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THE UPDATED WHO CLASSIFICATION OF HEMATOLOGICAL MALIGNANCIES
Department of Pathology, Stanford University, Stanford, CA; 2Department of Pathology, Weill Cornell Medical College, New York, NY; 3Department of
Pathology, Massachusetts General Hospital, Boston, MA; 4Institute of Pathology, University of Cologne, Cologne, Germany; 5Department of Pathology, Johns
Hopkins Medical Institutions, Baltimore, MD; 6Section of Hematology/Oncology, University of Chicago, Chicago, IL; 7Comprehensive Cancer Center, James
Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH; 8Department of Molecular Medicine, University of Pavia, and
Department of Hematology Oncology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy; and 9Department of Pathology, University of Chicago, Chicago, IL
Introduction
In collaboration with the Society for Hematopathology and the
European Association for Haematopathology, the World Health
Organization (WHO) published the third and fourth editions of the
WHO Classication of Tumours of Haematopoietic and Lymphoid
Tissues, in 2001 and 2008, respectively, as part of a series of WHO
Classication of Tumours blue book monographs. In the spring
of 2014, a clinical advisory committee (CAC) composed of ;100
pathologists, hematologists, oncologists, and geneticists from around
the world convened to propose revisions to the fourth edition of the
classication. The revision of the fourth edition follows the philosophy
of the third and fourth editions to incorporate clinical features,
morphology, immunophenotyping, cytogenetics, and molecular genetics
to dene disease entities of clinical signicance. The fourth edition of the
classication of hematopoietic and lymphoid tissues was the second
volume of the WHO blue book tumor series, and the series publication is
still in progress. A fth edition series cannot begin until the fourth edition
series is completed; but after 8 years of information and experience that
have emerged from scientic and clinical studies, a revision of these criteria
for hematopoietic and lymphoid neoplasms was felt to be necessary and
timely. In relation to myeloid neoplasms and acute leukemia, this revision
has been inuenced by several factors including the following:
Myeloproliferative neoplasms
The categories of MPNs have not signicantly changed since the 2008
fourth edition of the classication, but discoveries of new mutations and
improved understanding of the morphologic features of some entities
have impacted the diagnostic criteria for the disease entities.
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Table 1. (continued)
WHO myeloid neoplasm and acute leukemia classification
Blastic plasmacytoid dendritic cell neoplasm
Acute leukemias of ambiguous lineage
MPN, unclassifiable
Mastocytosis
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Mastocytosis
As mentioned, mastocytosis is no longer listed under the broad heading
of MPNs. Major advances in the understanding of mastocytosis
have been made since the 2008 classication,19 and these are
incorporated into the text of the monograph. Table 920 lists the 2016
categories of mastocytosis, which includes a shortening of the name
of the 2008 category of systemic mastocytosis with associated
clonal hematological non-mast-cell lineage disease (SH-AHNMD)
to the 2016 category of systemic mastocytosis with an associated
hematological neoplasm (SM-AHN). In many cases, the AHN is an
aggressive neoplasm that must be treated and the diagnosis should
clearly and separately indicate the presence of this disorder in a
distinct diagnosis line.
Myelodysplastic/myeloproliferative
neoplasms
The myelodysplastic syndrome (MDS)/MPN category was introduced
in the third edition to include myeloid neoplasms with clinical,
laboratory, and morphologic features that overlap between MDS and
MPN.24 Based on accumulated scientic evidence, a provisional entity
within the MDS/MPN unclassiable group, refractory anemia with
ring sideroblasts associated with marked thrombocytosis (RARS-T),
has been accepted as a full entity, now termed MDS/MPN with ring
sideroblasts and thrombocytosis in the 2016 revision. The 2016 revised
criteria for diseases in this category are summarized in Tables 11-14.25
In MDS/MPN, the karyotype is often normal or shows abnormalities in common with MDS. Targeted sequencing of genes mutated in
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Myelodysplastic syndromes
The MDS are a group of clonal BM neoplasms characterized by
ineffective hematopoiesis, manifested by morphologic dysplasia in
hematopoietic cells and by peripheral cytopenia(s). The revised
classication introduces renements in morphologic interpretation
and cytopenia assessment and addresses the inuence of rapidly
accumulating genetic information in MDS diagnosis and classication.
Cytopenia is a sine qua non for any MDS diagnosis and in prior
classications, MDS nomenclature included references to cytopenia or to specic types of cytopenia (eg, refractory anemia).
However, the WHO classication relies mainly on the degree of
dysplasia and blast percentages for disease classication and specic
cytopenias have only minor impact on MDS classication. Moreover, the lineage(s) manifesting signicant morphologic dysplasia
frequently do not correlate with the specic cytopenia(s) in
individual MDS cases.47-49 For these reasons, the terminology for
adult MDS has changed to remove terms such as refractory anemia
and refractory cytopenia and replaces them with myelodysplastic
syndrome followed by the appropriate modiers: single vs multilineage dysplasia, ring sideroblasts, excess blasts, or the del(5q)
cytogenetic abnormality (see Table 15). There are no changes to
childhood MDS; refractory cytopenia of childhood remains as a
provisional entity within this category.
One of the biggest challenges in this category is separating MDS from
reactive causes of cytopenia and dysplasia. Although the threshold to
dene dysplasia will remain as 10% dysplastic cells in any hematopoietic
lineage, it is recognized that dysplasia in excess of 10% may occur in
some normal individuals and even more frequently in nonneoplastic
causes of cytopenia.50,51 Moreover, identication of dysplasia is not
always reproducible among even experienced hematopathologists.52,53
For these reasons, possible reactive etiologies of dysplasia should always
be carefully considered prior to making a diagnosis of MDS, particularly
when the dysplasia is subtle and limited to 1 lineage. Some dysplastic
changes, particularly the presence of micromegakaryocytes (which can
be highlighted by immunostaining for megakaryocyte markers in the
BM trephine), are relatively specic for myelodysplasia and have high
reproducibility.53
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ARBER et al
The myeloblast percentage, as determined by counting wellprepared, cellular BM aspirate smears and/or touch preparations and a
PB smear, remains critical in dening the WHO MDS categories and as
risk strata in the Revised International Prognostic Scoring System
(IPSS-R).54 The presence of 1% blasts in the PB, with ,5% BM blasts,
denes 1 type of MDS, unclassiable (MDS-U). However, because 1%
blasts may not be reproducible as a single observation, this nding must
now be demonstrated on at least 2 separate occasions in order to
diagnose MDS-U according to this criterion. There is a major change in
the diagnostic criteria for myeloid neoplasms with erythroid predominance (erythroid precursors $50% of all BM cells). In the updated
classication, the denominator used for calculating blast percentage
in all myeloid neoplasms is all nucleated BM cells, not just
the nonerythroid cells. This will result in most cases previously
diagnosed as the erythroid/myeloid subtype of acute erythroid leukemia
now being classied as MDS with excess blasts, as discussed in AML,
not otherwise specied (see Table 16).
Despite the lowering of the neutropenia prognostic threshold in the
IPSS-R to 0.8 3 109/L,54 the WHO thresholds dening cytopenia
will remain as in the original IPSS (hemoglobin, ,10 g/dL; platelets,
,100 3 109/L; absolute neutrophil count, ,1.8 3 109/L); a diagnosis
of MDS may be made in rare cases with milder levels of cytopenia, but
at least 1 cytopenia must be present in order to make the diagnosis. It
should be noted that some ethnic groups may have a reference range for
normal absolute neutrophil count that is lower than 1.8 3 109/L, and
thus caution should be exercised in interpreting neutropenia if it is the
only cytopenia. MDS-U will continue to include cases with single
lineage dysplasia or isolated del(5q) and pancytopenia, but in such
cases all PB counts must be below the WHO thresholds given in this
paragraph.
The same cytogenetic abnormalities listed in the 2008 WHO classication55 remain MDS-dening in a cytopenic patient, even in the
absence of diagnostic morphologic dysplasia. In such cases, the
abnormality must be demonstrated by conventional karyotyping, not by
uorescence in situ hybridization (FISH) or sequencing technologies.
The presence of 18, 2Y, or del(20q) is not considered to be MDSdening in the absence of diagnostic morphologic features of MDS. In
spite of the increased knowledge of the prognostic importance of
genetic ndings in MDS, del(5q) remains as the only cytogenetic or
molecular genetic abnormality that denes a specic MDS subtype.
Based on recent data showing no adverse effect of 1 chromosomal abnormality in addition to the del(5q),56-58 the entity MDS with isolated
del(5q) may be diagnosed if there is 1 additional cytogenetic abnormality besides the del(5q), unless that abnormality is monosomy
7 or del(7q). Even though cytogenetic ndings are not used to dene
other specic subtypes of MDS, they are strongly correlated with
prognosis, as reected in the 5 cytogenetic prognostic groups in the
IPSS-R scheme54,58; thus, a complete BM karyotype remains a
critical test in any newly diagnosed MDS case.
As with all the other myeloid neoplasms, a large amount of data has
recently become available on recurring mutations in MDS. Targeted
sequencing of a limited number of genes can detect mutations in 80% to
90% of MDS patients; the most commonly mutated genes in MDS are
SF3B1, TET2, SRSF2, ASXL1, DNMT3A, RUNX1, U2AF1, TP53, and
EZH2.59,60 Importantly, acquired clonal mutations identical to those
seen in MDS can occur in the hematopoietic cells of apparently healthy
older individuals without MDS, so-called clonal hematopoiesis of
indeterminate potential (CHIP).30,31,61 Although some patients with
CHIP subsequently develop MDS, the natural history of this condition
is not yet fully understood; thus, the presence of MDS-associated
somatic mutations alone is not considered diagnostic of MDS in this
classication, even in a patient with unexplained cytopenia, where these
mutations may be commonly found.62 Further study is required to
determine the optimal management and monitoring of such patients and
to investigate possible links between specic mutations, mutant allele
MF-1
MF-2
Semiquantitative grading of BM fibrosis (MF) with minor modifications concerning collagen and osteosclerosis. Fiber density should be assessed only in hematopoietic areas.
*In grades MF-2 or MF-3 an additional trichrome stain is recommended.
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BLOOD, 19 MAY 2016 x VOLUME 127, NUMBER 20
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Table 10. Molecular genetic abnormalities in myeloid/lymphoid neoplasms associated with eosinophilia
Disease
PDGFRA
Presentation
Genetics
Eosinophilia
Serum tryptase
Treatment
Respond to TKI
Eosinophilia
Monocytosis mimicking CMML
FGFR1
PCM1-JAK2
Eosinophilia
Translocations of 8p11.2
FGFR1-various partners
Eosinophilia
t(8;9)(p22;p24.1) PCM1-JAK2
Respond to TKI
other partners
, Increased.
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BLOOD, 19 MAY 2016 x VOLUME 127, NUMBER 20
such cases have ,20% total blast cells and are now classied as MDS
(usually MDS with excess blasts). This change was based on the close
biologic relationship of erythroid/myeloid type acute erythroid
leukemia to MDS in terms of its clinical presentation, morphologic
features, and genetic abnormalities, as well as the low reproducibility of
nonerythroid blast counts and an attempt to achieve uniformity in
expressing blast percentages across all myeloid neoplasms.102-106
Cases with $50% or more erythroid cells and $20% total myeloblasts
usually meet criteria for AML with myelodysplasia-related changes
and should be diagnosed as such; cases with $20% total myeloblasts
not meeting criteria for AML with myelodysplasia-related changes
or AML with recurrent genetic abnormalities should be categorized as
1 of the other subtypes of AML, NOS. Pure erythroid leukemia
remains as an AML, NOS subtype and is now the only type of
acute erythroid leukemia. Table 16 summarizes the current diagnostic
approach to neoplastic marrow specimens with 50% or more erythroid
precursors.
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Myeloid sarcoma
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Dysplastic
lineages
Cytopenias*
Ring sideroblasts as % of
marrow erythroid elements
BM and PB blasts
Cytogenetics by conventional
karyotype analysis
1 or 2
,15%/,5%
(MDS-SLD)
rods
2 or 3
,15%/,5%
1-3
(MDS-MLD)
rods
$15%/$5%
1 or 2
dysplasia (MDS-RS-SLD)
rods
2 or 3
1-3
$15%/$5%
1-3
1-2
None or any
dysplasia (MDS-RS-MLD)
rods
rods
(7q)
MDS with excess blasts
(MDS-EB)
MDS-EB-1
0-3
1-3
None or any
BM 5%-9% or PB 2%-4%, no
Any
Auer rods
MDS-EB-2
0-3
1-3
None or any
BM 10%-19% or PB 5%-19%
Any
or Auer rods
MDS, unclassifiable (MDS-U)
with 1% blood blasts
1-3
1-3
BM ,5%, PB 5 1%, no
None or any
Any
Auer rods
with single lineage dysplasia
None or any
and pancytopenia
Any
rods
,15%
1-3
abnormality
MDS-defining abnormality
rods
1-3
1-3
BM ,5%, PB ,2%
None
Any
*Cytopenias defined as: hemoglobin, ,10 g/dL; platelet count, ,100 3 10 /L; and absolute neutrophil count, ,1.8 3 10 /L. Rarely, MDS may present with mild anemia or
thrombocytopenia above these levels. PB monocytes must be ,1 3 109/L
If SF3B1 mutation is present.
One percent PB blasts must be recorded on at least 2 separate occasions.
Cases with $15% ring sideroblasts by definition have significant erythroid dysplasia, and are classified as MDS-RS-SLD.
9
Table 16. Diagnostic approach to myeloid neoplasms when erythroid precursors comprise 50% of BM nucleated cells
BM erythroid precursors
$50%
Myeloblast % of all
cells in BM (or PB)
NA
Prior
Recurring WHO
therapy? genetic abnormality?
Yes
NA
Meets criteria
for AML-MRC?
NA
$50%
$20%
No
Yes
NA
$50%
$20%
No
No
Yes
$50%
$20%
No
No
No
abnormality
related changes
leukemia (erythroid/
myeloid type)
$50%
No
No*
NA
nonerythroid cells
MDS
leukemia (erythroid/
myeloid subtype)
$50%
No
No*
NA
MDS
MDS
No
No*
NA
nonerythroid cells
.80% immature erythroid
,20%
proerythroblasts
type)
type)
AML-MRC, acute myeloid leukemia with myelodysplasia-related changes; NA, not applicable.
*Cases of AML t(8;21)(q22;q22.1);RUNX1-RUNX1T1, AML with inv(16)(p13.1q22) or t(16;16)(p13.1;q22);CBFB-MYH11 or APL with PML-RARA, may rarely occur in this
setting with ,20% blasts and those diagnoses would take precedence over a diagnosis of AML, NOS, or MDS.
Classify based on myeloblast percentage of all BM cells and of PB leukocytes and other MDS criteria.
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BLOOD, 19 MAY 2016 x VOLUME 127, NUMBER 20
Unbalanced abnormalities
27/del(7q)
del(5q)/t(5q)
disorders
i(17q)/t(17p)
213/del(13q)
del(11q)
del(12p)/t(12p)
Myeloid neoplasms with germ line predisposition and other organ dysfunction
Myeloid neoplasms with germ line GATA2 mutation
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idic(X)(q13)
Balanced abnormalities
t(11;16)(q23.3;p13.3)
t(3;21)(q26.2;q22.1)
t(1;3)(p36.3;q21.2)
t(2;11)(p21;q23.3)
t(5;12)(q32;p13.2)
t(5;7)(q32;q11.2)
t(5;17)(q32;p13.2)
t(5;10)(q32;q21.2)
t(3;5)(q25.3;q35.1)
measure these are not yet standard and the prognostic implications
still controversial; thus, most differentiation stage subgroups are
not formally included in the classication. However, 1 subset with unique
biology is recognized as a new provisional entity (see next paragraph).
Indolent T-lymphoblastic proliferation, which was briey mentioned in the
fourth edition classication, is now a more readily recognized nonneoplastic entity that may mimic T-lymphoblastic lymphoma.127 It typically
involves lymphoid tissue of the upper aerodigestive tract but may occur in
other locations. Local recurrences are common and systemic dissemination
is rare. Histologic examination of involved lymph nodes shows inltration
and sometimes replacement by proliferations of lymphoblasts that are less
cytologically atypical than the usual T-lymphoblastic lymphoma.
Although the blasts have an immature thymic phenotype that can be
demonstrated by TdT staining in lymph nodes, the phenotype reects a
developmentally normal, nonaberrant phenotype and the proliferations are
not clonal. These latter features allow this indolent entity to be
distinguished from T-lymphoblastic lymphoma.
Early T-precursor (ETP) ALL leukemia has a unique
immunophenotypic and genetic makeup indicating only limited
Table 19. Criteria for lineage assignment for a diagnosis of MPAL
Lineage assignment criteria
Myeloid lineage
MPO* (flow cytometry, immunohistochemistry, or cytochemistry)
or
Monocytic differentiation (at least 2 of the following: nonspecific esterase
cytochemistry, CD11c, CD14, CD64, lysozyme)
T-lineage
Strong cytoplasmic CD3 (with antibodies to CD3 e chain)
or
Surface CD3
B-lineage
Strong CD19 with at least 1 of the following strongly expressed: CD79a,
cytoplasmic CD22, or CD10
or
Weak CD19 with at least 2 of the following strongly expressed: CD79a,
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ARBER et al
Acknowledgments
This work was supported by the Clinical Advisory Committee
meeting (Chicago, IL, March 31-April 1, 2014) from the following
Authorship
Contribution: All authors were involved in the writing and editing of
the manuscript.
Conict-of-interest disclosure: The authors declare no competing
nancial interests.
Correspondence: Daniel A. Arber, Department of Pathology,
Stanford University, 300 Pasteur Dr H1401 M/C 5627, Stanford, CA
94305; e-mail: darber@stanford.edu.
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