Acute myelogenous leukemia (AML) is the most common type
of acute leukemia in adults, 45% of all leukemias and 80-90%
of acute leukemias.
The seven major types of acute nonlymphoid or myeloid
leukemia are:
Acute nonlymphocytic (ANLL
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% Adult cases
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M1 Myeloblastic (AML)
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10-20%
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M2 AML with differentiation
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30-40%
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M3 Promyelocytic (APML)
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10-15%
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M4 Myelomonocytic (AMML, Naegeli)
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10-15%
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M5a Monoblastic (AMoL, Schilling)
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10-15%
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M5b AMoL with differentiation
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<5%
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M6 Erythroleukemia (Di Guglielmo)
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<5%
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M7 Megakaryoblastic
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<5%
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Other (e.g. biphenotypic)
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<5%
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Definition: AML involves the malignant
proliferation of immature cells or blasts which are
of nonlymphoid or myelogenous type. This proliferation
originates in the bone marrow, but involves the peripheral
blood and other organs.
Diagnosis of AML: The presence of >
30% blasts in the marrow as determined by a hematologist on
bone marrow aspirate. Frequently see increased peripheral
WBC count but it can be increased, normal or decreased.
Diagnosis of MDS: Marrow blasts are
increased but are fewer than 30%, is a myelodysplastic
syndrome (MDS). (More about MDS later.) Differentiate
AML type by cell morphology, cytochemistry, phenotype,
and genotype.
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Myeloblasts have nuclei with fine, delicate chromatin and
most often prominant nucleoli. The cytoplasm of myeloblasts
tends to be moderate in volume and lightly basophilic
without granules (primary azurophilic granules may be seen
in myeloblasts). Auer rods, which are angular,
crystalline, and red staining, are unique to
myeloblasts but only seen in about 20% of myeloid
leukemias.
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Note that myeloblasts do not magically mature from
myeloblasts with no granules to fully granulated
promyelocytes. Three stages in the cytoplasmic maturation of
a myeloblast are recognized.
Type I myeloblasts have no azuriphilic primary
granules nor Auer rods.
Type II myeloblasts have a few ( ²20)
azuriphilic primary granules. Auer rods may be seen.
Type III myeloblasts have ³20 azuriphilic
primary granules without a Golgi zone. Promyelocytes are
larger, have a lower N/C ratio with denser chromatin, and
usually have a pale paranuclear Golgi.
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No azuriphilic primary granules.
No Auer rods.
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Few (<20) azuriphilic primary granules.
Auer rods may be seen.
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>20 azuriphilic
primary granules without a Golgi zone.
Auer rods may be seen.
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**** 2YMS do not need to know the different subtypes of
blasts but should recognize that differentiation occurrs
progressively, from no granules to a point when sufficient
granules are present we call the cell a
promyelocyte.****
Promyelocytes: larger, lower N/C ratio, denser chromatin,
pale paranuclear Golgi
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Cytochemical studies show at least some of the blasts of
most nonlymphoid leukemias to be positive for
myeloperoxidase, and/or nonspecific esterase.
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M1
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M2
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M3
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M4
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M5
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M6
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M7
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MPO
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+
|
+
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+
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+
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- / +
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-
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-
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NSE
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-
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-
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- / +
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+
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++
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+
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+ / -
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PAS
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-
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-
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-
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-
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- / +
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+
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+
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Myeloperoxidase
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Nonspecific esterase
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Periodic Acid Schiff
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Immunophenotypic studies show expression of CD13
and/or CD33 on 95% of all nonlymphoid leukemias.
CD15 and CD14 are other commonly positive markers on
nonlymphoid leukemias.
B and T lymphocyte markers should be negative although
some myeloid leukemias express CD7.
The immunophenotype of AML does not correlate well with
the FAB categories.
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Chromosomal abnormalities are important diagnostic
and prognostic findings. The most important are the
t(8;21) in M2; t(15;17) in M3, and t(9;11) in M5.
Abnormalities of chromosome 16 are associated with
eosinophilic differentiation.
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Remember, that the definitive diagnosis of
leukemia rests on the finding of increased blasts on
bone marrow examination, although it most often presents
as blasts in the peripheral blood.
The white blood cell (WBC) count although usually
high, is often normal or occassionally even
low. The percent of blasts in the peripheral blood is
highly variable and may range from 0-100%.
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