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LLT1 overexpression renders allogeneic-NK resistance and facilitates the generation of enhanced universal CAR-T cells.
J Exp Clin Cancer Res
January 2025
State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300020, China.
Background: The benefit of universal CAR-T cells over autologous CAR-T cell therapy is that they are a treatment that is ready to use. However, the prevention of graft-versus-host disease (GVHD) and host-versus-graft reaction (HVGR) remains challenging. Deleting class I of human leukocyte antigen (HLA-I) and class II of human leukocyte antigen (HLA-II) can prevent rejection by allogeneic T cells; however, natural killer (NK) cell rejection due to the loss of self-recognition remains unresolved.
View Article and Find Full Text PDFAssociation of age, race, and ethnicity with access, response, and toxicities from CAR-T therapy in children and adults with B-cell malignancies: a review.
J Immunother Cancer
January 2025
Department of Medicine and Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
Chimeric antigen receptor T cell (CAR-T) therapies are now standard-of-care for several B-cell malignancies, and additional indications are being evaluated. In this review, we survey data on how outcomes after CAR-T therapies vary according to age, race, and ethnicity. We also review the representation of age, racial, and ethnic groups in key CAR-T clinical trials.
View Article and Find Full Text PDFTargeting LMO2-induced autocrine FLT3 signaling to overcome chemoresistance in early T-cell precursor acute lymphoblastic leukemia.
Leukemia
January 2025
Australian Centre for Blood Diseases (ACBD), School of Translational Medicine, Monash University, Melbourne, VIC, Australia.
Early T-cell Precursor Acute Lymphoblastic Leukemia (ETP-ALL) is an immature subtype of T-cell acute lymphoblastic leukemia (T-ALL) commonly show deregulation of the LMO2-LYL1 stem cell transcription factors, activating mutations of cytokine receptor signaling, and poor early response to intensive chemotherapy. Previously, studies of the Lmo2 transgenic mouse model of ETP-ALL identified a population of stem-like T-cell progenitors with long-term self-renewal capacity and intrinsic chemotherapy resistance linked to cellular quiescence. Here, analyses of Lmo2 transgenic mice, patient-derived xenografts, and single-cell RNA-sequencing data from primary ETP-ALL identified a rare subpopulation of leukemic stem cells expressing high levels of the cytokine receptor FLT3.
View Article and Find Full Text PDFVenetoclax and azacitidine in combination with homoharringtonine, cytarabine, and aclarubicin for salvage therapy of relapsed/refractory T cell acute lymphoblastic leukemia.
Int J Hematol
January 2025
Department of Hematology, The 920th Hospital of Joint Logistics Support Force, No.212, Da Guan Road, Xishan District, Kunming, 650100, Yunnan, China.
Background: The treatment of relapsed/refractory T cell acute lymphoblastic leukemia (R/R T-ALL) is a significant challenge in hematologic oncology, and no standard salvage treatment plan exists. Both Chinese and international clinical guidelines recommend combination chemotherapy including venetoclax.
Methods: Efficacy and safety of venetoclax, azacitidine, homoharringtonine, cytarabine, and aclarubicin (VA-HAA) combination therapy were retrospectively analyzed in 3 patients with R/R T-ALL at the Department of Hematology, 920th Hospital of the Joint Logistics Support Force, Chinese People's Liberation Army.
A complete response with daratumumab, venetoclax, azacitidine and dexamethasone in a heavily pre-treated, chemo-refractory early T-precursor acute lymphoblastic leukemia/lymphoma patient.
Ann Hematol
January 2025
Department of Hematology, Faculty of Medicine, Istanbul Medipol University, Istanbul, Turkey.
Early T-precursor acute lymphoblastic leukemia/lymphoma (ETP-ALL/LBL) is a rare and aggressive subtype of T-cell leukemia with poor prognosis and resistance to standard treatments. We report a 21-year-old male with ETP-ALL/LBL who, after an initial complete remission with the HOELZER protocol, experienced early relapse and was refractory to subsequent FLEND and BFM protocols. Following disease progression and complications, he was treated with a combination of daratumumab, venetoclax, azacitidine, and dexamethasone.
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