BTKCys481Ser drives ibrutinib resistance via ERK1/2 and protects BTKwild-type MYD88-mutated cells by a paracrine mechanism
Author:
Affiliation:
1. Bing Center for Waldenstrom’s Macroglobulinemia,
2. Department of Medical Oncology, Dana Farber Cancer Institute, and
3. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA
Abstract
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Link
http://ashpublications.org/blood/article-pdf/131/18/2047/1406067/blood811752.pdf
Reference36 articles.
1. A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemia;Yang;Blood,2013
2. Targeting B cell receptor signaling with ibrutinib in diffuse large B cell lymphoma;Wilson;Nat Med,2015
3. HCK is a survival determinant transactivated by mutated MYD88, and a direct target of ibrutinib;Yang;Blood,2016
4. Ibrutinib in previously treated Waldenström’s macroglobulinemia;Treon;N Engl J Med,2015
5. Mutated MYD88 activates the BCR component SYK, and provides a rationale therapeutic target in Waldenstrom’s Macroglobulinemia [abstract];Munshi;Blood,2017
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2. BTK and PLCG2 remain unmutated in one-third of patients with CLL relapsing on ibrutinib;Blood Advances;2023-06-16
3. B-cell Receptor Pathway Mutations Are Infrequent in Patients with Chronic Lymphocytic Leukemia on Continuous Ibrutinib Therapy;Clinical Cancer Research;2023-06-14
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