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
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 Leukemia
Morphology
MPO
SBB
Specific esterase
Nonspecific esterase
PAS
M0
Acute myeloblastic
leukemia: mimally
differentiated
>30% blasts
No granules
Not present
Not present
Not present
Not present
Not present
M1
Acute myeloblastic
leukemia with no
maturation
>30% blasts
Few 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% blasts
Prominent 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
leukemia
With 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%
Megakaryoblasts
Cytoplasmic 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% myeloblasts
Auer rods common
M3: promyelocytic leukemia (faggot cell)
Faggot cells with bundles of Auer rods
Genetic translocation t(15;17)
Hypergranulation
M4: Acute myelomonocytic leukemia
(AMML)
Monoblasts and promonocytes seen
Some neutrophil precursors seen
Vacuolization often seen
M5: Acute monoblastic leukemia
Monoblasts
Promonocytes
M6: Acute erythroid leukemia
Striking poik
High 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