1. Acute Myeloid Leukemias (AML)
MLAB 1415: Hematology
Keri Brophy-Martinez

2. 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

3. 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

4. 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

5. Clinical findings CLASSIC TRIAD Anemia Infection
Bleeding/easy bruising/petechiae
Fever
Shortness of breath
Fatigue
Weight loss
Pallor

6. Lab Features: Peripheral blood
WBC count:
variable at diagnosis
( 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
Hypogranular, giant forms
Megakaryocyte fragments

7. Lab Features: MISC. BONE MARROW Hypercellular Decreased fat content
>20 nonerythroid blasts
Fibrosis
MISC
Hyperuricemic
Increased LDH

8. Who Classification of acute leukemia
AML with recurrent genetic abnormalities
AML with myelodysplasia- related changes
AML and MDS- therapy related
AML- not otherwise categorized

9. WHO Classification of Acute Myelocytic Leukemias

10. FAB Classification of Acute Leukemia
Morphology
MPO
SBB
Specific esterase
Nonspecific esterase
PAS M0
Acute myeloblastic leukemia: mimally differentiated
>30% blasts
No granules
Not present M1
Acute myeloblastic leukemia with no maturation
Few granules
+/- Auer rods
Present
Can be Present M2
Acute myeloblastic leukemia with maturation
>30% blasts Granules common
+ Auer rods M3
Acute promyelocytic leukemia
Prominent granules
++ Auer rods
Faggot cells M4
Acute myelomonocytic leukemia
>20%monocytes
M4 eo
With eosinophilia
>5% abn eos M5
Acute monoblastic leukemia with or withour maturation
>30% blasts>80% monocytes with/without differentiation M6
Acute erythroleukemia
>30% myeloblasts
>50% megaloblasts
Present:
Myeloblasts
Not Present
Erythroblasts M7
Acute megakaryocytic leukemia
>30%
Megakaryoblasts
Cytoplasmic budding
Not present/Present

11. M1: AML without maturation
Myeloblast with Auer rod
High N:C ratio
Fine chromatin
Prominent nuclei

12. M2: Aml with maturation All stages of neutrophil maturation
>20% myeloblasts
Auer rods common

13. M3: promyelocytic leukemia (faggot cell)
Faggot cells with bundles of Auer rods
Genetic translocation t(15;17)
Hypergranulation

14. M4: Acute myelomonocytic leukemia (AMML)
Monoblasts and promonocytes seen
Some neutrophil precursors seen
Vacuolization often seen

15. M5: Acute monoblastic leukemia
Monoblasts
Promonocytes

16. M6: Acute erythroid leukemia
Striking poik
High number of RBC precursors
>20 Myeloblasts

17. M7: Acute Megakaryoblastic Leukemia
Peripheral blood
May see micromegakaryoblasts
Megakaryocyte fragments
Cytopenias
Dysplastic segmented neutrophils and platelets
Bone marrow
Often get “dry tap”
Fibrosis

18. 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

19. References
McKenzie, Shirlyn B., and J. Lynne. Williams. "Chapter 21." Introduction. Clinical Laboratory Hematology. Boston: Pearson, Print