eMedicine Specialties > Hematology > Stem Cells and Disorders

Acute Myelogenous Leukemia

Author: Karen Seiter, MD, Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College
Contributor Information and Disclosures

Updated: Mar 4, 2009

Introduction

Background

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.

For excellent patient education resources, visit eMedicine's Blood and Lymphatic System Center and Skin, Hair, and Nails Center. Also, see eMedicine's patient education articles Leukemia and Bruises.

Pathophysiology

The underlying pathophysiology in acute myelogenous leukemia (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

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, blood, and, frequently, the spleen and liver.

Frequency

United States

Estimates of new cases of acute myelogenous leukemia (AML) in the United States in 2007 were 13,410 (7060 men; 6350 women).

International

Acute myelogenous leukemia (AML) is more commonly diagnosed in developed countries.

Mortality/Morbidity

  • In 2007, an estimated 8990 deaths from acute myelogenous leukemia (AML) occurred in the United States. Of these, 5020 occurred in men and 3970 occurred in women.
  • In adults, treatment results are generally analyzed separately for younger (18-60 y) and older (>60 y) patients with acute myelogenous leukemia (AML).
    • 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.

Race

  • Acute myelogenous leukemia (AML) is more common in whites than in other populations.

Sex

  • Acute myelogenous leukemia (AML) is more common in men than in women. The difference is even more apparent in older patients. This is likely because myelodysplastic syndromes (MDSs) are more common in men, and advanced MDS frequently evolves into AML. Some have proposed that the increased prevalence of acute myelogenous leukemia (AML) in men may be related to occupational exposures.

Age

  • The prevalence of acute myelogenous leukemia (AML) increases with age. The median age of onset is approximately 70 years. However, acute myelogenous leukemia (AML) affects all age groups.

Clinical

History

  • Patients with acute myelogenous leukemia (AML) present with symptoms resulting from bone marrow failure, organ infiltration with leukemic cells, or both. The time course is variable.
    • Some patients, particularly younger ones, present with acute symptoms over a few days to 1-2 weeks.
    • Others have a longer course, with fatigue or other symptoms lasting from weeks to months. A longer course may suggest an antecedent hematologic disorder (AHD) such as MDS.
  • Symptoms of bone marrow failure are related to anemia, neutropenia, and thrombocytopenia.
    • The most common symptom of anemia is fatigue. Patients often retrospectively note a decreased energy level over past weeks.
    • Other symptoms of anemia include dyspnea upon exertion, dizziness, and, in patients with coronary artery disease, anginal chest pain. In fact, myocardial infarction may be the first presenting symptom of acute leukemia in an older patient.
    • Patients often have decreased neutrophil levels despite an increased total white blood cell (WBC) count.
    • Patients with acute myelogenous leukemia (AML) present with fever, which may occur with or without specific documentation of an infection. Patients with the lowest absolute neutrophil counts (ANCs) (ie, <500 cells/µL, especially <100 cells/µL) have the highest risk of infection.
    • Patients often have a history of upper respiratory infection symptoms that have not improved despite empiric treatment with oral antibiotics.
    • Patients present with bleeding gums and multiple ecchymoses. Bleeding may be caused by thrombocytopenia, coagulopathy that results from disseminated intravascular coagulation (DIC), or both.
    • Potentially life-threatening sites of bleeding include the lungs, gastrointestinal tract, and the central nervous system
  • Alternatively, symptoms may be the result of organ infiltration with leukemic cells.
    • The most common sites of infiltration include the spleen, liver, gums, and skin.
    • Infiltration occurs most commonly in patients with the monocytic subtypes of acute myelogenous leukemia (AML).
    • Patients with splenomegaly note fullness in the left upper quadrant and early satiety.
    • Patients with gum infiltration often present to their dentist first. Gingivitis due to neutropenia can cause swollen gums, and thrombocytopenia can cause the gums to bleed.
    • Patients with markedly elevated WBC counts (>100,000 cells/µL) can present with symptoms of leukostasis (ie, respiratory distress and altered mental status). Leukostasis is a medical emergency that requires immediate intervention.
    • Patients with a high leukemic cell burden may present with bone pain caused by increased pressure in the bone marrow.

Physical

  • Physical signs of anemia, including pallor and a cardiac flow murmur, are frequently present in those with acute myelogenous leukemia (AML).
  • Fever and other signs of infection can occur, including lung findings of pneumonia.
  • Patients with thrombocytopenia usually demonstrate petechiae, particularly on the lower extremities. The petechiae are small, often punctate, hemorrhagic rashes that are not palpable. Areas of dermal bleeding or bruises (ie, ecchymoses) that are large or present in several areas may indicate a coexistent coagulation disorder such as DIC. Purpura is characterized by flat bruises that are larger than petechiae but smaller than ecchymoses.
  • Signs relating to organ infiltration with leukemic cells include hepatosplenomegaly and, to a lesser degree, lymphadenopathy. Occasionally, patients have skin rashes due to infiltration of the skin with leukemic cells (leukemia cutis). Chloromata are extramedullary deposits of leukemia. Rarely, a bony or soft-tissue chloroma may precede the development of marrow infiltration by acute myelogenous leukemia (AML) (granulocytic sarcoma).
  • Signs relating to leukostasis include respiratory distress and altered mental status.

Causes

  • Although several factors have been implicated in the causation of acute myelogenous leukemia (AML), most patients who present with de novo AML have no identifiable risk factor.
  • Antecedent hematologic disorders
    • The most common risk factor for acute myelogenous leukemia (AML) is the presence of an antecedent hematologic disorder, the most common of which is MDS. MDS is a disease of the bone marrow 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 acute myelogenous leukemia (AML), whereas patients with high-risk MDS (eg, refractory anemia with excess blasts-type 2) frequently do develop AML.
    • Other antecedent hematologic disorders that predispose patients to acute myelogenous leukemia (AML) include aplastic anemia, myelofibrosis, paroxysmal nocturnal hemoglobinuria, and polycythemia vera.
  • Congenital disorders
    • Some congenital disorders that predispose patients to acute myelogenous leukemia (AML) include Bloom syndrome, Down syndrome, congenital neutropenia, Fanconi anemia, and neurofibromatosis.
    • Usually, these patients develop acute myelogenous leukemia (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 acute myelogenous leukemia (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.3 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 acute myelogenous leukemia (AML) following chemotherapy for other malignancies.4
  • Familial syndromes
    • Germ-line mutations in the gene AML1 (RUNX1, CBFA2) occur in the familial platelet disorder with predisposition for myelogenous leukemia (AML), an autosomal-dominant disorder characterized by moderate thrombocytopenia, a defect in platelet function, and propensity to develop AML.
    • 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 myelogenous leukemia (AML).5
    • 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 myelogenous leukemia (AML). 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.
  • Previous exposure to chemotherapeutic agents for another malignancy
    • 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 myelogenous leukemia (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.6
    • 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 myelogenous leukemia (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 chromosome band 11q23. Less commonly, patients developed leukemia with other balanced translocations, such as inversion 16 or t(15;17).7
    • 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.

More on Acute Myelogenous Leukemia

Overview: Acute Myelogenous Leukemia
Differential Diagnoses & Workup: Acute Myelogenous Leukemia
Treatment & Medication: Acute Myelogenous Leukemia
Follow-up: Acute Myelogenous Leukemia
References
[ CLOSE WINDOW ]

References

  1. Vardiman JW, Harris NL, Brunning RD. The World Health Organization (WHO) classification of the myeloid neoplasms. Blood. Oct 1 2002;100(7):2292-302. [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. Larson RA, Wang Y, Banerjee M, 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. Jul 15 1999;94(2):803-7. [Medline]. [Full Text].

  4. Allan JM, Wild CP, Rollinson S, et al. Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapy-induced leukemia. Proc Natl Acad Sci U S A. Sep 25 2001;98(20):11592-7. [Medline]. [Full Text].

  5. Smith ML, Cavenagh JD, Lister TA, Fitzgibbon J. Mutation of CEBPA in familial acute myeloid leukemia. N Engl J Med. Dec 2 2004;351(23):2403-7. [Medline]. [Full Text].

  6. 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. Apr 1 2003;21(7):1195-204. [Medline]. [Full Text].

  7. Andersen MK, Larson RA, Mauritzson N, et al. 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. Apr 2002;33(4):395-400. [Medline].

  8. Griswold IJ, Shen LJ, La Rosee P, et al. Effects of MLN518, a dual FLT3 and KIT inhibitor, on normal and malignant hematopoiesis. Blood. Nov 1 2004;104(9):2912-8. [Medline]. [Full Text].

  9. Thiede C, Steudel C, Mohr B, 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. Jun 15 2002;99(12):4326-35. [Medline]. [Full Text].

  10. Mayer RJ, Davis RB, Schiffer CA, et al, for the Cancer and Leukemia Group B. Intensive postremission chemotherapy in adults with acute myeloid leukemia. N Engl J Med. Oct 6 1994;331(14):896-903. [Medline]. [Full Text].

  11. Lowenberg B, Verdonck LJ, Dekker AW, et al. Autologous bone marrow transplantation in acute myeloid leukemia in first remission: results of a Dutch prospective study. J Clin Oncol. Feb 1990;8(2):287-94. [Medline].

  12. Grimwade D, Walker H, Oliver F, et al, for The Medical Research Council Adult and Children's Leukaemia Working Parties. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1,612 patients entered into the MRC AML 10 trial. Blood. Oct 1 1998;92(7):2322-33. [Medline]. [Full Text].

  13. Zittoun RA, Mandelli F, Willemze R, et al, for The European Organization for Research and Treatment of Cancer (EORTC) and the Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto (GIMEMA) Leukemia Cooperative Groups. Autologous or allogeneic bone marrow transplantation compared with intensive chemotherapy in acute myelogenous leukemia. N Engl J Med. Jan 26 1995;332(4):217-23. [Medline]. [Full Text].

  14. Harousseau JL, Cahn JY, Pignon B, et al, for The Groupe Ouest Est Leucemies Aigues Myeloblastiques (GOELAM). Comparison of autologous bone marrow transplantation and intensive chemotherapy as postremission therapy in adult acute myeloid leukemia. Blood. Oct 15 1997;90(8):2978-86. [Medline]. [Full Text].

  15. 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.

  16. Menzin J, Lang K, Earle CC, Kerney D, Mallick R. The outcomes and costs of acute myeloid leukemia among the elderly. Arch Intern Med. Jul 22 2002;162(14):1597-603. [Medline]. [Full Text].

  17. Lowenberg B, Zittoun R, Kerkhofs H, 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. Sep 1989;7(9):1268-74. [Medline].

  18. Kantarjian H, O'Brien S, Cortes J, 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. Mar 1 2006;106(5):1090-8. [Medline]. [Full Text].

  19. 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. Mar 15 2007;109(6):1114-24. [Medline]. [Full Text].

  20. Giles F, Rizzieri D, Karp J, et al. Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia. J Clin Oncol. Jan 1 2007;25(1):25-31. [Medline]. [Full Text].

  21. Faderl S, Verstovsek S, Cortes J, et al. Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older. Blood. Jul 1 2006;108(1):45-51. [Medline]. [Full Text].

  22. Blum W, Klisovic RB, Hackanson B, et al. Phase I study of decitabine alone or in combination with valproic acid in acute myeloid leukemia. J Clin Oncol. Sep 1 2007;25(25):3884-91. [Medline]. [Full Text].

  23. Silverman LR, McKenzie DR, Peterson BL, et al. Further analysis of trials with azacitidine in patients with myelodysplastic syndrome: studies 8421, 8921, and 9221 by the Cancer and Leukemia Group B. J Clin Oncol. Aug 20 2006;24(24):3895-903. [Medline]. [Full Text].

  24. Chen ZX, Xue YQ, Zhang R, et al. A clinical and experimental study on all-trans retinoic acid-treated acute promyelocytic leukemia patients. Blood. Sep 15 1991;78(6):1413-9. [Medline]. [Full Text].

  25. Fenaux P, Chastang C, Chevret S, et al, for the European APL Group. 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. Blood. Aug 15 1999;94(4):1192-200. [Medline]. [Full Text].

  26. de Botton S, Fawaz A, Chevret S, 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. Jan 1 2005;23(1):120-6. [Medline]. [Full Text].

  27. Frankel SR, Eardley A, Lauwers G, Weiss M, Warrell RP Jr. The "retinoic acid syndrome" in acute promyelocytic leukemia. Ann Intern Med. Aug 15 1992;117(4):292-6. [Medline].

  28. Sanz MA, Martin G, Gonzalez M, et al, for the Programa de Estudio y Traitmiento de las Hemopatias Malignas. Risk-adapted treatment of acute promyelocytic leukemia with all-trans-retinoic acid and anthracycline monochemotherapy: a multicenter study by the PETHEMA group. Blood. Feb 15 2004;103(4):1237-43. [Medline]. [Full Text].

  29. Estey E, Kornblau S, Pierce S, et al. A stratification system for evaluating and selecting therapies in patients with relapsed or primary refractory acute myelogenous leukemia. Blood. Jul 15 1996;88(2):756. [Medline]. [Full Text].

  30. Sievers EL, Larson RA, Stadtmauer EA, et al, for the Mylotarg Study Group. Efficacy and safety of gemtuzumab ozogamicin in patients with CD33-positive acute myeloid leukemia in first relapse. J Clin Oncol. Jul 1 2001;19(13):3244-54. [Medline]. [Full Text].

  31. Wadleigh M, Richardson PG, Zahrieh D, et al. Prior gemtuzumab ozogamicin exposure significantly increases the risk of veno-occlusive disease in patients who undergo myeloablative allogeneic stem cell transplantation. Blood. Sep 1 2003;102(5):1578-82. [Medline]. [Full Text].

  32. Ohno R, Tomonaga M, Kobayashi T, et al. Effect of granulocyte colony-stimulating factor after intensive induction therapy in relapsed or refractory acute leukemia. N Engl J Med. Sep 27 1990;323(13):871-7. [Medline].

  33. Dombret H, Chastang C, Fenaux P, et al, for the AML Cooperative Study Group. A controlled study of recombinant human granulocyte colony-stimulating factor in elderly patients after treatment for acute myelogenous leukemia. N Engl J Med. Jun 22 1995;332(25):1678-83. [Medline]. [Full Text].

  34. Godwin JE, Kopecky KJ, Head DR, 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. May 15 1998;91(10):3607-15. [Medline]. [Full Text].

  35. Rowe JM, Andersen JW, Mazza JJ, 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. Jul 15 1995;86(2):457-62. [Medline]. [Full Text].

  36. Stone RM, Berg DT, George SL, et al, for the Cancer and Leukemia Group B. Granulocyte-macrophage colony-stimulating factor after initial chemotherapy for elderly patients with primary acute myelogenous leukemia. N Engl J Med. Jun 22 1995;332(25):1671-7. [Medline]. [Full Text].

  37. Zittoun R, Suciu S, Mandelli F, 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. Jul 1996;14(7):2150-9. [Medline].

  38. Ades L, Chevret S, Raffoux E, et al, for the European Acute Promyelocytic Leukemia Group. 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. Dec 20 2006;24(36):5703-10. [Medline]. [Full Text].

  39. American Cancer Society. Cancer facts & figures 2005. Available at http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts__Figures_2005.asp. Accessed February 27, 2009.

  40. American Cancer Society. Cancer facts & figures 2008. Available at http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts_and_Figures_2008.asp?from=fast. Accessed February 27, 2009.

  41. Brownson RC, Chang JC, Davis JR. Cigarette smoking and risk of adult leukemia. Am J Epidemiol. Nov 1 1991;134(9):938-41. [Medline].

  42. Cassileth PA, Harrington DP, Appelbaum FR, et al. Chemotherapy compared with autologous or allogeneic bone marrow transplantation in the management of acute myeloid leukemia in first remission. N Engl J Med. Dec 3 1998;339(23):1649-56. [Medline]. [Full Text].

  43. de Lima M, Anagnostopoulos A, Munsell M, 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. Aug 1 2004;104(3):865-72. [Medline]. [Full Text].

  44. Estey EH, Thall PF, Giles FJ, et al. Gemtuzumab ozogamicin with or without interleukin 11 in patients 65 years of age or older with untreated acute myeloid leukemia and high-risk myelodysplastic syndrome: comparison with idarubicin plus continuous-infusion, high-dose cytosine arabinoside. Blood. Jun 15 2002;99(12):4343-9. [Medline]. [Full Text].

  45. Falini B, Mecucci C, Tiacci E, et al, for the GIMEMA Acute Leukemia Working Party. Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype. N Engl J Med. Jan 20 2005;352(3):254-66. [Medline]. [Full Text].

  46. Frohling S, Schlenk RF, Stolze I, et al. CEBPA mutations in younger adults with acute myeloid leukemia and normal cytogenetics: prognostic relevance and analysis of cooperating mutations. J Clin Oncol. Feb 15 2004;22(4):624-33. [Medline]. [Full Text].

  47. Giles FJ, Kantarjian HM, Kornblau SM, et al. Mylotarg (gemtuzumab ozogamicin) therapy is associated with hepatic venoocclusive disease in patients who have not received stem cell transplantation. Cancer. Jul 15 2001;92(2):406-13. [Medline]. [Full Text].

  48. Karp JE. Farnesyl protein transferase inhibitors as targeted therapies for hematologic malignancies. Semin Hematol. Jul 2001;38(3 suppl 7):16-23. [Medline].

  49. Slavin S, Nagler A, Shapira et al. Treatment of leukemia by alloreactive lymphocytes and nonmyeloablative stem cell transplantation. J Clin Immunol. Mar 2002;22(2):64-9. [Medline].

  50. Song WJ, Sullivan MG, Legare RD, et al. Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to develop acute myelogenous leukaemia. Nat Genet. Oct 1999;23(2):166-75. [Medline].

  51. Storb RF, Champlin R, Riddell SR, et al. Non-myeloablative transplants for malignant disease. Hematology Am Soc Hematol Educ Program. 2001;375-91. [Medline]. [Full Text].

  52. Valk PJ, Verhaak RG, Beijen MA, et al. Prognostically useful gene-expression profiles in acute myeloid leukemia. N Engl J Med. Apr 15 2004;350(16):1617-28. [Medline]. [Full Text].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

acute myelogenous leukemia, acute myeloid leukemia, AML, acute nonlymphoblastic leukemia, acute nonlymphocytic leukemia, acute non-lymphoblastic leukemia, acute non-lymphocytic leukemia, nonlymphoblastic leukemia, nonlymphocytic leukemia, non-lymphoblastic leukemia, non-lymphocytic leukemia, leukemia, cancer, bone marrow cancer, bone marrow failure,

radiation exposure, Bloom syndrome, Down syndrome, trisomy 21, congenital neutropenia, Fanconi anemia, neurofibromatosis, acute promyelocytic leukemia, APL, M3, promyelocytic leukemia, immature bone marrow cells, chromosomal translocation, genetic abnormality, cytogenetic abnormalities, anemia, thrombocytopenia, neutropenia, myelodysplastic syndrome, MDS, antecedent hematologic disorder, AHD, disseminated intravascular coagulation, DIC,

organ infiltration with leukemic cells, leukostasis, familial erythroleukemia, bone marrow transplantation, bone marrow transplant, BMT, allogeneic BMT, autologous BMT, alkylating agents, topoisomerase-II inhibitors, acute monocytic leukemia, M5, acute myelomonocytic leukemia, M4, blast count, acute undifferentiated leukemia, M0, acute megakaryocytic leukemia, M7, bone marrow aspiration, arabinosylcytosine, araC, ara-C, fibrinolysis,

all-trans-retinoic acid, ATRA, retinoic acid syndrome, malignant disease of bone marrow, bleeding gums, multiple ecchymoses, gingivitis, petechiae, leukemia cutis, chloromata, soft-tissue chloroma, granulocytic sarcoma, Li-Fraumeni syndrome, aplastic anemia, pancytopenia, myelofibrosis, paroxysmal nocturnal hemoglobinuria, polycythemia vera

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Karen Seiter, MD, Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College
Karen Seiter, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, and American Society of Hematology
Disclosure: Novartis Honoraria Speaking and teaching; Celgene Honoraria Speaking and teaching; Schering Honoraria Speaking and teaching

Medical Editor

Clarence Sarkodee-Adoo, MD, Consulting Staff, Department of Bone Marrow Transplantation, City of Hope Samaritan BMT Program
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ronald A Sacher, MB, BCh, MD, FRCPC, Director of the Hoxworth Blood Center, Professor, Departments of Internal Medicine and Pathology, University of Cincinnati Medical Center
Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Society of Hematology
Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD, Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Thomas Jefferson University
Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, and New York Academy of Sciences
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.