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Obecabtagene Autoleucel: First Approval.
Mol Diagn Ther
January 2025
Springer Nature, Private Bag 65901, Mairangi Bay, Auckland, 0754, New Zealand.
Obecabtagene autoleucel (AUCATZYL) is a CD19-directed genetically modified autologous T cell immunotherapy which is being developed by Autolus for the treatment of hematological cancers and systemic lupus erythematosus. In comparison with other chimeric antigen receptor T (CAR T) therapies, obecabtagene autoleucel has a fast off-rate binder for CD19. Obecabtagene autoleucel received approval following positive results from the FELIX phase I/II trial in adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL), and it is the first CAR T therapy that does not have mandatory Risk Evaluation Mitigation Strategy monitoring requirements.
View Article and Find Full Text PDFPeriductal fibroblasts participate in liver homeostasis, fibrosis, and tumorigenesis.
J Exp Med
April 2025
Key Laboratory of Multi-Cell System, Shanghai Institute of Biochemistry and Cell Biology, CAS Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Hepatic fibroblasts comprise groups of stromal cells in the liver that are phenotypically distinct from hepatic stellate cells. However, their physiology is poorly understood. By single-cell RNA sequencing, we identified Cd34 and Dpt as hepatic fibroblast-specific genes.
View Article and Find Full Text PDFComparative Safety of Ibrutinib Versus Zanubrutinib in Patients With Chronic Lymphocytic Leukemia: A Prospective Cohort Study.
Hematol Oncol
March 2025
Department of Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
This study compares the safety profiles of two Bruton's tyrosine kinase (BTK) inhibitors, Ibrutinib and Zanubrutinib, in patients with chronic lymphocytic leukemia (CLL). While Ibrutinib has transformed CLL treatment, it is associated with significant adverse events (AEs). Zanubrutinib, a second-generation BTK inhibitor, offers potential for improved safety.
View Article and Find Full Text PDFTargeting the Menin-KMT2A interaction in leukemia: Lessons learned and future directions.
Int J Cancer
January 2025
DGHO, Deutsche Gesellschaft für Hämatologie und Medizinische Onkologie e.V. working group, Clinical and Translational Epigenetics, Berlin, Germany.
Chromosomal rearrangements involving the Mixed Lineage Leukemia gene (MLL1, KMT2A) are defining a genetically distinct subset in about 10% of human acute leukemias. Translocations involving the KMT2A-locus at chromosome 11q23 are resulting in the formation of a chimeric oncogene, where the N-terminal part of KMT2A is fused to a variety of translocation partners. The most frequently found fusion partners of KMT2A in acute leukemia are the C-terminal parts of AFF1, MLLT3, MLLT1 and MLLT10.
View Article and Find Full Text PDFSynergistic effect of inhibiting CHK2 and DNA replication on cancer cell growth.
Elife
January 2025
Institut de Génétique Humaine, Univ. de Montpellier, CNRS, Montpellier, France.
Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS to unbearable levels or inhibit checkpoint kinases involved in the DNA damage response. Thus far, treatments that combine these two strategies have shown promise but also have severe adverse effects.
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