[1]Meng X, Min Q, Wang J Y. B cell lymphoma[J]. Adv Exp Med Biol, 2020, 1254: 161-181.
[2]Young R M, Phelan J D, Wilson W H, et al. Pathogenic B-cell receptor signaling in lymphoid malignancies: new insights to improve treatment[J]. Immunol Rev, 2019, 291(1): 190-213.
[3]Tkachenko A, Kupcova K, Havranek O. B-cell receptor signaling and beyond: the role of Igα (CD79a)/Igβ (CD79b) in normal and malignant B cells[J]. Int J Mol Sci, 2023, 25(1): 10.
[4]Young R M, Wu T Y, Schmitz R, et al. Survival of human lymphoma cells requires B-cell receptor engagement by self-antigens[J]. Proc Natl Acad Sci U S A, 2015, 112(44): 13447-13454.
[5]Melchers F. Checkpoints that control B cell development[J]. J Clin Invest, 2015, 125(6): 2203-2210.
[6]Dong Y, Pi X, Bartels-Burgahn F, et al. Structural principles of B cell antigen receptor assembly[J]. Nature, 2022, 612(7938): 156-161.
[7]Pinto D, Montani E, Bolli M, et al. A functional BCR in human IgA and IgM plasma cells[J]. Blood, 2013, 121(20): 4110-4114.
[8]Shimizu T, Mundt C, Licence S, et al. VpreB1/VpreB2/lambda 5 triple-deficient mice show impaired B cell development but functional allelic exclusion of the IgH locus[J]. J Immunol, 2002, 168(12): 6286-6293.
[9]Tiegs S L, Russell D M, Nemazee D. Receptor editing in self-reactive bone marrow B cells[J]. J Exp Med, 1993, 177(4): 1009-1020.
[10]Blanc P, Moro-Sibilot L, Barthly L, et al. Mature IgM-expressing plasma cells sense antigen and develop competence for cytokine production upon antigenic challenge[J]. Nat Commun, 2016, 7(1): 13600.
[11]Wienands J, Larbolette O, Reth M.Evidence for a preformed transducer complex organized by the B cell antigen receptor[J]. Proc Natl Acad Sci U S A, 1996, 93(15): 7865-7870.
[12]Davis R E, Ngo V N, Lenz G, et al. Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma[J]. Nature, 2010, 463(7277): 88-92.
[13]Wang L D, Clark M R. B-cell antigen-receptor signalling in lymphocyte development[J]. Immunology, 2003, 110(4): 411-420.
[14]Monroe J G. ITAM-mediated tonic signalling through pre-BCR and BCR complexes[J]. Nat Rev Immunol, 2006, 6(4): 283-294.
[15]Lenz G, Nagel I, Siebert R, et al. Aberrant immunoglobulin class switchrecombination and switch translocations in activated B cell-like diffuse large B cell lymphoma[J]. J Exp Med, 2007, 204(3): 633-643.
[16]Horikawa K, Martin S W, Pogue S L, et al. Enhancement and suppression of signaling by the conserved tail of IgG memory-type B cell antigen receptors[J]. J Exp Med, 2007, 204(4): 759-769.
[17]Dogan I, Bertocci B, Vilmont V, et al. Multiple layers of B cell memory with different effector functions[J]. Nat Immunol, 2009, 10(12): 1292-1299.
[18]Chen L F, Monti S, Juszczynski P, et al. SYK inhibition modulates distinct PI3K/AKT-dependent survival pathways and cholesterol biosynthesis in diffuse large B cell lymphomas[J]. Cancer Cell, 2013, 23(6): 826-838.
[19]Xu W D, Berning P, Lenz G. Targeting B-cell receptor and PI3K signaling in diffuse large B-cell lymphoma[J]. Blood, 2021, 138(13): 1110-1119.
[20]Küppers R. Mechanisms of B-cell lymphoma pathogenesis[J]. Nat Rev Cancer, 2005, 5(4): 251-262.
[21]Refaeli Y, Young R M, Turner B C, et al. The B cell antigen receptor and overexpression of MYC can cooperate in the genesis of B cell lymphomas[J]. PLoS Biol, 2008, 6(6): e152.
[22]Wang M L, Rule S, Martin P, et al. Targeting BTK with ibrutinib in relapsed or refractory mantle-cell lymphoma[J]. N Engl J Med, 2013, 369(6): 507-516.
[23]Swerdlow S H, Campo E, Pileri S A, et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms[J]. Blood, 2016, 127(20): 2375-2390.
[24]Rosenwald A, Wright G, Leroy K, et al. Molecular diagnosis of primary mediastinal B cell lymphoma identifies a clinically favorable subgroup of diffuse large B cell lymphoma related to Hodgkin lymphoma[J]. J Exp Med, 2003, 198(6): 851-862.
[25]Rosenwald A, Wright G, Chan W C, et al. The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma[J]. N Engl J Med, 2002, 346(25): 1937-1947.
[26]Havranek O, Xu J D, Köhrer S, et al. Tonic B-cell receptor signaling in diffuse large B-cell lymphoma[J]. Blood, 2017, 130(8): 995-1006.
[27]Zhang J, Liu D, Shen R, et al.Abstract 2599: discovery and pharmacological characterization of the second generation of Btk inhibitors with improved target selectivity and enhanced in vivo efficacy[J]. Cancer Res, 2015, 75(15_Supplement): 2599.
[28]Carnero Contentti E, Correale J. Bruton's tyrosine kinase inhibitors: a promising emerging treatment option for multiple sclerosis[J]. Expert Opin Emerg Drugs, 2020, 25(4): 377-381.
[29]Herman S E M, Farooqui M, Bezabhie R, et al. In vivo effects of ibrutinib on bcr signaling, tumor cell activation and proliferation in blood and tissue-resident cells of chronic lymphocytic leukemia patients[J]. Blood, 2012, 120(21): 185.
[30]Fruman D A, Chiu H, Hopkins B D, et al. The PI3K pathway in human disease[J]. Cell, 2017, 170(4): 605-635.
[31]Lannutti B J, Meadows S A, Herman S E M, et al. CAL-101, a p110delta selectivephosphatidylinositol-3-kinase inhibitor for the treatment of B-cell malignancies, inhibits PI3K signaling and cellular viability[J]. Blood, 2011, 117(2): 591-594.
[32]Aydin E, Faehling S, Saleh M, et al. Phosphoinositide 3-kinase signaling in the tumor microenvironment: what do we need to consider when treating chronic lymphocytic leukemia with PI3K inhibitors?[J]. Front Immunol, 2020, 11: 595818.
[33]Serrat N, Guerrero-Hernández M, Matas-Céspedes A, et al. PI3Kδ inhibition reshapes follicular lymphoma-immune microenvironment cross talk and unleashes the activity of venetoclax[J]. Blood Adv, 2020, 4(17): 4217-4231.
[34]Pecoraro C, Faggion B, Balboni B, et al. GSK3β as a novel promising target to overcome chemoresistance in pancreatic cancer[J]. Drug Resist Updat, 2021, 58: 100779.
[35]Gacche R N, Assaraf Y G. Redundant angiogenic signaling and tumor drug resistance[J]. Drug Resist Updat, 2018, 36: 47-76.
[36]Kobayashi T, Nakamura S, Taniguchi T, et al. Purification and characterization of a cytosolic protein-tyrosine kinase from porcine spleen[J]. Eur J Biochem, 1990, 188(3): 535-540.
[37]Riccaboni M, Bianchi I, Petrillo P. Spleen tyrosine kinases: biology, therapeutic targets and drugs[J]. Drug Discov Today, 2010, 15(13/14): 517-530.
[38]Liu D L, Mamorska-Dyga A. Syk inhibitors in clinical development for hematological malignancies[J]. J Hematol Oncol, 2017, 10(1): 145.
[39]Horwitz S M, Feldman T A, Ye J C, et al. Phase 2a study of the dual SYK/JAK inhibitor cerdulatinib (ALXN2075) as monotherapy in patients with relapsed/refractory peripheral T-cell lymphoma[J]. Blood, 2021, 138: 622.
[40]Liu X F, Zhou H, Hu Y, et al. Sovleplenib (HMPL-523), a novel Syk inhibitor, for patients with primary immune thrombocytopenia in China: a randomised, double-blind, placebo-controlled, phase 1b/2 study[J]. Lancet Haematol, 2023, 10(6): e406-e418.
[41]Lenz G, Tilly H, Ziepert M, et al. Pola-R-CHP or R-CHOEP for first-line therapy of younger patients with high-risk diffuse large B-cell lymphoma: a retrospective comparison of two randomized phase 3 trials[J]. Leukemia, 2024, 38(12): 2709-2711.
[42]Tilly H, Morschhauser F, Sehn L H, et al. Polatuzumab vedotin in previously untreated diffuse large B-cell lymphoma[J]. N Engl J Med, 2022, 386(4): 351-363.
[43]Sehn L H, Hertzberg M, Opat S, et al. Polatuzumab vedotin plus bendamustine and rituximab in relapsed/refractory DLBCL: survival update and new extension cohort data[J]. Blood Adv, 2022, 6(2): 533-543.
[44]Srivastava S, Riddell S R. Engineering CAR-T cells: design concepts[J]. Trends Immunol, 2015, 36(8): 494-502.
[45]Leung I, Templeton M L, Lo Y, et al. Compromised antigen binding and signaling interfere with bispecific CD19 and CD79a chimeric antigen receptor function[J]. Blood Adv, 2023, 7(12): 2718-2730.
[46]Julamanee J, Terakura S, Umemura K, et al. Composite CD79A/CD40 co-stimulatory endodomain enhances CD19CAR-T cell proliferation and survival[J]. Mol Ther, 2021, 29(9): 2677-2690.
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