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Acute Myeloid Leukemias (AML). MLAB 1415: Hematology Keri Brophy-Martinez. Overview of AML. Also known as Acute myelocytic leukemia Acute myelogenous leukemia Acute nonlymphocytic leukemia - PowerPoint PPT Presentation
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Acute Myeloid Leukemias (AML)MLAB 1415: HematologyKeri Brophy-Martinez
Overview of AML Also known as
Acute myelocytic leukemia Acute myelogenous leukemia Acute nonlymphocytic leukemia
Stem cell disorder characterized by malignant neoplastic proliferation and accumulation of immature and nonfunctional hematopoietic cells in the BM Chemo/radiation Exposure to benzene History of MDS
Overview of AML All acute leukemias begin BEFORE clinical signs and
symptoms occur As the tumor volume expands, normal functional
marrow cells decrease Characterized by two major features
Ability to proliferate continuously Due to mutations affecting growth factors Transcription errors
Arrested development of normal cells Lacks apoptosis
Etiology• Classified by the cellular
appearance of the primary stem cell• Common myeloid
progenitor (CMP)• AML or ANLL
• Common lymphoid progenitor (CLP)• ALL
• Peak incidence in adults over 60
Clinical findings
• CLASSIC TRIAD• Anemia• Infection• Bleeding/easy bruising/petechiae
• Fever• Shortness of breath• Fatigue• Weight loss• Pallor
Lab Features: Peripheral blood WBC count:
variable at diagnosis ( 1-200 x 109/L)
>20% blasts present Auer rods: fused primary granules in myeloblasts RBCs
Decreased Hgb < 10g/dL Inclusions reflect rbc maturation defects
Howell-Jolly, Pappenheimer, basophilic stippling
nRBCs present Platelets
Decreased Hypogranular, giant forms Megakaryocyte fragments
Lab Features: MISC.
• BONE MARROW• Hypercellular• Decreased fat content• >20 nonerythroid blasts• Fibrosis
• MISC• Hyperuricemic• Increased LDH
Who Classification of acute leukemia
• AML with recurrent genetic abnormalities• AML with myelodysplasia- related changes• AML and MDS- therapy related• AML- not otherwise categorized
WHO Classification of Acute Myelocytic Leukemias
FAB Classification of Acute LeukemiaMorphology MPO SBB Specific esterase Nonspecific esterase PAS
M0 Acute myeloblastic leukemia: mimally differentiated
>30% blastsNo granules
Not present Not present Not present Not present Not present
M1 Acute myeloblastic leukemia with no maturation
>30% blastsFew granules+/- Auer rods
Present Present Can be Present Not present Not present
M2 Acute myeloblastic leukemia with maturation
>30% blasts Granules common+ Auer rods
Present Present Can be Present Not present Not present
M3 Acute promyelocytic leukemia
>30% blastsProminent granules++ Auer rods Faggot cells
Present Present Present Not present Not present
M4 Acute myelomonocytic leukemia
>30% blasts>20%monocytes+ Auer rods
Present Present Present Present Not present
M4 eo Acute myelomonocytic leukemiaWith eosinophilia
>30% blasts>20%monocytes>5% abn eos+ Auer rods
Present Present Present Present Not present
M5 Acute monoblastic leukemia with or withour maturation
>30% blasts>80% monocytes with/without differentiation
Can be Present Can be Present Can be Present Present Not present
M6 Acute erythroleukemia
>30% myeloblasts>50% megaloblasts+ Auer rods
Present:Myeloblasts
Present:Myeloblasts
Present:Myeloblasts
Not Present Present:Erythroblasts
M7 Acute megakaryocytic leukemia
>30% MegakaryoblastsCytoplasmic budding
Not present Not present Can be Present Not present/Present Not present
M1: AML without maturation
• Myeloblast with Auer rod
• High N:C ratio• Fine chromatin• Prominent nuclei
M2: Aml with maturation
All stages of neutrophil maturation>20% myeloblastsAuer rods common
M3: promyelocytic leukemia (faggot cell)
Faggot cells with bundles of Auer rodsGenetic translocation t(15;17)Hypergranulation
M4: Acute myelomonocytic leukemia (AMML)
Monoblasts and promonocytes seenSome neutrophil precursors seenVacuolization often seen
M5: Acute monoblastic leukemia
MonoblastsPromonocytes
M6: Acute erythroid leukemia
Striking poikHigh number of RBC precursors>20 Myeloblasts
M7: Acute Megakaryoblastic Leukemia
• Peripheral blood• May see micromegakaryoblasts• Megakaryocyte fragments• Cytopenias• Dysplastic segmented neutrophils and platelets
• Bone marrow• Often get “dry tap” • Fibrosis
Prognosis of all AMLs and therapy
• Death often occurs from infection and hemorrhage in weeks to months unless therapy is started
• Chemotherapy• Reduces tumor load
• Bone marrow transplants
References• McKenzie, Shirlyn B., and J. Lynne. Williams. "Chapter 21."
Introduction. Clinical Laboratory Hematology. Boston: Pearson, 2010. Print