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The significance of endogenous immune surveillance in acute lymphoblastic leukemia (ALL) remains controversial. Using clinical B-ALL samples and a novel mouse model, we show that neoantigen-specific CD4+ T cells are induced to adopt type-1 regulatory (Tr1) function in the leukemia microenvironment. Tr1s then inhibit cytotoxic CD8+ T cells, preventing effective leukemia clearance.

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Umbilical cord blood (UCB) represents a valuable graft source in the absence of a human leukocyte antigen (HLA)-matched donor for hematopoietic cell transplantation (HCT). Donor-specific anti-HLA antibodies (DSAs), targeting grafts with mismatched HLA antigens, pose a significant obstacle by increasing the risk of primary graft failure, delayed engraftment, and decreased survival. Existing literature on HLA desensitization has primarily focused on haploidentical transplants, and there is a lack of experience regarding the optimal strategy in UCB transplantation.

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Utility of Daratumumab as Bridging Therapy in De Novo T-Cell Acute Lymphoblastic Lymphoma.

Pediatr Blood Cancer

January 2025

Department of Clinical Haematology, Oncology, Blood and Marrow Transplantation, Perth Children's Hospital, Perth, Western Australia, Australia.

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Background: Multiple factors have been described to influence the risk of acute or chronic graft-versus-host disease (aGVHD or cGVHD) after allogeneic hematopoietic cell transplantation (HCT), including underlying chronic myeloid leukemia (CML) and high-dose total body irradiation (TBI). However, the impact of the underlying disease or low-dose TBI on the risk of GVHD in the modern era has not been determined.

Objective: To determine risk factors for GVHD in the modern era in the setting of antithymocyte globulin (ATG)-based GVHD prophylaxis.

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INTRODUCTION ETV6::JAK2 is a fusion known to drive Acute Lymphoblastic Leukaemia (ALL) in the presence of other genomic lesions which define the JAK/STAT class of Philadelphia-like Acute Lymphoblastic Leukaemia (Ph-like ALL). Ph-like ALL comprises approximately 15% of ALL. Patients with mutations or gene fusions signaling through the JAK/STAT pathway have particularly poor prognosis.

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