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Optimizing drug combinations for T-PLL: restoring DNA damage and P53-mediated apoptotic responses.
Blood
October 2024
Department I of Internal Medicine, Center for Integrated Oncology Aachen-Bonn-Cologne-Duesseldorf, University Hospital Cologne, University of Cologne, Cologne, Germany.
T-prolymphocytic leukemia (T-PLL) is a mature T-cell neoplasm associated with marked chemotherapy resistance and continued poor clinical outcomes. Current treatments, that is, the CD52-antibody alemtuzumab, offer transient responses, with relapses being almost inevitable without consolidating allogeneic transplantation. Recent more detailed concepts of T-PLL's pathobiology fostered the identification of actionable vulnerabilities: (1) altered epigenetics, (2) defective DNA damage responses, (3) aberrant cell-cycle regulation, and (4) deregulated prosurvival pathways, including T-cell receptor and JAK/STAT signaling.
View Article and Find Full Text PDFThe PPP2R1A cancer hotspot mutant p.R183W increases clofarabine resistance in uterine serous carcinoma cells by a gain-of-function mechanism.
Cell Oncol (Dordr)
October 2024
Laboratory of Protein Phosphorylation and Proteomics, Department of Cellular and Molecular Medicine, University of Leuven (KU Leuven), Gasthuisberg O&N1, Herestraat 49, PO-box 901, Leuven, B-3000, Belgium.
Purpose: Uterine serous carcinoma (USC) is generally associated with poor prognosis due to a high recurrence rate and frequent treatment resistance; hence, there is a need for improved therapeutic strategies. Molecular analysis of USC identified several molecular markers, useful to improve current treatments or identify new druggable targets. PPP2R1A, encoding the Aα subunit of the tumor suppressive Ser/Thr phosphatase PP2A, is mutated in up to 40% of USCs.
View Article and Find Full Text PDFPharmacological modulation of inflammatory oligodendrocyte progenitor cells using three multiple sclerosis disease modifying therapies in vitro.
Neurotherapeutics
July 2024
Department of Neurology, Johns Hopkins University School of Medicine, United States; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, United States. Electronic address:
Preclinical studies of pro-remyelinating therapies for multiple sclerosis tend to neglect the effect of the disease-relevant inflammatory milieu. Interferon-gamma (IFN-γ) is known to suppress oligodendrocyte progenitor cell (OPC) differentiation and induce a recently described immune OPC (iOPC) phenotype characterized by expression of major histocompatibility complex (MHC) molecules. We tested the effects of cladribine (CDB), dimethylfumarate (DMF), and interferon-beta (IFN-β), existing anti-inflammatory therapies for MS, on the IFN-γ-induced iOPC formation and OPC differentiation block.
View Article and Find Full Text PDFInhibition of chitin deacetylases to attenuate plant fungal diseases.
Nat Commun
June 2023
School of Bioengineering, Dalian University of Technology, 116024, Dalian, China.
Phytopathogenic fungi secrete chitin deacetylase (CDA) to escape the host's immunological defense during infection. Here, we showed that the deacetylation activity of CDA toward chitin is essential for fungal virulence. Five crystal structures of two representative and phylogenetically distant phytopathogenic fungal CDAs, VdPDA1 from Verticillium dahliae and Pst_13661 from Puccinia striiformis f.
View Article and Find Full Text PDFImmune Response to Seasonal Influenza Vaccination in Multiple Sclerosis Patients Receiving Cladribine.
Cells
April 2023
Department of Neurology and Center for Translational Neuro and Behavioral Science, University Medicine Essen, 45127 Essen, Germany.
Cladribine has been approved for the treatment of multiple sclerosis (MS) and its administration results in a long-lasting depletion of lymphocytes. As lymphopenia is known to hamper immune responses to vaccination, we evaluated the immunogenicity of the influenza vaccine in patients undergoing cladribine treatment at different stages vs. controls.
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