more fixes

+@article{hodsonRegulationNormalBcell2016,

+ title = {Regulation of Normal {{B-cell}} Differentiation and Malignant {{B-cell}} Survival by {{OCT2}}},

+ 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.},

+ date = {2016-04-05},

+ journaltitle = {Proceedings of the National Academy of Sciences of the United States of America},

+ shortjournal = {Proc Natl Acad Sci U S A},

+ volume = {113},

+ number = {14},

+ eprint = {26993806},

+ eprinttype = {pmid},

+ pages = {E2039-2046},

+ issn = {1091-6490},

+ doi = {10.1073/pnas.1600557113},

+ 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.},

+ langid = {english},

+ pmcid = {PMC4833274},

+ keywords = {Animals,B-Lymphocytes,cancer biology,Cell Differentiation,Cell Line Tumor,Cell Survival,germinal center,lymphoma,Lymphoma Large B-Cell Diffuse,lymphopedia,Mice,Mice Knockout,Organic Cation Transport Proteins,Organic Cation Transporter 2},

+ file = {/Users/rmorin/Zotero/storage/IMDHB5EC/Hodson et al. - 2016 - Regulation of normal B-cell differentiation and ma.pdf;/Users/rmorin/Zotero/storage/YQRVND4V/Hodson et al. - 2016 - Regulation of normal B-cell differentiation and ma.pdf}

+}

+

+@article{gaoSGK1MutationsDLBCL2021,

+ title = {{{SGK1}} Mutations in {{DLBCL}} Generate Hyperstable Protein Neoisoforms That Promote {{AKT}} Independence},

+ author = {Gao, Jie and Sidiropoulou, Eirini and Walker, Ieuan and Krupka, Joanna A. and Mizielinski, Karol and Usheva, Zelvera and Samarajiwa, Shamith A. and Hodson, Daniel J.},

+ date = {2021-09-16},

+ journaltitle = {Blood},

+ shortjournal = {Blood},

+ volume = {138},

+ number = {11},

+ eprint = {33988691},

+ eprinttype = {pmid},

+ pages = {959--964},

+ issn = {1528-0020},

+ doi = {10.1182/blood.2020010432},

+ abstract = {Serum and glucocorticoid-regulated kinase 1 (SGK1) is one of the most frequently mutated genes in diffuse large B-cell lymphoma (DLBCL). However, little is known about its function or the consequence of its mutation. The frequent finding of truncating mutations has led to the widespread assumption that these represent loss-of-function variants and, accordingly, that SGK1 must act as a tumor suppressor. In this study, instead, the most common SGK1 mutations led to production of aberrantly spliced messenger RNA neoisoforms in which translation is initiated from downstream methionines. The resulting N-terminal truncated protein isoforms showed increased expression related to the exclusion of an N-terminal degradation domain. However, they retained a functional kinase domain, the overexpression of which rendered cells resistant to AKT inhibition, in part because of increased phosphorylation of GSK3B. These findings challenge the prevailing assumption that SGK1 is a tumor-suppressor gene in DLBCL and provide the impetus to explore further the pharmacological inhibition of SGK1 as a therapeutic strategy for DLBCL.},

+ langid = {english},

+ pmcid = {PMC8701626},

+ keywords = {Cells Cultured,Enzyme Stability,Humans,Immediate-Early Proteins,Lymphoma Large B-Cell Diffuse,lymphopedia,Phosphorylation,Protein Domains,Protein Isoforms,Protein Serine-Threonine Kinases,Proto-Oncogene Proteins c-akt},

+ file = {/Users/rmorin/Zotero/storage/J9ETHUL6/Gao et al. - 2021 - SGK1 mutations in DLBCL generate hyperstable prote.pdf;/Users/rmorin/Zotero/storage/TXGZRW9Y/Gao et al. - 2021 - SGK1 mutations in DLBCL generate hyperstable prote.pdf}

+}

+