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+@article{venturuttiTBL1XR1MutationsDrive2020b,
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+ title = {{{TBL1XR1 Mutations Drive Extranodal Lymphoma}} by {{Inducing}} a {{Pro-tumorigenic Memory Fate}}},
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+ author = {Venturutti, Leandro and Teater, Matt and Zhai, Andrew and Chadburn, Amy and Babiker, Leena and Kim, Daleum and Béguelin, Wendy and Lee, Tak C. and Kim, Youngjun and Chin, Christopher R. and Yewdell, William T. and Raught, Brian and Phillip, Jude M. and Jiang, Yanwen and Staudt, Louis M. and Green, Michael R. and Chaudhuri, Jayanta and Elemento, Olivier and Farinha, Pedro and Weng, Andrew P. and Nissen, Michael D. and Steidl, Christian and Morin, Ryan D. and Scott, David W. and Privé, Gilbert G. and Melnick, Ari M.},
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+ date = {2020-07-23},
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+ journaltitle = {Cell},
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+ shortjournal = {Cell},
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+ volume = {182},
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+ number = {2},
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+ eprint = {32619424},
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+ eprinttype = {pmid},
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+ pages = {297-316.e27},
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+ issn = {1097-4172},
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+ doi = {10.1016/j.cell.2020.05.049},
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+ abstract = {The most aggressive B cell lymphomas frequently manifest extranodal distribution and carry somatic mutations in the poorly characterized gene TBL1XR1. Here, we show that TBL1XR1 mutations skew the humoral immune response toward generating abnormal immature memory B cells (MB), while impairing plasma cell differentiation. At the molecular level, TBL1XR1 mutants co-opt SMRT/HDAC3 repressor complexes toward binding the MB cell transcription factor (TF) BACH2 at the expense of the germinal center (GC) TF BCL6, leading to pre-memory transcriptional reprogramming and cell-fate bias. Upon antigen recall, TBL1XR1 mutant MB cells fail to differentiate into plasma cells and instead preferentially reenter new GC reactions, providing evidence for a cyclic reentry lymphomagenesis mechanism. Ultimately, TBL1XR1 alterations lead to a striking extranodal immunoblastic lymphoma phenotype that mimics the human disease. Both human and murine lymphomas feature expanded MB-like cell populations, consistent with a MB-cell origin and delineating an unforeseen pathway for malignant transformation of the immune system.},
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+ langid = {english},
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+ pmcid = {PMC7384961},
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+ keywords = {ABC-DLBCL,Animals,BACH2,Basic-Leucine Zipper Transcription Factors,BCL6,cell fate,cell of origin,Chromatin,extranodal lymphoma,germinal center,Germinal Center,Histone Deacetylases,Humans,Immunologic Memory,Lymphoma Large B-Cell Diffuse,memory B cells,Mice,Mice Inbred C57BL,Mice Knockout,Mutagenesis Site-Directed,Nuclear Proteins,Nuclear Receptor Co-Repressor 2,Precursor Cells B-Lymphoid,Protein Binding,Proto-Oncogene Proteins c-bcl-6,Receptors Cytoplasmic and Nuclear,Repressor Proteins,RNA Interference,RNA Small Interfering,TBL1XR1,Transcription Genetic},
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+ file = {/Users/rmorin/Zotero/storage/PTBY7V7T/Venturutti et al. - 2020 - TBL1XR1 Mutations Drive Extranodal Lymphoma by Ind.pdf}
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+}
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+
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@article{huNovelMissenseM206K2013b,
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title = {A Novel Missense ({{M206K}}) {{STAT3}} Mutation in Diffuse Large {{B}} Cell Lymphoma Deregulates {{STAT3}} Signaling},
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author = {Hu, Guangzhen and Witzig, Thomas E. and Gupta, Mamta},