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+@article{hodsonRegulationNormalBcell2016a,
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+ title = {Regulation of Normal {{B-cell}} Differentiation and Malignant {{B-cell}} Survival by {{OCT2}}},
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+ author = {Hodson, Daniel J. and Shaffer, Arthur L. and Xiao, Wenming and Wright, George W. and Schmitz, Roland and Phelan, James D. and Yang, Yandan and Webster, Daniel E. and Rui, Lixin and Kohlhammer, Holger and Nakagawa, Masao and Waldmann, Thomas A. and Staudt, Louis M.},
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+ date = {2016-04-05},
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+ journaltitle = {Proceedings of the National Academy of Sciences of the United States of America},
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+ shortjournal = {Proc Natl Acad Sci U S A},
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+ volume = {113},
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+ number = {14},
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+ eprint = {26993806},
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+ eprinttype = {pmid},
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+ pages = {E2039-2046},
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+ issn = {1091-6490},
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+ doi = {10.1073/pnas.1600557113},
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+ abstract = {The requirement for the B-cell transcription factor OCT2 (octamer-binding protein 2, encoded by Pou2f2) in germinal center B cells has proved controversial. Here, we report that germinal center B cells are formed normally after depletion of OCT2 in a conditional knockout mouse, but their proliferation is reduced and in vivo differentiation to antibody-secreting plasma cells is blocked. This finding led us to examine the role of OCT2 in germinal center-derived lymphomas. shRNA knockdown showed that almost all diffuse large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivator OCA-B. Genome-wide chromatin immunoprecipitation (ChIP) analysis and gene-expression profiling revealed the broad transcriptional program regulated by OCT2 that includes the expression of STAT3, IL-10, ELL2, XBP1, MYC, TERT, and ADA. Importantly, genetic alteration of OCT2 is not a requirement for cellular addiction in DLBCL. However, we detected amplifications of the POU2F2 locus in DLBCL tumor biopsies and a recurrent mutation of threonine 223 in the DNA-binding domain of OCT2. This neomorphic mutation subtly alters the DNA-binding preference of OCT2, leading to the transactivation of noncanonical target genes including HIF1a and FCRL3 Finally, by introducing mutations designed to disrupt the OCT2-OCA-B interface, we reveal a requirement for this protein-protein interface that ultimately might be exploited therapeutically. Our findings, combined with the predominantly B-cell-restricted expression of OCT2 and the absence of a systemic phenotype in our knockout mice, suggest that an OCT2-targeted therapeutic strategy would be efficacious in both major subtypes of DLBCL while avoiding systemic toxicity.},
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+ langid = {english},
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+ pmcid = {PMC4833274},
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+ keywords = {Animals,B-Lymphocytes,cancer biology,Cell Differentiation,Cell Line Tumor,Cell Survival,germinal center,lymphoma,Lymphoma Large B-Cell Diffuse,Mice,Mice Knockout,Organic Cation Transport Proteins,Organic Cation Transporter 2},
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+ file = {/Users/rmorin/Zotero/storage/IMDHB5EC/Hodson et al. - 2016 - Regulation of normal B-cell differentiation and ma.pdf}
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+}
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@article{melznerBiallelicMutationSOCS12005a,
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title = {Biallelic Mutation of {{SOCS-1}} Impairs {{JAK2}} Degradation and Sustains Phospho-{{JAK2}} Action in the {{MedB-1}} Mediastinal Lymphoma Line},
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author = {Melzner, Ingo and Bucur, Alexandra Juliana and Brüderlein, Silke and Dorsch, Karola and Hasel, Cornelia and Barth, Thomas F. E. and Leithäuser, Frank and Möller, Peter},