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Inhibition of Bruton's tyrosine kinase restricts neuroinflammation following intracerebral hemorrhage.
Theranostics
January 2025
Department of Neurology, Tianjin Neurological Institute, Tianjin Institute of Immunology, State Key Laboratory of Experimental Hematology, International Joint Laboratory of Ocular Diseases, Ministry of Education, Haihe Laboratory of Cell Ecosystem, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin & Ministry of Education, Tianjin Medical University General Hospital, Tianjin 300052, China.
Intracerebral hemorrhage (ICH) is a devastating form of stroke with a lack of effective treatments. Following disease onset, ICH activates microglia and recruits peripheral leukocytes into the perihematomal region to amplify neural injury. Bruton's tyrosine kinase (BTK) controls the proliferation and survival of various myeloid cells and lymphocytes.
View Article and Find Full Text PDFFungal infection in patients treated with Bruton's Tyrosine Kinase inhibitor, from epidemiology to clinical outcome: A systematic review.
Clin Microbiol Infect
December 2024
Sorbonne Université, CIMI-Paris, AP-HP, Service de Parasitologie-Mycologie, Hopital de La Pitie-Salpetriere, F-75013 Paris, France. Electronic address:
Background: Bruton Tyrosine Kinase inhibitor (BTKi) emerged as key treatment for B-cell lymphomas. Despite its efficacy in the treatment of malignancies, numerous cases of invasive fungal infections (IFI) have been reported in patients receiving ibrutinib, a first generation BTKi. Cases of invasive aspergillosis have also been reported with acalabrutinib and zanubrutinib.
View Article and Find Full Text PDFOptimal use of BTK inhibitors in Waldenström's macroglobulinemia: combination or single drug approach?
Ther Adv Hematol
December 2024
Department of Clinical Therapeutics, Faculty of Medicine, National and Kapodistrian University of Athens, 80 Vassilisis Sofias Avenue, Athens 11527, Greece.
Waldenström macroglobulinemia is an indolent B-cell lymphoma which although remains incurable, there are a lot of treatment options. Today, Bruton tyrosine kinase inhibitors have a central role in the management of the disease either as monotherapy or combination with other regimens, due to their efficacy, ease of administration, and safety profile. However, there is still active clinical investigation to further increase their efficacy and improve safety profile.
View Article and Find Full Text PDFInsights into genetic aberrations and signalling pathway interactions in chronic lymphocytic leukemia: from pathogenesis to treatment strategies.
Biomark Res
December 2024
L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Rudolf Weigl 12, 53-114, Wroclaw, Poland.
Chronic lymphocytic leukemia (CLL) is prevalent in adults and is characterized by the accumulation of mature B cells in the blood, bone marrow, lymph nodes, and spleens. Recent progress in therapy and the introduction of targeted treatments [inhibitors of Bruton's tyrosine kinase (BTKi) or inhibitor of anti-apoptotic B-cell lymphoma-2 (Bcl-2i) protein (venetoclax)] in place of chemoimmunotherapy have significantly improved the outcomes of patients with CLL. These advancements have shifted the importance of traditional predictive markers, leading to a greater focus on resistance genes and reducing the significance of mutations, such as TP53 and del(17p).
View Article and Find Full Text PDFImpact of the clinically approved BTK inhibitors on the conformation of full-length BTK and analysis of the development of BTK resistance mutations in chronic lymphocytic leukemia.
Elife
December 2024
Roy J. Carver Department of Biochemistry, Biophysics and Molecular Biology, Iowa State University, Ames, United States.
Inhibition of Bruton's tyrosine kinase (BTK) has proven to be highly effective in the treatment of B-cell malignancies such as chronic lymphocytic leukemia (CLL), autoimmune disorders, and multiple sclerosis. Since the approval of the first BTK inhibitor (BTKi), Ibrutinib, several other inhibitors including Acalabrutinib, Zanubrutinib, Tirabrutinib, and Pirtobrutinib have been clinically approved. All are covalent active site inhibitors, with the exception of the reversible active site inhibitor Pirtobrutinib.
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