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Chapter 66 Acute Lymphoblastic Leukemia in Adults 1033

10 3
10 2
CD19 FITC 10 1 0

10

10 3 10 0 10 1 10 2 10 3 10 0 10 1 10 10 3 10 0 10 1 10 2 10 3
2
CD34 PC5 CD10 PE CD20 FITC
10 3
10 2
10 2
SS log 10 1 LAMBDA PE 10 1 0

10 0 10
2
10 0 10 1 10 2 10 3 10 0 10 1 10 10 3 10 0 10 1 10 2 10 3
HLA-DR FITC KAPPA FITC cyCD79a PE
10 3
10 0 10 1 10 2 10 3
CD33 PE 10 1
CD45 ECD 10 2

10 0
2
10 0 10 1 10 2 10 3 10 0 10 1 10 10 3 10 0 10 1 10 2 10 3
cyTDT FITC CD19 PC5 cylgM PE
Fig. 66.4 AN EXAMPLE OF FLOW CYTOMETRIC EVALUATION IN A CASE OF B-ACUTE LYM-
PHOBLASTIC LEUKEMIA. Selected histograms from a panel of markers used in the evaluation of acute
lymphoblastic leukemia by flow cytometry are illustrated. The blasts are first identified by weak CD45
expression and low side scatter (left histogram, circled population). This is a useful gating strategy because it
allows for an easy identification of the blast population and its separation from lymphocytes (with bright
CD45) and nucleated red blood cells (with absent CD45 expression). Because no single antigen is specific for
a lineage, multiple antigens are evaluated using multicolor flow cytometry. The phenotype illustrated is that
+
+
+
of a common precursor B-acute lymphoblastic leukemia. In this case, the blasts are CD34 , HLA-DR , TdT ,
−
−
+
−
−
+
+
CD19 , CD10 , CD20 , cyCD79a , κ , λ , and cyIgµ . There is weak and partial expression of the myeloid
marker CD33.
TABLE Immunophenotypes of B and T-Lymphocyte Progenitors
66.3
B Lineage CD10 CD19 CD22 CD79a TdT CyIgµ
Early precursor (pro-B) − + + + + −
Intermediate (common) + + + + + −
Pre-B +/− + + + + +
T Lineage CD1a CD2 CD3 CD4 CD7 CD8 CD34
ETP a − +/− C +/− +/− − +
Pro-T − − C − + − +/−
Pre-T − + C − + − +−
Cortical T + + C + + + −
Medullary T − + C, S b + b −
a ETP ALL CD5-/lo, CD1a-, CD8- with stem cell myeloid markers, notably CD34, CD117, CD33, and CD13.
b Medullary T lymphocytes are positive for either CD4 or CD8, but not both.
C, Cytoplasmic; CyIgµ, cytoplasmic µ heavy chain; ETP, early T-cell precursor; S, surface; TdT, terminal deoxynucleotidyl transferase.

on treatment outcome. In addition, specific cytogenetic or molecular The ongoing revision of the WHO classification will build upon the
abnormalities are associated with unique phenotypic characteristics framework established in 2008 to incorporate subsequent discoveries
+
and are amenable to targeted therapy. Although Ph ALL is the first on molecular genetics of ALL in order to potentially identify groups
subset of ALL to use a molecularly targeted TKI therapy as frontline of ALL likely to benefit from specific targeted therapy (see discussion
treatment, it is likely that more genetically-defined entities will be on Philadelphia chromosome-like ALL (Ph-like ALL) later).
targeted for specific therapy. This was recognized in the 2008 WHO Hyperdiploidy, defined by the presence of more than 50 chromo-
classification with a specific discussion on lymphoblastic leukemia/ somes, is seen in almost 25% of pediatric patients and 4% to 5% of
lymphoma with recurrent cytogenetic abnormalities (Table 66.4). adult ALL patients. In addition to routine karyotyping or fluorescence