ORIGINAL RESEARCH article
Front. Oncol.
Sec. Pediatric Oncology
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1641088
Expression of aberrant markers in monitoring of measurable residual disease in B-cell precursor acute lymphoblastic leukemia patients during remission-inducing therapy phase
Provisionally accepted- 1Medical University of Silesia in Katowice, Department of Pediatric, Hematology and Oncology in Zabrze, Katowice, Poland
- 2Medical Univeristy of Silesia in Katowice, Department of Microbiology and Immunology in Zabrze, Poland, Katowice, Poland
- 3Department of Pediatric, Hematology, Oncology and Transplantology, Medical University of Lublin, Poland, Lublin, Poland
- 4Department of Pediatrics, Oncology and Hematology, Medical University of Łódź, Poland, Lodz, Poland
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
B-cell acute lymphoblastic leukemia (BCP-ALL) is characterized by an abnormal proliferation of immature cells in bone marrow. Leukemic blasts at diagnosis exhibit a so-called leukemia associated immunophenotype (LAIP), which is further used for determination of measurable residual disease (MRD) levels at particular time points during the therapy. Nevertheless, in some patients LAIP proves insufficient for discrimination of blasts from their normal counterparts, therefore, search for novel, aberrant markers is essential. A crucial requirement for these antigens is their expression variability throughout the entire treatment monitoring period.The aim of the study was to assess the expression level of four markers: CD66c, CD304, CD72 and CD86 on leukemic cells at diagnosis and at day 15 and 33 of treatment to compare stability of their expression. We also correlated the results obtained with the most common genetic aberrations
Keywords: Flow Cytometry, measurable residual disease, B-cell precursor acute lymphoblastic leukemia, Childhood acute leukemia, antigen expression hyper-hypodiploidy, BCR::ABL1, KMT2A::AFF1, ETV6::RUNX1
Received: 04 Jun 2025; Accepted: 07 Aug 2025.
Copyright: © 2025 Słota, Sędek, Lejman, Perkowski, Lasia, Bulsa, Mlynarski, Kowalczyk and Szczepański. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Łukasz Słota, Medical University of Silesia in Katowice, Department of Pediatric, Hematology and Oncology in Zabrze, Katowice, Poland
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.