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• W1518069585 abstract "// Ning Ding 1 , Xitao Li 2 , Yunfei Shi 3 , Lingyan Ping 1 , Lina Wu 4 , Kai Fu 5 , Lixia Feng 1 , Xiaohui Zheng 1 , Yuqin Song 1 , Zhengying Pan 2 and Jun Zhu 1 1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Lymphoma, Peking University Cancer Hospital and Institute, Beijing, China 2 Key Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Xili, Shenzhen, China 3 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Pathology, Peking University Cancer Hospital and Institute, Beijing, China 4 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Central Laboratory, Peking University Cancer Hospital and Institute, Beijing, China 5 Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA Correspondence to: Jun Zhu, email: // Zhengying Pan, email: // Yuqin Song, email: // Keywords : BCR signaling, Btk, irreversible inhibitor, targeted therapy, B-cell lymphoma Received : December 17, 2014 Accepted : March 26, 2015 Published : April 14, 2015 Abstract The B-cell receptor (BCR) signaling pathway has gained significant attention as a therapeutic target in B-cell malignancies. Recently, several drugs that target the BCR signaling pathway, especially the Btk inhibitor ibrutinib, have demonstrated notable therapeutic effects in relapsed/refractory patients, which indicates that pharmacological inhibition of BCR pathway holds promise in B-cell lymphoma treatment. Here we present a novel covalent irreversible Btk inhibitor PLS-123 with more potent anti-proliferative activity compared with ibrutinib in multiple cellular and in vivo models through effective apoptosis induction and dual-action inhibitory mode of Btk activation. The phosphorylation of BCR downstream activating AKT/mTOR and MAPK signal pathways was also more significantly reduced after treatment with PLS-123 than ibrutinib. Gene expression profile analysis further suggested that the different selectivity profile of PLS-123 led to significant downregulation of oncogenic gene PTPN11 expression, which might also offer new opportunities beyond what ibrutinib has achieved. In addition, PLS-123 dose-dependently attenuated BCR- and chemokine-mediated lymphoma cell adhesion and migration. Taken together, Btk inhibitor PLS-123 suggested a new direction to pharmacologically modulate Btk function and develop novel therapeutic drug for B-cell lymphoma treatment." @default.
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• W1518069585 date "2015-04-14" @default.
• W1518069585 modified "2023-10-17" @default.
• W1518069585 title "Irreversible dual inhibitory mode: the novel Btk inhibitor PLS-123 demonstrates promising anti-tumor activity in human B-cell lymphoma" @default.
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• W1518069585 doi "https://doi.org/10.18632/oncotarget.3824" @default.
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