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Blood Cell Identification – Graded Case History
This peripheral blood smear is from a 39-year-old male who recently returned from a trip to Nigeria. He presented to the emergency room with a fever. He started having symptoms on the plane on the way home ten days ago. He complains now of myalgias, arthralgias, nausea, decreased appetite, cough, headache, and persistent fever. A peripheral smear is submitted for review. Laboratory data include; WBC = 5.0 x 10
9/L;
HGB = 12.6g/dL; HCT = 37.8%; MCV = 76.2fL.
BC
P-0
1
Referees Participants
Identification No. % No. % Evaluation
Plasmodium sp. (malaria) 76 100.0 4484 99.5 Good
The red blood cells identified by the arrows are infected by Plasmodium sp., as correctly identified by
100.0% of the referees and 99.5% of the participants.
There are five species of Plasmodium that cause the clinical disease known as malaria:
P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. The different shapes and appearance of
the various stages of development and their variations between species are distinctive allowing
identification on thick and thin peripheral blood smears. The ring forms of all five types of malaria are
usually less than 2 μm in diameter. Potential look-alikes include platelets overlying red blood cells,
clumps of bacteria or platelets that may be confused with schizonts, masses of fused platelets that may
be confused with a gametocyte, precipitated stain, Babesia infection, and contaminating
microorganisms (bacteria, fungi, etc.).
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Blood Cell Identification – Graded
BC
P-0
2
Referees Participants
Identification No. % No. % Evaluation
Lymphocyte, large granular 50 56.2 2733 53.4 Good
Lymphocyte, reactive (to include plasmacytoid and immunoblastic forms)
33 37.1 1881 36.8 Acceptable
Lymphocyte 1 1.1 165 3.2 Acceptable
Monocyte 3 3.4 248 4.9 Unacceptable
Neutrophil, myelocyte 1 1.1 45 0.9 Unacceptable
Lymphocyte with phagocytized bacteria
1 1.1 6 0.1 Unacceptable
The white blood cell identified by the arrow is a large granular lymphocyte, as correctly identified by
56.2% of the referees and 53.4% of the participants. Large granular lymphocytes are defined as
medium to large cells with round nuclei, dense chromatin, and no visible nucleoli. Their cytoplasm is
moderate to abundant, clear or lightly basophilic, and contains several coarse, unevenly distributed,
azurophilic granules. These lymphocytes are found in blood smears from normal individuals and can be
increased in response to infections, such as infectious mononucleosis or in this case, malarial infection.
4
Blood Cell Identification – Graded
BC
P-0
3
Referees Participants
Identification No. % No. % Evaluation
Platelet, normal 89 100.0 5102 99.7 Good
The blood component identified by the arrow is a platelet, as correctly identified by 100.0% of the
referees and 99.7% of the participants. Platelets (also known as thrombocytes) are small, blue-gray
fragments of megakaryocytic cytoplasm typically measuring 1.5 to 3 μm in diameter. Fine, purple-red
granules are aggregated at the center or dispersed throughout the cytoplasm. They are typically single
but may form aggregates.
5
Blood Cell Identification – Graded
BC
P-0
4
Referees Participants
Identification No. % No. % Evaluation
Neutrophil, segmented or band 73 82.0 4083 80.0 Good
Neutrophil, toxic (to include toxic
granulation and/or Döhle bodies, and/or toxic vacuolization)
16 18.0 1005 19.6 Unacceptable
The white blood cell identified by the arrow is a normal segmented neutrophil, as correctly identified by
82.0% of the referees and 80.0% of the participants. Neutrophils have a segmented nucleus with
condensed nuclear chromatin. The nuclear segments are connected by thin filaments with no internal
chromatin structure. The cytoplasm is pale pink with specific granules.
Toxic changes in neutrophils include toxic granulation, Döhle bodies, and cytoplasmic vacuolization.
The neutrophil in image BCP-04 lacks toxic granulation and Döhle bodies, and contains only a few very
small cytoplasmic vacuoles, a finding likely representing EDTA degenerative change. Toxic granulation
and Döhle bodies each may be present in an individual cell without the other finding; either finding
alone is sufficient to designate the neutrophil as “toxic.” In contrast, since small cytoplasmic vacuoles
can be a degenerataive artifact of EDTA storage, cytoplasmic vacuolization is best considered toxic
only if accompanied by toxic granulation and/or Döhle bodies.
Toxic granulation is the presence of large purple or dark blue granules within segmented neutrophils,
bands, or metamyelocytes (Images 1-3). In image BCP-04, very small normal primary granules are
discernable, but they do not appear enlarged and are not as basophilic in their staining characteristics
as toxic granules. Döhle bodies are found within neutrophilic cytoplasm and appear as single or multiple
blue to grey-blue inclusions of variable size and shape (Image 2, arrow), a feature lacking in this case.
These inclusions represent denatured aggregates of free ribosomes or stacks of endoplasmic reticulum.
Vacuoles within the cytoplasm of cells showing toxic granulation and/or Döhle bodies constitute toxic
vacuolization. These toxic vacuoles (Image 3) are variable in size, may coalesce, and generally are
larger and more numerous than those associated with degenerative change. EDTA storage may
produce degenerative vacuolization that is comprised of a few, small, punch-out appearing vacuoles, as
in this case.
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Blood Cell Identification - Graded
BC
P-0
4
Image 1
Image 2
Image 3
7
Blood Cell Identification – Graded
BC
P-0
5
Referees Participants
Identification No. % No. % Evaluation
Erythrocyte with overlying
platelet 86 96.6 4825 94.3 Good
Platelet, normal 3 3.4 260 5.1 Unacceptable
The blood cell identified by the arrow is an erythrocyte with an overlying platelet, as correctly identified
by 96.6% of the referees of the 94.3% of the participants. This artifact is important to distinguish from
red cell inclusions or parasites. Many times, platelets overlying red cells are surrounded by a thin clear
zone or halo, which is not a feature of most genuine red cell inclusions. Of interest, the red blood cell
above the red blood cell identified in this photo is infected by Plasmodium sp.
8
Discussion
This case illustrates a blood smear from a patient infected with Plasmodium sp. There are five species of
Plasmodium that cause the clinical disease known as malaria: P. falciparum, P. vivax, P. ovale, P. malariae, and
P. knowlesi. Malarial infection is transmitted by infected Anopheles mosquitos. The distribution of malarial
endemic regions spans >95 countries, with ~500 million cases reported each year. Those most at risk for infection
are children <5 years of age, pregnant women, refugees from endemic countries, and non-immune travelers to
endemic regions.
The life cycle of Plasmodium begins with the bite of the vector, an Anopheles mosquito, whose saliva contains
infective sporozoites that can be injected through its proboscis. As the infected saliva enters the human host, the
sporozoites circulate in the bloodstream for 20-30 minutes before entering the liver, where they will lay dormant
as they multiply for the next 10 days. At the end of the 10 days, multiple of these small ring forms (called
merozoites) break free from the parenchymal cells of the liver and are released into the bloodstream to infect
erythrocytes.
The pathophysiology of infection belies its clinical presentation, wherein parasite-infected red blood cells
accumulate in various organs, including the heart, brain, liver, and lungs. Patients may have a non-specific
presentation of malaise, fever, and myalgias, which typically occur 7-30 days after the mosquito bite. This quickly
progresses to splenomegaly, anemia, and jaundice. In severe infections (usually caused by P. falciparum), the
patient may develop cerebral encephalopathy, hypoglycemia, hypotension, liver dysfunction, disseminated
intravascular coagulation, acute renal failure, and hemoglobinuria (“blackwater fever”).
Identification of malarial infection in humans is performed by examining Romanowsky stained (often Giemsa)
thick and thin peripheral blood smears under a 100x oil immersion objective. Ideally, the blood smears are
obtained at different intervals in the day to account for the fluctuating numbers of circulating parasites in the blood
stream. Of the five malarial species, P. vivax (most common), P. falciparum, and P. malariae are the most
commonly seen. P. ovale and P. knowlesi are rarer species.
A stepwise approach to the laboratory characterization of malarial species in blood smears is recommended, as
microscopic examination remains the “gold standard” for detection. As P. falciparum causes the most virulent of
the malarial infections, with potential for severe symptoms and rapid progression to death, it is imperative to first
exclude this species. The following features will be seen in a P. falciparum infection (see Image 1): a) banana- or
crescent-shaped gametocytes are pathognomonic (but uncommonly seen); b) tiny ring forms (trophozoites),
which occupy <1/3 the diameter of the red blood cell; c) multiple ring forms in one red blood cell, with 2 nuclei in
the same ring; d) “heavy” malarial load, with >20% of erythrocytes infected by parasites, indicating a severe
infection; e) “applique” effect, whereas ring forms appear “stuck-on” the red blood cell membrane.
9
Image 1
If none of the above 5 features are seen, a search for evidence of other malarial organisms, including P. vivax, is
undertaken. Features of P. vivax infection include (see Image 2): a) somewhat irregularly-shaped erythrocytes,
which are enlarged, pale, and contain pink-red staining granules (so-called Schuffner’s dots); b) “ameboid” quality
of erythrocyte, wherein mature trophozoites begin to fill the entire red blood cell; c) merozoites with 12-14 or more
individual schizonts (early segmented form with more than one nucleus); d) large and circular gametocytes
(arrowhead) which fill more than half the cell diameter; e) finely granular and brownish pigment in both the
gametocyte and schizont.
Image 2
10
When blood smears are positive for parasites, a quantification/percentage of erythrocytes by parasites must be
provided to the clinician to provide an index of malarial load. Other laboratory tests available include the rapid
antigen tests or rapid diagnostic tests (RDTs) which utilize a qualitative immunochromatographic assay/stain
method -- useful in the rapid diagnosis or exclusion of P. falciparum. This rapid screen does not detect
parasitemia levels less than 0.5%. All positive RDTs must be confirmed on microscopy. Nucleic acid testing is
very sensitive and specific, using PCR (polymerase chain reaction) testing as its platform. Often, results are not
available quickly enough in the routine laboratory setting, limiting its utility in the rapid diagnosis of acutely ill
patients. For now, its use is confined to confirmation of the specific species of malaria. Serologic testing for IgG
malaria antibody using an ELISA method is limited to screening for chronic malaria or retrospectively diagnosing
malaria in a previously non-immune individual.
References:
1. Centers for Disease Control and Prevention: Malaria References and Resources. Centers for Disease
Control and Prevention. Atlanta: Georgia [8 Feb 2010; Accessed: 8 Jan 2011].
2. Collins WE, Jeffrey GM. Plasmodium malariae: parasite and disease. Clin Microbiol Rev 2007;20:579-
592.
3. Winn W, Allen S, Janda W, Koneman E, et al. Koneman’s Color Atlas and Textbook of Diagnostic
Microbiology, 6th ed. Philadelphia: Lippincott Williams and Wilkins, 2006.
4. World Heath Organization: Malaria fact sheet. World Health Organization. Geneva: Switzerland
[Accessed: 8 Jan 2011].
Joan E. Etzell, MD, Vice Chair
Maria Vergara-Lluri, MD
Hematology and Clinical Microscopy Resource Committee
11
Blood Cell Identification – Ungraded
Case History
This peripheral blood smear is from a 17-year-old patient who presents to the emergency room with ecchymoses. Laboratory data include: WBC = 58.2 x 10
9/L; HGB = 6.6 g/dL; PLT = 6.6 x10
9/L; Fibrinogen = 63
mg/L; Prolonged PT and PTT; and markedly elevated D-dimer level.
BC
P-0
6
Referees Participants
Identification No. % No. % Evaluation
Lymphocyte 78 89.7 4466 88.7 Educational
Lymphocyte, reactive (to include plasmacytoid and immunoblastic forms)
4 4.6 162 3.2 Educational
Nucleated red cell, normal or abnormal morphology
4 4.6 189 3.8 Educational
Neutrophil with dysplastic nucleus and/or hypogranular cytoplasm
1 1.2 24 0.5 Educational
The white blood cell indicated by the arrow is a lymphocyte, as correctly identified by 89.7% of the referees
and 88.7% of the participants. Lymphocytes may exhibit variation in size ranging from 7 to 15 µm and in
N:C ratio from 5:1 to 2:1. Most lymphocytes have round to oval nuclei that may be slightly indented or
notched. The chromatin is diffusely dense or coarse and clumped. Most lymphocytes have a scant amount
of pale blue to moderately basophilic, agranular cytoplasm. Some lymphocytes show a perinuclear clear
zone or halo which surrounds the nucleus. Also of note, the cell in the lower left of this image is an
abnormal promyelocyte with multiple Auer rods, a finding that is common in acute promyelocytic leukemia
with t(15;17).
12
Blood Cell Identification – Ungraded
BC
P-0
7
Referees Participants Performance
Identification No. % No. % Evaluation
Fragmented red cell
(schistocyte, helmet cell, keratocyte, triangular cell)
87 100.0 4958 98.9 Educational
The red blood cell identified by the arrow is a fragmented red cell, as correctly identified by 100.0% of the
referees and 98.9% of the participants. This cell is also known as a triangulocyte or a schistocyte. Other
fragmented red blood cells include helmet cells and keratocytes (horn cells). Fragments should not have
central pallor; such cells are best considered non-specific poikilocytes. Fragmented cells are seen in
severe burns, disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TIP)
and other microangiopathic hemolytic anemias. Patients with acute promyelocytic leukemia, as in this
case, are at risk for disseminated intravascular coagulation (DIC). When present in large numbers, red cell
fragments may cause the MCV to fall into the microcytic range or interfere with platelet enumeration.
13
Blood Cell Identification – Ungraded
BC
P-0
8
Referees Participants Performance
Identification No. % No. % Evaluation
Neutrophil, segmented or band 84 96.6 4836 96.4 Educational
Neutrophil with dysplastic nucleus and/or hypogranular cytoplasm
3 3.4 130 2.6 Educational
The arrowed cells are neutrophils, as correctly identified by 96.6% of the referees and 96.4% of the
participants. The upper arrowed cell slightly to the right is a segmented neutrophil while the lower arrowed
cell would be considered a band neutrophil. The nucleus of a band neutrophil is indented to more than half
the distance to the farthest nuclear margin, but in no area is the chromatin condensed to a single filament.
The nucleus can assume many shapes: band-like, sausage-like; S, C, or U-shaped; and twisted and
folded on itself. The cytoplasm has specific granules predominating in the pale cytoplasm. Band
neutrophils comprise 5-10 percent of the nucleated blood under normal conditions, but may be increased
in the blood in a number of physiologic and pathologic states. Band neutrophils comprise 10-15% of the
nucleated cells in the bone marrow. The other leukocytes in this image are abnormal promyelocytes.
14
Blood Cell Identification – Ungraded
BC
P-0
9
Referees BCP Participants Performance
Identification No. % No. % Evaluation
Platelet, normal 83 95.4 4870 97.1 Educational
Platelet, hypogranular 3 3.5 119 2.4 Educational
Stain precipitate 1 1.1 4 0.1 Educational
The blood component identified by the arrow is a platelet, as correctly identified by 95.4% of the referees
and 97.1% of the participants. Platelets, also known as thrombocytes, are small, blue gray fragments of
cytoplasm measuring 1.5 to 3 µm in diameter. Fine, purple-red granules are aggregated at the center or
dispersed throughout the cytoplasm. Platelets may vary in shape but most are round or elliptical. They are
typically single but may form aggregates.
15
Blood Cell Identification – Ungraded
BC
P-1
0
Referees Participants Performance
Identification No. % No. % Evaluation
Neutrophil promyelocyte,
abnormal with/without Auer rod(s)
55 64.7 3208 64.1 Educational
Myeloblast with Auer rod 20 23.5 1075 21.5 Educational
Neutrophil, myelocyte 3 3.5 207 4.1 Educational
Eosinophil, any stage 2 2.4 108 2.2 Educational
Leukocyte with phagocytized bacteria
2 2.4 91 1.8 Educational
Monocyte, immature (promonocyte, monoblast)
1 1.2 1 <0.1 Educational
Neutrophil, promyelocyte 1 1.2 31 0.6 Educational
Plasma cell, abnormal (malignant, myeloma cell)
1 1.2 22 0.4 Educational
The arrowed cell is an abnormal promyelocyte containing multiple Auer, as correctly identified by 64.7% of
the referees and 64.1% of the participants; these cells are also sometimes referred to as myeloblasts with
Auer rod as identified by 23.5% of referees and 21.5% of participants. Auer rods are inclusions which
represent a crystallization of azurophilic (primary) granules. A cell containing multiple Auer rods is referred
to as a faggot cell (from the English faggot, meaning a cord of wood). Faggot cells are most commonly
seen in acute promyelocytic leukemia.
16
Discussion
Acute promyelocytic leukemia with t(15;17)(q22;q21); PML-RARA
Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia characterized by the
t(15;17)(q22;q21) resulting in the fusion of the promyelocytic leukemia gene (PML) and retinoic acid receptor
alpha (RARα) gene (PML/RARα). The fusion product PML-RARα homodimerizes, binds to DNA and works as a
transcriptional repressor which inhibits expression of target genes necessary for granulocytic differentiation.
Variant chromosomal translocations, such as t(11;17), t(5;17), can be detected in up to 2% of APL cases.
This leukemia accounts for approximately 10-15% of acute myeloid leukemia cases in the United States. Most
patients present with leukopenia along with a coagulopathy, fibrinolysis and proteolysis, which can be life
threatening and requires emergent therapy along with prompt diagnosis by integration of morphologic findings,
immunophenotype and cytogenetic/FISH studies. This type of leukemia is very uncommon in children less than
10 years of age, and its incidence increases steadily until it plateaus during early adulthood and remains constant
until it decreases after age 60.
The two main morphologic types of APL are the classic hypergranular or typical variant, as in this case, which
comprises the majority of APL cases, and the microgranular or hypogranular variant, comprising approximately
15-20% of APL cases. Leukopenia is typically seen in association with the hypergranular variant, with rare
circulating leukemic promyelocytes found in the peripheral blood. A leukocytosis is more commonly seen in the
microgranular variant. The microgranular subtype is also associated with the short bcr 3 type PML-RARA fusion
gene and FLT3 mutations.
Leukemic promyelocytes of either subtype can be classified as blasts in a peripheral blood or bone marrow
differential. The leukemic promyelocytes of the hypergranular variant demonstrate nuclear irregularity and
variability with reniform or bilobed nuclei. Nucleoli are variably prominent. The cytoplasm is abundant and
characterized by the presence of numerous large azurophilic cytoplasmic granules that can often obscure the
nucleus. These leukemic promyelocytes can also contain numerous bundles of Auer rods (faggot cells) as seen in
images BCP-06, -09 and -10. Myeloblasts which may or may not contain single Auer rods may also be seen. The
Auer rods of the hypergranular variant are usually larger than in other types of AML. The microgranular variant
blast contains a primarily bilobed, reniform or monocytoid like nucleus; the cytoplasm appears agranular or may
contain fine dust like azurophilic granules. Multiple Auer rods are less frequently seen in this variant.
The immunophenotype of hypergranular APL blasts demonstrates bright expression of CD33 and cytoplasmic
myeloperoxidase, variable CD13 expression and largely lack of expression of HLA-DR and CD34. Blasts of the
hypogranular variant demonstrate similar findings although may also show dim expression of HLA-DR and CD34;
the blasts also commonly express the T-lineage associated marker CD2, a finding which has been associated
with a less favorable prognosis. CD56 expression can be seen in 15-20% of APL and has been associated with a
less favorable clinical course. CD117 expression can be seen in both variants. The blasts do not typically express
CD15 or CD11b. Lack of expression of CD34 and HLA-DR is not specific for a diagnosis of APL, and integration
of ancillary studies, such as conventional cytogenetic or FISH results, should be used in confirming a diagnosis.
Very strong myeloperoxidase expression is seen in the abnormal promyelocytes by cytochemistry as well as by
flow cytometry which can be helpful in distinguishing these blasts, especially the hypogranular blasts, from
monoblasts. Sudan black B and chloroacetate esterase cytochemical staining are strongly positive in the blasts of
both variants.
17
This prognosis of APL is favorable, especially when compared to other subtypes of acute myeloid leukemia. The
current standard approach to therapy is with the concomitant administration of targeted terminal granulocytic
differentiation therapy with all-trans retinoic acid (ATRA), and anthracycline based chemotherapy. This
combination leads to complete remission in 90-95% of patients. Arsenic trioxide (ATO) is also an effective therapy
in patients who have relapsed. Minimal residual disease (MRD) monitoring can be performed by sequential
quantitative reverse transcription polymerase chain reaction (RT-PCR). This can be used to predict relapse,
especially in cases with evidence of morphologic remission, and to direct preemptive therapy.
Measures to counteract the coagulopathy associated with APL should be instituted immediately if this diagnosis is
considered, as intracerebral and pulmonary hemorrhages can occur prior to and during induction of therapy.
Relapse can occur in 10-20% of patients. Patients at high risk for relapse include those with an elevated WBC
(>10000/uL or 10 x 109/L) at diagnosis, age over 55 years, expression of CD56 on the blasts as well as the
predominance of the PML-RARAbcr3 isoform. Overall survival is approximately 80%.
References:
1. Akagi T, Shih L, Kato M, et al. Hidden abnormalities and novel classification of t(15;17) acute
promyelocytic leukemia (APL) based on genomic alterations. Blood, 2009; 113: 1741-1748.
2. Cassinat B, de Botton S, Kelaidi C, et al. When can real-time quantitative PT-PCR effectively define
molecular relapse in acute promyelocytic leukemia patients? Leukemia Research, 2009; 33: 1178-1182.
3. Chauffaille M, Borri D, Proto-Siqueira R, et al. Acute promyelocytic leukemia with t(15;17): frequency of
additional clonal chromosomome abnormalites and FLT3 mutations. Leukemia and Lymphoma, 2008;
49: 2387-2389.
4. Collins S. Retinoic acid receptors, hematopoiesis and leukemogenesis. Current Opinion in Hematology,
2008; 15: 346-351.
5. Dunphy CH, Polski JM, Johns G, et al. Acute promyelocytic leukemia, hypogranular variant, with
uncharacteristic staining with chloroacetate esterase. Leukemia and Lymphoma, 2001; 42: 215-219.
6. Foucar K,Reichard K, Czuchlewski D. Bone Marrow Pathology. ASCP Press: Chicago, 2010.
7. Grimwade D, Jovanovic JV, Hills RK, et al. Prospective minimal residual disease monitoring to predict
relapse of acute promyelocytic leukemia and to direct pre-emptive arsenic trioxide therapy. Journal of
Clinical Oncology, 2009; 27: 3650-3658.
8. Jaffe ES, Harris NL, Vardiman JW, Campo E, Arber DA. Hematopathology. Saunders/Elsevier:
Philadelphia, 2011.
9. Kelaidi C, Chevret S, de Botton S, et al. Improved outcome of acute promyelocytic leukemia with high
WBC counts over the last 15 years: the European APL group experience. Journal of Clinical Oncology,
2009; 27: 2668-2676.
10. Lin P, Hao S, Medeiros J, et al. Expression of CD2 in acute promyelocytic leukemia correlates with short
form of PML-RAR transcripts and poorer prognosis. American Journal of Clinical Pathology, 2004; 121:
402-407.
11. Nowak D, Stewart D, Koeffler HP. Differentiation therapy of leukemia: 3 decades of development. Blood,
2009; 113: 3655-3665.
12. Ravandi F, Estey E. Jones D, et al. Effective treatment of acute promyelocytic leukemia with all-trans-
retinoic acid, arsenic trioxide, and gemtuzumab ozogamicin. Journal of Clinical Oncology, 2009; 27: 504-
510.
13. Sanz M, Grimwade D, Tallman MS, et al. Management of acute promyelocytic leukemia:
recommendations from an expert panel on behalf of the European LeukemiaNet. Blood, 2009; 113:
1875-1891.
18
14. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Vardiman JW. World Health
Organization Classification of Tumours of Hematopoietic and Lymphoid Tissues. IARC Press: Lyon, 2008,
p112-113.
15. Tallman MS.Treatment of relapsed or refractory acute promyelocytic leukemia. Best Practice & Research,
2007; 20: 57-65.
16. Tallman, M. What is the role of arsenic in newly diagnosed APL? Best Practice & Research, 2008; 21:
659-666.
17. Tallman M, Altman J. Curative strategies in acute promyelocytic leukemia. American Society of
Hematology, 2008; 391-399.
18. Wang Z, Chen Z. Acute promyelocytic leukemia: from highly fatal to highly curable. Blood, 2008; 111:
2505-2515.
Lydia C. Contis, MD
Alice L. Werner, MD
Hematology and Clinical Microscopy Resource Committee
Recommended