DLBCL_genes.md
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|[ETS1](ETS1)|Tier 1 GE[@morinFrequentMutationHistonemodifying2011]|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)|[@paneaWholeGenomeLandscape2019]||
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|[ETV6](ETV6)|Tier 1 GE[@lohrDiscoveryPrioritizationSomatic2012a]|[Lohr et al](papers/lohrDiscoveryPrioritizationSomatic2012a)|||
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|[EZH2](EZH2)|Tier 1 GE[@morinSomaticMutationsAltering2010a], FE[@yapSomaticMutationsEZH22011b]|[Morin et al](papers/morinSomaticMutationsAltering2010a)|[@loveGeneticLandscapeMutations2012; @mottokIntegrativeGenomicAnalysis2019b]||
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-|[FAS](FAS)|Tier 1 GE[@schollMutationsRegionFAS2007]|[Scholl et al](papers/schollMutationsRegionFAS2007)|[@spinaGeneticsNodalMarginal2016b]||
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-|[FBXO11](FBXO11)|Tier 1 GE[@hubschmannMutationalMechanismsShaping2021b]|[Hubschmann et al](papers/hubschmannMutationalMechanismsShaping2021b)|[@parryWholeExomeSequencing2013; @richterRecurrentMutationID32012a]||
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+|[FAS](FAS)|Tier 1 GE[@schollMutationsRegionFAS2007], FE[@seebergerLossFasCD952001]|[Scholl et al](papers/schollMutationsRegionFAS2007)|[@spinaGeneticsNodalMarginal2016b]||
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+|[FBXO11](FBXO11)|Tier 1 GE[@hubschmannMutationalMechanismsShaping2021b], FE[@schneiderFBXO11InactivationLeads2016b]|[Hubschmann et al](papers/hubschmannMutationalMechanismsShaping2021b)|[@parryWholeExomeSequencing2013; @richterRecurrentMutationID32012a]||
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|[FBXW7](FBXW7)|Tier 1 GE[@zhangGeneticHeterogeneityDiffuse2013]|[Zhang et al](papers/zhangGeneticHeterogeneityDiffuse2013)|||
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|[FOXO1](FOXO1)|Tier 1 GE[@morinFrequentMutationHistonemodifying2011], FE[@trinhAnalysisFOXO1Mutations], CE[@trinhAnalysisFOXO1Mutations]|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)|[@dunsCharacterizationDLBCLPMBL2021b; @schmitzBurkittLymphomaPathogenesis2012]||
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|[GNA13](GNA13)|Tier 1 GE[@morinFrequentMutationHistonemodifying2011], FE[@muppidiLossSignalingGa132014b]|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)|[@loveGeneticLandscapeMutations2012; @reichelFlowSortingExome2015a]||
morinlab.bib
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+@article{schneiderFBXO11InactivationLeads2016b,
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+ title = {{{FBXO11}} Inactivation Leads to Abnormal Germinal-Center Formation and Lymphoproliferative Disease},
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+ author = {Schneider, Christof and Kon, Ning and Amadori, Letizia and Shen, Qiong and Schwartz, Friederike H. and Tischler, Benjamin and Bossennec, Marion and Dominguez-Sola, David and Bhagat, Govind and Gu, Wei and Basso, Katia and Dalla-Favera, Riccardo},
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+ date = {2016-08-04},
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+ journaltitle = {Blood},
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+ shortjournal = {Blood},
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+ volume = {128},
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+ number = {5},
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+ eprint = {27166359},
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+ eprinttype = {pmid},
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+ pages = {660--666},
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+ issn = {1528-0020},
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+ doi = {10.1182/blood-2015-11-684357},
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+ abstract = {The BCL6 proto-oncogene encodes a transcriptional repressor that is required for the germinal center (GC) reaction and is implicated in lymphomagenesis. BCL6 protein stability is regulated by F-box protein 11 (FBXO11)-mediated ubiquitination and degradation, which is impaired in ∼6\% of diffuse large B-cell lymphomas that carry inactivating genetic alterations targeting the FBXO11 gene. In order to investigate the role of FBXO11 in vivo, we analyzed GC-specific FBXO11 knockout mice. FBXO11 reduction or loss led to an increased number of GC B cells, to an altered ratio of GC dark zone to light zone cells, and to higher levels of BCL6 protein in GC B cells. B-cell receptor-mediated degradation of BCL6 was reduced in the absence of FBXO11, suggesting that FBXO11 contributes to the physiologic downregulation of BCL6 at the end of the GC reaction. Finally, FBXO11 inactivation was associated with the development of lymphoproliferative disorders in mice.},
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+ langid = {english},
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+ pmcid = {PMC9709922},
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+ keywords = {Animals,B-Lymphocytes,Cell Line Tumor,Down-Regulation,F-Box Proteins,Gene Deletion,Gene Silencing,Gene Targeting,Germinal Center,Humans,Immunoglobulin M,Lymphocyte Count,Lymphoproliferative Disorders,Mice,Organ Specificity,Proto-Oncogene Mas,Proto-Oncogene Proteins c-bcl-6},
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+ file = {/Users/rmorin/Zotero/storage/9A8EFBYB/Schneider et al. - 2016 - FBXO11 inactivation leads to abnormal germinal-cen.pdf}
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+}
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+
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+
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+@article{seebergerLossFasCD952001,
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+ title = {Loss of {{Fas}} ({{CD95}}/{{APO-1}}) Regulatory Function Is an Important Step in Early {{MALT-type}} Lymphoma Development},
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+ author = {Seeberger, H. and Starostik, P. and Schwarz, S. and Knörr, C. and Kalla, J. and Ott, G. and Müller-Hermelink, H. K. and Greiner, A.},
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+ date = {2001-07},
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+ journaltitle = {Laboratory Investigation; a Journal of Technical Methods and Pathology},
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+ shortjournal = {Lab Invest},
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+ volume = {81},
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+ number = {7},
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+ eprint = {11454987},
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+ eprinttype = {pmid},
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+ pages = {977--986},
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+ issn = {0023-6837},
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+ doi = {10.1038/labinvest.3780310},
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+ abstract = {Fas (CD95, APO-1) mutations were found in autoimmune diseases and some lymphomas, suggesting impairment of Fas-mediated cell death signaling that may cause tumor development. Because mucosa-associated lymphoid tissue (MALT)-type lymphoma B cells recognize autoantigens and proliferate in response to antigen and T cell-mediated signals, it is suggestive that autoreactive B cell lymphoma precursor cells may have escaped the Fas-mediated checkpoint that normally operates in healthy individuals. Using different biochemical, molecular, and functional approaches, we analyzed the Fas signaling in malignant B cells from seven MALT-type lymphomas that were additionally characterized for the t(11;18)(q21;q21) and four gastric diffuse large B cell lymphomas (DLBL). All DLBLs and three of seven MALT-type lymphomas were resistant to Fas-mediated apoptosis in vitro. Moreover, four of five MALT-type lymphomas analyzed and one of three DLBLs analyzed showed mutations in Fas mRNA transcripts but no loss of heterozygosity in the Fas promotor region. Alternative mechanisms of resistance to apoptosis, such as decreased expression of Fas or production of soluble Fas were not operative. Therefore, it is suggestive that a subgroup of MALT-type lymphoma B cells, irrespective of t(11;18)(q21;q21), escape the censoring Fas pathway by mutating and inactivating Fas. This identifies a key regulatory step in early MALT-type lymphomagenesis.},
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+ langid = {english},
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+ keywords = {Adult,Aged,Apoptosis,B-Lymphocytes,Base Sequence,Caspase 3,Caspase 8,Caspase 9,Caspases,DNA Primers,fas Receptor,Female,Humans,Loss of Heterozygosity,Lymphoma B-Cell Marginal Zone,Male,Middle Aged,Mutation,Promoter Regions Genetic,RNA Messenger,Sequence Homology Nucleic Acid}
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+}
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+
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@article{kizhakeyilDDX3XLossAdverse2021,
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title = {{{DDX3X}} Loss Is an Adverse Prognostic Marker in Diffuse Large {{B-cell}} Lymphoma and Is Associated with Chemoresistance in Aggressive Non-{{Hodgkin}} Lymphoma Subtypes},
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author = {Kizhakeyil, Atish and Zaini, Nurmahirah Binte Mohammed and Poh, Zhi Sheng and Wong, Brandon Han Siang and Loh, Xinpeng and Ng, Aik Seng and Low, Zun Siong and Prasannan, Praseetha and Gong, Chun and Tan, Michelle Guet Khim and Nagarajan, Chandramouli and Huang, Dachuan and Lu, Pang Wan and Lim, Jing Quan and Barrans, Sharon and Ong, Choon Kiat and Lim, Soon Thye and Chng, Wee Joo and Follows, George and Hodson, Daniel J. and Du, Ming Qing and Goh, Yeow Tee and Tan, Suat Hoon and Grigoropoulos, Nicholas Francis and Verma, Navin Kumar},