Bruton tyrosine kinase represents a promising therapeutic target for treatment of chronic lymphocytic leukemia and is effectively targeted by PCI-32765.

By S. E. Herman, Amber L. Gordon, E. Hertlein, A. Ramanunni, Xiaoli Zhang, S. Jaglowski, J. Flynn, Jeffrey A Jones, K. Blum, J. Buggy and 3 more. Blood, 2011

834 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6fe7953490a1d457e0111cac2ae23bea2be86276

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Simar Pal Singh
Floris Dammeijer
R. Hendriks
Ta-Ming Liu
S. Jaglowski
N. Muthusamy
J. Dubovsky
Lisa L. Smith

Citations in the corpus

Ibrutinib Regimens versus Chemoimmunotherapy in Older Patients with Untreated CLL (2018, neutral): “1) 34/542 (6) 14/181 (8) 9/181 (5) 11/180 (6)”
Role of Bruton’s tyrosine kinase in B cells and malignancies (2018, background): “Hereby, BTK is essential for constitutively active pathways implicated in CLL cell survival, including AKT, ERK and NF-кB, both in patient cells and mouse models [133, 141–143].”
Ibrutinib is an irreversible molecular inhibitor of ITK driving a Th1-selective pressure in T lymphocytes. (2013, background): “Ibrutinib is an irreversible inhibitor of Bruton tyrosine kinase (BTK) that blocks downstream B-cell receptor activation.(15,16) Numerous in vitro and in vivo studies confirm the specific activity of ibrutinib against BTK-restricted targets.”
Three-year follow-up of treatment-naïve and previously treated patients with CLL and SLL receiving single-agent ibrutinib. (2015, neutral): “Median platelets, 3 10(9)/L (range) 113 (32-217) 105 (2-310) 105 (2-310) #100 3 10(9)/L, n (%) 12 (39) 49 (49) 61 (46)”