morinlab.bib
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+@article{pfeiferPTENLossDefines2013,
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+ title = {{{PTEN}} Loss Defines a {{PI3K}}/{{AKT}} Pathway-Dependent Germinal Center Subtype of Diffuse Large {{B-cell}} Lymphoma},
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+ author = {Pfeifer, Matthias and Grau, Michael and Lenze, Dido and Wenzel, Sören-Sebastian and Wolf, Annette and Wollert-Wulf, Brigitte and Dietze, Kerstin and Nogai, Hendrik and Storek, Benjamin and Madle, Hannelore and Dörken, Bernd and Janz, Martin and Dirnhofer, Stephan and Lenz, Peter and Hummel, Michael and Tzankov, Alexandar and Lenz, Georg},
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+ date = {2013-07-23},
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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 = {110},
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+ number = {30},
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+ eprint = {23840064},
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+ eprinttype = {pmid},
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+ pages = {12420--12425},
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+ issn = {1091-6490},
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+ doi = {10.1073/pnas.1305656110},
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+ abstract = {Diffuse large B-cell lymphoma (DLBCL) represents a heterogeneous diagnostic category with distinct molecular subtypes that can be defined by gene expression profiling. However, even within these defined subtypes, heterogeneity prevails. To further elucidate the pathogenesis of these entities, we determined the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) in 248 primary DLBCL patient samples. These analyses revealed that loss of PTEN was detectable in 55\% of germinal center B-cell-like (GCB) DLBCLs, whereas this abnormality was found in only 14\% of non-GCB DLBCL patient samples. In GCB DLBCL, the PTEN status was inversely correlated with activation of the oncogenic PI3K/protein kinase B (AKT) pathway in both DLBCL cell lines and primary patient samples. Reexpression of PTEN induced cytotoxicity in PTEN-deficient GCB DLBCL cell line models by inhibiting PI3K/AKT signaling, indicating an addiction to this pathway in this subset of GCB DLBCLs. PI3K/AKT inhibition induced down-regulation of the transcription factor MYC. Reexpression of MYC rescued GCB DLBCL cells from PTEN-induced toxicity, identifying a regulatory mechanism of MYC expression in DLBCL. Finally, pharmacologic PI3K inhibition resulted in toxicity selectively in PTEN-deficient GCB DLBCL lines. Collectively, our results indicate that PTEN loss defines a PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that pharmacologic inhibition of PI3K might represent a promising therapeutic approach in these lymphomas.},
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+ langid = {english},
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+ pmcid = {PMC3725065},
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+ keywords = {Cohort Studies,Humans,Lymphoma Large B-Cell Diffuse,lymphopedia,p38 Mitogen-Activated Protein Kinases,Phosphatidylinositol 3-Kinases,PTEN Phosphohydrolase,Signal Transduction},
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+ file = {/Users/rmorin/Zotero/storage/XALB6YM6/Pfeifer et al. - 2013 - PTEN loss defines a PI3KAKT pathway-dependent ger.pdf}
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+}
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+
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@article{hodsonRegulationNormalBcell2016,
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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.},