Noncatalytic Bruton's tyrosine kinase activates PLCγ2 variants mediating ibrutinib resistance in human chronic lymphocytic leukemia cells
نویسندگان
چکیده
منابع مشابه
Beyond Ibrutinib Resistance in Chronic Lymphocytic Leukemia
Despite ibrutinib activity in multiple B-cell malignancies, cases of primary and secondary resistance have emerged. The overall reported frequency of resistance is low. Resistance has been found to be caused by a mutation in the BTK binding site of ibrutinib or gain-of-function mutations in PLCG2, which lead to autonomous BCR activity. Improved understanding of mechanisms of primary and seconda...
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BACKGROUND The receptor tyrosine kinase like orphan receptor (ROR)-1 gene is overexpressed in chronic lymphocytic leukemia (CLL). Because Stat3 is constitutively activated in CLL and sequence analysis revealed that the ROR1 promoter harbors gamma-interferon activation sequence-like elements typically activated by Stat3, we hypothesized that Stat3 activates ROR1. METHODOLOGY/PRINCIPAL FINDINGS...
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The Bruton tyrosine kinase inhibitor (BTKi) ibrutinib is a new targeted therapy for patients with chronic lymphocytic leukemia (CLL). Ibrutinib is given orally on a continuous schedule and induces durable remissions in the majority of CLL patients. However, a small proportion of patients initially responds to the BTKi and then develops resistance. Estimating the frequency, timing, and individua...
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New treatment options are urgently needed for patients with relapsed chronic lymphocytic leukemia (CLL) who fail to respond to currently available therapies or cannot achieve a sustained response. Moreover, targeted agents with less myelotoxicity are necessary to treat patients with multiple comorbidities who would otherwise be unable to tolerate standard regimens. Ibrutinib, a Bruton's tyrosin...
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ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 2020
ISSN: 0021-9258
DOI: 10.1074/jbc.ra119.011946