Abstract
An increasing number of evidences suggest a genetic predisposition in acute lymphoblastic leukemia (ALL) that might favor the occurrence of the driver genetic alterations. Such genetic background might also translate into phenotypic alterations of residual hematopoietic cells. Whether such phenotypic alterations are present in bone marrow (BM) cells from childhood B-cell precursor (BCP)-ALL remains to be investigated. Here we analyzed the immunophenotypic profile of BM and peripheral blood (PB) maturing/matured neutrophils from 118 children with BCP-ALL and their relationship with the features of the disease. Our results showed altered neutrophil phenotypes in most (77%) BCP-ALL cases. The most frequently altered marker was CD10 (53%), followed by CD33 (34%), CD13 (15%), CD15/CD65 (10%) and CD123 (7%). Of note, patients with altered neutrophil phenotypes had younger age (p = 0.03) and lower percentages of BM maturing neutrophils (p = 0.004) together with greater BM lymphocyte (p = 0.04), and mature B-cell (p = 0.03) counts. No significant association was found between an altered neutrophil phenotype and other disease features. These findings point out the potential existence of an altered residual hematopoiesis in most childhood BCP-ALL cases.
Highlights
B‐cell precursor acute lymphoblastic leukemia (BCP‐ALL) is a genetically and clinically heterogeneous malignancy characterized by the clonal expansion of tumor B‐cell precursors [1]
Childhood BCP‐ALL is a relatively heterogeneous group of de novo acute leukemias, which is characterized by an abnormal expansion of genetically altered B‐cell precursors blocked at relatively early stages of B‐lymphoid maturation [3]
Accumulating evidences suggest that a genetic predisposition might exist which favors the development of childhood BCP‐ALL [4,5,6,7,8,9, 11]
Summary
B‐cell precursor acute lymphoblastic leukemia (BCP‐ALL) is a genetically and clinically heterogeneous malignancy characterized by the clonal expansion of tumor B‐cell precursors [1]. Several distinct genetic/molecular subtypes of BCP‐ALL have been identified which show an age‐associated distribution with prognostic impact [2, 3]. Chromosomal alterations from such BCP‐ALL‐associated genetic subgroups appear to be associated with the development of the disease and they frequently are a hallmark of the tumor. Around 2% of children with BCP‐ALL present with a transient (preleukemic) aplastic phase, 2 to 9 months before initial diagnosis [10, 11]. Efforts devoted to the analysis of BCP‐ALL tumor cells have concentrated in the characterization of the oncogenetic steps that occur within the BCP‐ALL blast cell compartment [2, 12]; in contrast, fewer studies have investigated the features of residual hematopoietic cells at diagnosis
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