. Treatment of leukemia by
alloreactive lymphocytes and nonmyeloablative stem cell transplantation. J Clin
Immunol. 2002 Mar. 22(2):64-9. [Medline].
56. Storb RF, Champlin R, Riddell SR, Murata M, Bryant S, Warren EH. Non-myeloablative
transplants for malignant disease. Hematology Am Soc Hematol Educ Program. 2001.
375-91. [Medline]. [Full Text].
57. Chen ZX, Xue YQ, Zhang R, Tao RF, Xia XM, Li C, et al. A clinical and experimental
study on all-trans retinoic acid-treated acute promyelocytic leukemia patients. Blood.
1991 Sep 15. 78(6):1413-9. [Medline]. [Full Text].
58. Fenaux P, Chastang C, Chevret S, Sanz M, Dombret H, Archimbaud E, et al. A
randomized comparison of all transretinoic acid (ATRA) followed by chemotherapy and
ATRA plus chemotherapy and the role of maintenance therapy in newly diagnosed acute
promyelocytic leukemia. The European APL Group. Blood. 1999 Aug 15. 94(4):1192-
200. [Medline]. [Full Text].
59. de Botton S, Fawaz A, Chevret S, Dombret H, Thomas X, Sanz M, et al. Autologous and
allogeneic stem-cell transplantation as salvage treatment of acute promyelocytic leukemia
initially treated with all-trans-retinoic acid: a retrospective analysis of the European acute
promyelocytic leukemia group. J Clin Oncol. 2005 Jan 1. 23(1):120-6. [Medline]. [Full
Text].
60. Frankel SR, Eardley A, Lauwers G, Weiss M, Warrell RP Jr. The "retinoic acid
syndrome" in acute promyelocytic leukemia. Ann Intern Med. 1992 Aug 15. 117(4):292-
6. [Medline].
61. Ads L, Chevret S, Raffoux E, de Botton S, Guerci A, Pigneux A, et al. Is cytarabine
useful in the treatment of acute promyelocytic leukemia? Results of a randomized trial
from the European Acute Promyelocytic Leukemia Group. J Clin Oncol. 2006 Dec 20.
24(36):5703-10. [Medline]. [Full Text].
62. Sanz MA, Martn G, Gonzlez M, Len A, Rayn C, Rivas C, et al. Risk-adapted
treatment of acute promyelocytic leukemia with all-trans-retinoic acid and anthracycline
monochemotherapy: a multicenter study by the PETHEMA group. Blood. 2004 Feb 15.
103(4):1237-43. [Medline]. [Full Text].
63. Lo-Coco F, Avvisati G, Vignetti M, Thiede C, Orlando SM, Iacobelli S, et al. Retinoic
acid and arsenic trioxide for acute promyelocytic leukemia. N Engl J Med. 2013 Jul 11.
369(2):111-21. [Medline].
64. Estey E, Kornblau S, Pierce S, Kantarjian H, Beran M, Keating M. A stratification
system for evaluating and selecting therapies in patients with relapsed or primary
refractory acute myelogenous leukemia. Blood. 1996 Jul 15. 88(2):756. [Medline]. [Full
Text].
65. Giles F, O'Brien S, Cortes J, et al. Outcome of patients with acute myelogenous leukemia
after second salvage therapy. Cancer. 2005 Aug 1. 104(3):547-54. [Medline].
66. Wierzbowska A, Robak T, Pluta A, et al. Cladribine combined with high doses of
arabinoside cytosine, mitoxantrone, and G-CSF (CLAG-M) is a highly effective salvage
regimen in patients with refractory and relapsed acute myeloid leukemia of the poor risk:
a final report of the Polish Adult Leukemia Group. Eur J Haematol. 2008 Feb. 80(2):115-
26. [Medline].
67. Amadori S, Arcese W, Isacchi G, et al. Mitoxantrone, etoposide, and intermediate-dose
cytarabine: an effective and tolerable regimen for the treatment of refractory acute
myeloid leukemia. J Clin Oncol. 1991 Jul. 9(7):1210-4. [Medline].
68. Levis M, Ravandi F, Wang ES, et al. Results from a randomized trial of salvage
chemotherapy followed by lestaurtinib for patients with FLT3 mutant AML in first
relapse. Blood. 2011 Mar 24. 117(12):3294-301. [Medline]. [Full Text].
69. Cornely OA, Maertens J, Winston DJ, Perfect J, Ullmann AJ, Walsh TJ, et al.
Posaconazole vs. fluconazole or itraconazole prophylaxis in patients with neutropenia. N
Engl J Med. 2007 Jan 25. 356(4):348-59. [Medline]. [Full Text].
70. Ohno R, Tomonaga M, Kobayashi T, Kanamaru A, Shirakawa S, Masaoka T, et al. Effect
of granulocyte colony-stimulating factor after intensive induction therapy in relapsed or
refractory acute leukemia. N Engl J Med. 1990 Sep 27. 323(13):871-7. [Medline].
71. Dombret H, Chastang C, Fenaux P, Reiffers J, Bordessoule D, Bouabdallah R, et al. A
controlled study of recombinant human granulocyte colony-stimulating factor in elderly
patients after treatment for acute myelogenous leukemia. AML Cooperative Study Group.
N Engl J Med. 1995 Jun 22. 332(25):1678-83. [Medline]. [Full Text].
72. Godwin JE, Kopecky KJ, Head DR, Willman CL, Leith CP, Hynes HE, et al. A double-
blind placebo-controlled trial of granulocyte colony-stimulating factor in elderly patients
with previously untreated acute myeloid leukemia: a Southwest oncology group study
(9031). Blood. 1998 May 15. 91(10):3607-15. [Medline]. [Full Text].
73. Rowe JM, Andersen JW, Mazza JJ, Bennett JM, Paietta E, Hayes FA, et al. A
randomized placebo-controlled phase III study of granulocyte-macrophage colony-
stimulating factor in adult patients (> 55 to 70 years of age) with acute myelogenous
leukemia: a study of the Eastern Cooperative Oncology Group (E1490). Blood. 1995 Jul
15. 86(2):457-62. [Medline]. [Full Text].
74. Stone RM, Berg DT, George SL, Dodge RK, Paciucci PA, Schulman P, et al.
Granulocyte-macrophage colony-stimulating factor after initial chemotherapy for elderly
patients with primary acute myelogenous leukemia. Cancer and Leukemia Group B. N
Engl J Med. 1995 Jun 22. 332(25):1671-7. [Medline]. [Full Text].
75. Zittoun R, Suciu S, Mandelli F, de Witte T, Thaler J, Stryckmans P, et al. Granulocyte-
macrophage colony-stimulating factor associated with induction treatment of acute
myelogenous leukemia: a randomized trial by the European Organization for Research
and Treatment of Cancer Leukemia Cooperative Group. J Clin Oncol. 1996 Jul.
14(7):2150-9. [Medline].
76. [Guideline] Fey MF, Buske C, ESMO Guidelines Working Group. Acute myeloblastic
leukaemias in adult patients: ESMO Clinical Practice Guidelines for diagnosis, treatment
and follow-up. Ann Oncol. 2013 Oct. 24 Suppl 6:vi138-43. [Medline]. [Full Text].
77. Taskesen E, Bullinger L, Corbacioglu A, Sanders MA, Erpelinck CA, Wouters BJ, et al.
Prognostic impact, concurrent genetic mutations, and gene expression features of AML
with CEBPA mutations in a cohort of 1182 cytogenetically normal AML patients: further
evidence for CEBPA double mutant AML as a distinctive disease entity. Blood. 2011 Feb
24. 117(8):2469-75. [Medline].
78. Valk PJ, Verhaak RG, Beijen MA, Erpelinck CA, Barjesteh van Waalwijk van Doorn-
Khosrovani S, Boer JM, et al. Prognostically useful gene-expression profiles in acute
myeloid leukemia. N Engl J Med. 2004 Apr 15. 350(16):1617-28. [Medline]. [Full Text].
 79. Li R, Hu X, Wang L, Cheng H, Lv S, Zhang W, et al. Fludarabine and Cytarabine versus
High-dose Cytarabine in Consolidation Treatment of t(8; 21) Acute Myeloid Leukemia: a
prospective, randomized study. Am J Hematol. 2016 Sep 27. [Medline].
80. Poynter JN, Richardson M, Roesler M, Blair CK, Hirsch B, Nguyen P, et al. Chemical
exposures and risk of acute myeloid leukemia and myelodysplastic syndromes in a
population-based study. Int J Cancer. 2016 Sep 7. [Medline].

What to Read Next on Medscape

Related Conditions and Diseases

Pathology of Acute Leukemias of Ambiguous Lineage

Acute Lymphoblastic Leukemia Staging
Acute Myeloid Leukemia Staging
Pediatric Acute Myelocytic Leukemia
Genetics of Acute Myeloid Leukemia
Acute Lymphoblastic Leukemia (ALL) Guidelines

News & Perspective

CPX-351: Better Outcomes in Older High-Risk AML

Patients
At ASH, New Approaches Suggest 'Major Advances' Against AML
CAR T Cells Motoring to Market -- by Next Year?

Tools

Drug Interaction Checker

Pill Identifier
Calculators
Formulary
Slideshow

2016 in Review: Key Guidelines in Hematology and Oncology You

Need to Know

Most Popular Articles

According to Oncologist/Hematologists

1. Browned Toast, Potatoes May Raise Cancer Risk

2. Breast Cancer Campaign Based on Lemons Goes Viral
3. New Rx for Advanced Colorectal Cancer: Exercise
4. Indications for Adjuvant Radiation Therapy in Breast Cancer
5. The New Era of First-Line Immunotherapy for Advanced NSCLC

View More

Overview
o Practice Essentials
o Pathophysiology
o Etiology
o Epidemiology
o Prognosis
o Patient Education
o Show All
Presentation
DDx
 Workup
Treatment
Guidelines
Medication
Tables
References

Recommended

Diseases & Conditions Acute Lymphoblastic Leukemia Staging

Diseases & Conditions Acute

praktek Essentials
leukemia myelogenous akut (AML) adalah penyakit ganas dari sumsum tulang di mana prekursor
hematopoietik ditangkap dalam tahap awal pengembangan. Kebanyakan subtipe AML dibedakan dari
gangguan darah terkait lainnya dengan kehadiran lebih dari 20% ledakan di sumsum tulang.
Lihat Leukemia Kronis: 4 Kanker Membedakan, sebuah Images Kritis slideshow, untuk membantu
mendeteksi leukemia kronis dan menentukan jenis hadir tertentu.
Patofisiologi yang mendasari di AML terdiri dari penangkapan pematangan sel sumsum tulang pada
tahap awal pengembangan. (Lihat Patofisiologi.) Beberapa faktor telah terlibat dalam penyebab dari
AML, termasuk gangguan yg hematologi, sindrom familial, paparan lingkungan, dan pajanan obat.
Namun, sebagian besar pasien yang datang dengan de novo AML tidak memiliki faktor risiko
diidentifikasi. (Lihat Etiologi.)
Pasien dengan AML hadir dengan gejala yang dihasilkan dari kegagalan sumsum tulang, gejala akibat
infiltrasi organ dengan sel-sel leukemia, atau keduanya. Waktu kursus adalah variabel. (Lihat Presentasi.)
The pemeriksaan untuk AML meliputi tes darah, sumsum tulang aspirasi dan biopsi (tes diagnostik
definitif), dan analisis kelainan genetik. (Lihat hasil pemeriksaan.)
rejimen kemoterapi standar saat menyembuhkan hanya sebagian kecil pasien dengan AML. Akibatnya,
semua pasien harus dievaluasi untuk masuk ke uji klinis yang dirancang dengan baik. Jika percobaan
klinis tidak tersedia, pasien dapat diobati dengan terapi standar. (Lihat Treatment.) Diterima kembali
sering diperlukan untuk pengelolaan efek racun dari kemoterapi.
patofisiologi
Patofisiologi yang mendasari di AML terdiri dari penangkapan pematangan sel sumsum tulang pada
tahap awal pengembangan. Mekanisme penangkapan ini berada di bawah studi, tetapi dalam banyak
kasus, melibatkan aktivasi gen yang abnormal melalui translokasi kromosom dan kelainan genetik
lainnya. [1, 2, 3]
Penangkapan perkembangan hasil ini dalam 2 proses penyakit. Pertama, produksi sel darah normal
nyata menurun, yang menghasilkan berbagai derajat anemia, trombositopenia, dan neutropenia. Kedua,
proliferasi cepat dari sel-sel ini, bersama dengan penurunan kemampuan mereka untuk menjalani
program kematian sel (apoptosis), menyebabkan akumulasi dalam sumsum tulang, darah, dan, sering,
limpa dan hati.
Etiologi
Beberapa faktor telah terlibat dalam penyebab dari AML, termasuk gangguan yg hematologi, sindrom
familial, paparan lingkungan, dan pajanan obat. Namun, sebagian besar pasien yang datang dengan de
novo AML tidak memiliki faktor risiko diidentifikasi.
Gangguan hematologi yg
faktor risiko yang paling umum untuk AML adalah adanya gangguan hematologi yg, yang paling umum
dari yang myelodysplastic syndrome (MDS). MDS adalah penyakit sumsum tulang dari etiologi yang tidak
diketahui yang terjadi paling sering pada pasien yang lebih tua dan bermanifestasi sebagai cytopenias
progresif yang terjadi selama bulan ke tahun. Pasien dengan risiko rendah MDS (misalnya, anemia
refrakter dengan temuan Sitogenetika normal) umumnya tidak mengembangkan AML, sedangkan
pasien dengan risiko tinggi MDS (misalnya, anemia refrakter dengan kelebihan ledakan-tipe 2) sering
dilakukan.
Gangguan hematologi yg lain yang mempengaruhi pasien untuk AML meliputi anemia aplastik dan
mielofibrosis.
kelainan bawaan
Beberapa kelainan bawaan yang mempengaruhi pasien untuk AML termasuk sindrom Bloom, sindrom
Down, neutropenia kongenital, Fanconi anemia, dan neurofibromatosis. Biasanya, pasien tersebut
mengembangkan AML selama masa kanak-kanak; jarang, beberapa mungkin hadir di masa dewasa
muda.
kelainan genetik lebih halus, termasuk polimorfisme enzim yang memetabolisme karsinogen, juga
mempengaruhi pasien untuk AML. Misalnya, polimorfisme NAD (P) H: kuinon oksidoreduktase (NQO1),
enzim yang memetabolisme derivatif benzena, terkait dengan peningkatan risiko AML. [4] meningkat
Khususnya risiko ada untuk AML yang terjadi setelah kemoterapi untuk penyakit lain atau untuk de novo
AML dengan kelainan kromosom 5, 7, atau keduanya.
Demikian juga, polimorfisme di glutathione S -transferase berhubungan dengan AML sekunder setelah
kemoterapi untuk keganasan lainnya. [5]
sindrom keluarga
mutasi germline dalam AML1 gen (RUNX1, CBFA2) terjadi pada gangguan platelet keluarga dengan
predisposisi untuk AML, gangguan dominan autosomal yang ditandai dengan trombositopenia moderat,
cacat dalam fungsi trombosit, dan kecenderungan untuk mengembangkan AML. [6] Mutasi CEBPA
(alpha protein gen encoding CCAAT / enhancer mengikat, faktor diferensiasi granulositik dan anggota
keluarga bzip) digambarkan dalam sebuah keluarga dengan 3 anggota yang terkena AML. [7]
Holme dkk meneliti 27 keluarga dengan keluarga MDS / AML. Semua keluarga diskrining untuk RUNX1,
mutasi CEBPA, TERC, TERT, GATA2, TET2, dan NPM1. Lima dari 27 keluarga memiliki mutasi telomerase
(3 TERT, 2 TERC), salah satu memiliki mutasi RUNX1, dan empat memiliki mutasi GATA2 heterozigot. [8]
Gao et al recen

tly Ulasan mutasi GATA2 terkait dengan familial AML-MDS. [9] GATA2 merupakan faktor transkripsi yang
penting untuk diferensiasi hematopoietik dan pembentukan limfatik, dan mutasi GATA2 germline
terlibat dalam kelompok langka sindrom kompleks dengan tumpang tindih fitur klinis defisiensi imun,
lymphedema, dan kecenderungan untuk AML atau MDS.Some sindrom kanker turun-temurun , seperti
sindrom Li-Fraumeni, dapat bermanifestasi sebagai leukemia. Namun, kasus leukemia kurang umum
daripada tumor padat yang umumnya menjadi ciri penelitian syndromes.Environmental
exposuresSeveral ini menunjukkan hubungan antara paparan radiasi dan leukemia. Awal ahli radiologi
(sebelum penggunaan perisai yang tepat) ditemukan memiliki kemungkinan peningkatan
mengembangkan leukemia. Pasien yang menerima iradiasi terapi untuk ankylosing spondylitis berada
pada peningkatan risiko leukemia. Selamat dari ledakan bom atom di Jepang berada pada risiko yang
meningkat tajam untuk pengembangan leukemia.Persons yang merokok memiliki (rasio odds, 1,5) kecil
tapi signifikan secara statistik peningkatan risiko AML. [10] Dalam beberapa penelitian, risiko AML
sedikit meningkat pada orang yang merokok dibandingkan dengan mereka yang tidak smoke.Exposure
untuk benzena dikaitkan dengan anemia aplastik dan pansitopenia. Pasien-pasien ini sering
mengembangkan AML. Banyak dari pasien ini menunjukkan M6 morfologi. Paparan jelaga, kreosot,
tinta, pewarna dan solusi tanning dan debu batubara juga telah dikaitkan dengan AML. [80] Sebelumnya
paparan agentsAs kemoterapi lebih banyak pasien dengan kanker bertahan hidup keganasan utama
mereka dan lebih banyak pasien menerima kemoterapi intensif (termasuk transplantasi sumsum tulang
[BMT]), jumlah pasien dengan AML meningkat karena paparan agen kemoterapi. Misalnya, kejadian
kumulatif leukemia akut pada pasien dengan kanker payudara yang diobati dengan doxorubicin dan
siklofosfamid sebagai terapi adjuvan adalah 0,2-1,0% pada 5 tahun. [11] Pasien dengan paparan
sebelumnya untuk agen kemoterapi dapat dibagi menjadi 2 kelompok: (1) orang-orang dengan paparan
sebelumnya alkylating agen dan (2) orang-orang dengan paparan inhibitors.Patients topoisomerase-II
dengan paparan sebelumnya untuk agen alkylating, dengan atau tanpa radiasi, sering memiliki fase
myelodysplastic sebelum pengembangan AML. Sitogenetika pengujian sering mengungkapkan -5 dan /
atau -7 (5q- atau monosomi 7) .Patients dengan paparan sebelumnya terhadap inhibitor topoisomerase-
II tidak memiliki fase myelodysplastic. Sitogenetika pengujian mengungkapkan translokasi yang
melibatkan Band 11q23. Kurang umum, pasien mengembangkan leukemia dengan translokasi lainnya
yang seimbang, seperti inversi 16 atau t (15; 17). [12] Periode latensi khas antara paparan obat dan
leukemia akut adalah sekitar 3-5 tahun untuk alkylating agen / paparan radiasi, tetapi hanya 9-12 bulan
untuk topoisomerase inhibitors.EpidemiologyThe American Cancer Society memperkirakan bahwa
19.950 kasus baru AML ( 11.130 pada pria, 8820 perempuan) akan terjadi di Amerika Serikat pada tahun
2016, akuntansi untuk 31% dari semua kasus leukemia pada orang dewasa 20 tahun dan lebih tua. [13]
AML lebih sering didiagnosis di negara maju, dan lebih sering terjadi pada orang kulit putih daripada
prevalensi populations.The lain dari AML meningkat dengan usia. Usia rata-rata onset adalah sekitar 70
tahun. Namun, AML mempengaruhi semua usia groups.AML lebih sering terjadi pada pria dibandingkan
pada wanita. Perbedaan ini bahkan lebih jelas pada pasien yang lebih tua. Hal ini mungkin karena MDS
lebih sering terjadi pada laki-laki, dan maju MDS sering berkembang menjadi AML. Beberapa telah
mengusulkan bahwa peningkatan prevalensi AML pada pria mungkin terkait dengan eksposur pekerjaan
(lihat Etiologi) prognosis .PrognosisThe bergantung pada beberapa faktor. Bertambahnya usia
merupakan faktor yang merugikan, karena pasien yang lebih tua lebih sering mengalami gangguan yg
hematologi sebelumnya bersama dengan kondisi medis penyerta yang kompromi kemampuan untuk
memberikan dosis penuh kemoterapi. Sebuah sebelumnya gangguan yg hematologi (paling sering, MDS)
dikaitkan dengan hasil yang buruk untuk studi therapy.A oleh Arellano et al ditemukan leukopenia di
diagnosis tidak memiliki makna prognostik pada pasien dengan AML. [14] Temuan dari analisis
sitogenetika dari sumsum tulang merupakan salah satu faktor prognostik paling penting. Pasien dengan
t (8; 21), t (15; 17), atau inversi 16 memiliki prognosis yang terbaik, dengan tingkat kelangsungan hidup
jangka panjang dari sekitar 65%. Pasien dengan temuan sitogenetika yang normal memiliki prognosis
menengah dan memiliki tingkat kelangsungan hidup jangka panjang dari sekitar 25%. Pasien dengan
temuan sitogenetika berisiko miskin (terutama -7, -5) memiliki prognosis buruk, dengan tingkat
kelangsungan hidup jangka panjang kurang dari 10% kelainan sitogenetika .Lain, termasuk 8, 11q23, dan
lain-lain, telah dilaporkan berisiko menengah di beberapa seri dan risiko miskin di hadapan others.The
dari mutasi Flt3 dikaitkan dengan prognosis yang lebih buruk. Mutasi pada CEBPA berhubungan dengan
durasi remisi lebih lama dan lebih lama overa

kelangsungan hidup ll. Mutasi pada NPM berhubungan dengan respon meningkat menjadi studi
chemotherapy.A oleh Metzeler et al menentukan bahwa mutasi TET2 berdampak prognostik buruk di
bagian pasien dinyatakan menguntungkan berisiko menggunakan LeukemiaNet Eropa (ELN) klasifikasi
molekul-risiko pasien dengan primer AML cytogenetically normal. [15] Pada orang dewasa, hasil
pengobatan umumnya dianalisis secara terpisah untuk lebih muda (18-60 y) pasien dengan AML dan
untuk pasien yang lebih tua (> 60 y). Dengan rejimen kemoterapi standar saat ini, sekitar 30-35% dari
orang dewasa yang lebih muda dari 60 tahun bertahan hidup lebih lama dari 5 tahun dan dianggap
sembuh. Hasil pada pasien yang lebih tua lebih mengecewakan, dengan kurang dari 10% dari hidup
selama studi term.A panjang dengan Kayser et al menemukan bahwa terapi terkait AML (t-AML)
merupakan faktor prognostik yang merugikan bagi kematian pada remisi lengkap tapi tidak kambuh dan
kelangsungan hidup secara keseluruhan di muda pasien ditangani secara intensif. [16] Itu juga
merupakan faktor prognostik yang merugikan untuk kambuh tapi tidak mati di remisi lengkap di tua,
kurang ditangani secara intensif studi patients.A oleh Varadarajan et al menemukan bahwa setelah
pernah merokok menurun kelangsungan hidup secara keseluruhan pada pasien dengan AML. [17]
Crysandt dan collegeues menemukan bahwa pada pasien yang lebih muda dengan de novo AML,
kelebihan berat badan dan obesitas merupakan faktor risiko untuk respon gangguan untuk induksi
terapi dan bebas penyakit dan secara keseluruhan lebih pendek kelangsungan hidup. [18] The American
Cancer Society memperkirakan bahwa pada tahun 2015, 10.460 kematian akibat AML akan terjadi di
Amerika Serikat. Dari jumlah tersebut, 6110 diharapkan terjadi pada pria dan 4350 wanita. [13]
Kematian pada pasien dengan AML mungkin akibat dari infeksi yang tidak terkontrol atau perdarahan.
Hal ini dapat terjadi bahkan setelah penggunaan produk darah yang tepat dan EducationPatients
support.Patient antibiotik dengan AML harus diinstruksikan untuk segera memanggil penyedia layanan
kesehatan mereka jika mereka demam atau memiliki tanda-tanda sumber bleeding.For pendidikan
pasien, melihat darah dan limfatik System Center dan Kulit, rambut, dan kuku Center, serta Leukemia
dan Lebam.