Resistance to ABT-199 induced by microenvironmental signals in chronic lymphocytic leukemia can be counteracted by CD20 antibodies or kinase inhibitors
Molecular pathways: Targeting the microenvironment in chronic lymphocytic leukemia: Focus on the B-cell receptor
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Dichotomy in NF-kB signaling and chemoresistance in immunoglobulin variable heavy-chainmutated versus unmutated CLL cells upon CD40/TLR9 triggering
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ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets
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Updated results of a phase I first-in-human study of the Bcl-2 inhibitor ABT-199 (GDC-0199) in patients with relapsed/refractory R/R chronic lymphocytic leukemia (CLL)
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Idelalisib, an inhibitor of phosphatidylinositol 3-kinase p110delta, for relapsed/refractory chronic lymphocytic leukemia
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Increasing the efficacy of CD20 antibody therapy through the engineering of a new type II anti-CD20 antibody with enhanced direct and immune effector cellmediated B-cell cytotoxicity
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IL-21 and CD40L signals from autologous T cells can induce antigen-independent proliferation of CLL cells
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Concurrent up-regulation of BCL-XL and BCL2A1 induces approximately 1000-fold resistance to ABT-737 in chronic lymphocytic leukemia
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CD40 stimulation sensitizes CLL cells to rituximab-induced cell death
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CD40 stimulation sensitizes CLL cells to lysosomal cell death induction by type II anti-CD20 mAb GA101
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The Btk tyrosine kinase is a major target of the Bcr-Abl inhibitor dasatinib
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Acquired mutations in BCL2 family proteins conferring resistance to the BH3 mimetic ABT-199 in lymphoma
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