Detection of small abnormal B-Lymphoblast populations at diagnosis of chronic myelogenous leukemia,BCR-ABL1+: Incidence, phenotypic features, and clinical implications
| Autor: | Maria Gorgan, Elena Vrotsos, Joseph A. DiGiuseppe |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Histology medicine.drug_class Population Biology Tyrosine-kinase inhibitor Pathology and Forensic Medicine 03 medical and health sciences 0302 clinical medicine Immunophenotyping hemic and lymphatic diseases medicine education education.field_of_study medicine.diagnostic_test Lymphoblast hemic and immune systems Cell Biology medicine.disease Bone marrow examination Haematopoiesis 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Immunology Bone marrow Chronic myelogenous leukemia |
| Zdroj: | Cytometry Part B: Clinical Cytometry. 92:275-278 |
| ISSN: | 1552-4949 |
| Popis: | Background 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. Methods 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. Results 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). Conclusions In chronic-phase CML, a small ( |
| Databáze: | OpenAIRE |
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