Detection of small abnormal B-Lymphoblast populations at diagnosis of chronic myelogenous leukemia, BCR-ABL1+: Incidence, phenotypic features, and clinical implications.
According to the 2008 World Health Organization (WHO) Classification of Tumors of the Haematopoietic and Lymphoid Tissues, the finding of B lymphoblasts in the blood or bone marrow of a patient with chronic myelogenous leukemia, BCR-ABL1+ (CML) should raise a concern for progression of the disease to B-lymphoblastic blast phase. Data addressing the incidence and phenotypic features of abnormal B lymphoblasts in CML, and whether the detection of B lymphoblasts inexorably heralds blast phase in CML, though, are limited.



We reviewed a consecutive series of patients with newly diagnosed CML who had undergone bone marrow examination with flow cytometric immunophenotyping. Polychromatic immunophenotyping data were reviewed, and clinical follow-up data were obtained.



A precursor B-cell population with an abnormal composite immunophenotype was detected in 4 of 36 (11.1%) diagnostic bone marrow samples, at levels ranging from 0.01% to 0.30% of viable single cells acquired. The most common phenotypic aberrations were abnormally bright expression of CD10 and CD19 (seen in four and three cases, respectively), and abnormally dim expression of CD38 (seen in four cases). All three patients with adequate clinical follow-up have achieved and maintained a deep or major molecular response with a tyrosine kinase inhibitor, and none has progressed to B-lymphoblastic blast phase (follow-up duration: 17-46 months).



In chronic-phase CML, a small (<0.5%) abnormal B-lymphoblast population is present in a significant minority of diagnostic bone marrow samples, but does not inevitably herald progression to B-lymphoblastic blast phase. © 2015 International Clinical Cytometry Society.
Department of Pathology & Laboratory Medicine, Hartford Hospital, Hartford, Connecticut.
Elena
E
Vrotsos
Department of Pathology & Laboratory Medicine, Hartford Hospital, Hartford, Connecticut.
Maria
M
Gorgan
Department of Pathology & Laboratory Medicine, Hartford Hospital, Hartford, Connecticut.
Joseph A
0000-0002-2063-8832
JA
DiGiuseppe
D051997:ADP-ribosyl Cyclase 1 / Q000097:blood / Q000235:genetics; D000328:Adult; D000368:Aged; D018941:Antigens, CD19 / Q000097:blood / Q000235:genetics; D000970:Antineoplastic Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D015870:Gene Expression; D006801:Humans; D016130:Immunophenotyping; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood / Q000235:genetics; D008875:Middle Aged; D015260:Neprilysin / Q000097:blood / Q000235:genetics; D054448:Precursor Cells, B-Lymphoid / Q000276:immunology / Q000473:pathology*; D011379:Prognosis; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D016896:Treatment Outcome
D018941:Antigens, CD19; D000970:Antineoplastic Agents; D015415:Biomarkers; C000604811:CD19 molecule, human; D008562:Membrane Glycoproteins; D047428:Protein Kinase Inhibitors; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1; D015260:Neprilysin
CML; flow cytometry; immunophenotype; lymphoblasts; polychromatic