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http://dx.doi.org/10.1002/pbc.32035 | DOI Listing |
Pediatr Blood Cancer
September 2025
Seattle Children's Hospital, Seattle, Washington, USA.
Eur J Case Rep Intern Med
August 2025
Division of Hematology and Oncology, UNM Comprehensive Cancer Center, Albuquerque, USA.
Background: Blinatumomab and inotuzumab ozogamicin (InO) are B-cell targeted agents used in the frontline and relapsed/refractory treatment of B-cell acute lymphoblastic leukaemia (B-ALL). Blinatumomab, a bispecific T-cell engager that targets CD19 and CD3, and InO, an antibody-drug conjugate targeting CD22, have both shown efficacy. However, recent reports have noted lineage conversion as a complication when these agents are used individually or sequentially.
View Article and Find Full Text PDFPediatr Blood Cancer
August 2025
Division of Hematology/Oncology, Children's Hospital of Zhejiang University School of Medicine, Hangzhou, China.
Cureus
July 2025
Department of Hematology, Lyndon B. Johnson Hospital, Houston, USA.
Central nervous system (CNS) involvement in adult B-cell acute lymphoblastic leukemia (B-ALL) continues to pose treatment challenges, even with advancements in chemotherapy and targeted immunotherapy. Blinatumomab, a bispecific T-cell engager, has been shown to improve outcomes for patients with relapsed or refractory B-ALL; however, it can lead to immune-related neurotoxic effects, including immune effector cell-associated neurotoxicity syndrome (ICANS). We present an unusual case of a 38-year-old man with refractory B-ALL who experienced a parenchymal CNS relapse that manifested as foot drop during treatment with blinatumomab, likely as a result of ICANS.
View Article and Find Full Text PDFActa Naturae
January 2025
Almazov National Medical Research Centre, St. Petersburg, 197341 Russia.
A patient with an immunophenotype characteristic of B-cell acute lymphoblastic leukemia (B-ALL) was found to carry the chromosomal translocation t(9;22)(q34;q11), or Philadelphia (Ph) chromosome and less common variant of the chimeric oncogene BCR::ABL/p210. No additional mutations in the BCR::ABL gene, including point mutations, insertions, or deletions, were identified in the disease onset characterized by elevated blast cell (77.6%) and leukocyte (48×109/L) counts.
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