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