11b256947b38010ed5ac08c09ba5641c6bb5081d
DLBCL_genes.md
| ... | ... | @@ -50,7 +50,7 @@ link-citations: true |
| 50 | 50 | |[EZH2](EZH2)|Tier 1 GE[@morinSomaticMutationsAltering2010a], FE[@yapSomaticMutationsEZH22011b]|[Morin et al](papers/morinSomaticMutationsAltering2010a)|[@loveGeneticLandscapeMutations2012; @mottokIntegrativeGenomicAnalysis2019b]|| |
| 51 | 51 | |[FAS](FAS)|Tier 1 GE[@schollMutationsRegionFAS2007], FE[@seebergerLossFasCD952001]|[Scholl et al](papers/schollMutationsRegionFAS2007)|[@spinaGeneticsNodalMarginal2016b]|| |
| 52 | 52 | |[FBXO11](FBXO11)|Tier 1 GE[@hubschmannMutationalMechanismsShaping2021b], FE[@schneiderFBXO11InactivationLeads2016b]|[Hubschmann et al](papers/hubschmannMutationalMechanismsShaping2021b)|[@parryWholeExomeSequencing2013; @richterRecurrentMutationID32012a]|| |
| 53 | -|[FBXW7](FBXW7)|Tier 1 GE[@zhangGeneticHeterogeneityDiffuse2013]|[Zhang et al](papers/zhangGeneticHeterogeneityDiffuse2013)||| |
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| 53 | +|[FBXW7](FBXW7)|Tier 1 GE[@zhangGeneticHeterogeneityDiffuse2013], FE[@saffieFBXW7TriggersDegradation2020b]|[Zhang et al](papers/zhangGeneticHeterogeneityDiffuse2013)||| |
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| 54 | 54 | |[FOXO1](FOXO1)|Tier 1 GE[@morinFrequentMutationHistonemodifying2011], FE[@trinhAnalysisFOXO1Mutations], CE[@trinhAnalysisFOXO1Mutations]|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)|[@dunsCharacterizationDLBCLPMBL2021b; @schmitzBurkittLymphomaPathogenesis2012]|| |
| 55 | 55 | |[GNA13](GNA13)|Tier 1 GE[@morinFrequentMutationHistonemodifying2011], FE[@muppidiLossSignalingGa132014b]|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)|[@loveGeneticLandscapeMutations2012; @reichelFlowSortingExome2015a]|| |
| 56 | 56 | |[GNAI2](GNAI2)|Tier 1 GE[@morinMutationalStructuralAnalysis2013]|[Morin et al](papers/morinMutationalStructuralAnalysis2013)|[@grandeGenomewideDiscoverySomatic2019]|| |
morinlab.bib
| ... | ... | @@ -1,3 +1,23 @@ |
| 1 | +@article{saffieFBXW7TriggersDegradation2020b, |
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| 2 | + title = {{{FBXW7 Triggers Degradation}} of {{KMT2D}} to {{Favor Growth}} of {{Diffuse Large B-cell Lymphoma Cells}}}, |
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| 3 | + author = {Saffie, Rizwan and Zhou, Nan and Rolland, Delphine and Önder, Özlem and Basrur, Venkatesha and Campbell, Sydney and Wellen, Kathryn E. and Elenitoba-Johnson, Kojo S. J. and Capell, Brian C. and Busino, Luca}, |
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| 4 | + date = {2020-06-15}, |
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| 5 | + journaltitle = {Cancer Research}, |
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| 6 | + shortjournal = {Cancer Res}, |
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| 7 | + volume = {80}, |
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| 8 | + number = {12}, |
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| 9 | + eprint = {32350066}, |
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| 10 | + eprinttype = {pmid}, |
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| 11 | + pages = {2498--2511}, |
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| 12 | + issn = {1538-7445}, |
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| 13 | + doi = {10.1158/0008-5472.CAN-19-2247}, |
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| 14 | + abstract = {Mature B-cell neoplasms are the fifth most common neoplasm. Due to significant heterogeneity at the clinical and genetic levels, current therapies for these cancers fail to provide long-term cures. The clinical success of proteasome inhibition for the treatment of multiple myeloma and B-cell lymphomas has made the ubiquitin pathway an important emerging therapeutic target. In this study, we assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. FBXW7 targeted the frequently inactivated tumor suppressor KMT2D for protein degradation, subsequently regulating gene expression signatures related to oxidative phosphorylation (OxPhos). Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxPhos inhibition. These data elucidate a novel mechanism of regulation of KMT2D levels by the ubiquitin pathway and uncover a role of FBXW7 in regulating oxidative phosphorylation in B-cell malignancies. SIGNIFICANCE: These findings characterize FBXW7 as a prosurvival factor in B-cell lymphoma via degradation of the chromatin modifier KMT2D.}, |
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| 15 | + langid = {english}, |
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| 16 | + pmcid = {PMC7417195}, |
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| 17 | + keywords = {Animals,Cell Line Tumor,Cell Proliferation,Chromatin,DNA-Binding Proteins,F-Box-WD Repeat-Containing Protein 7,Female,Gene Expression Regulation Neoplastic,Gene Knockout Techniques,HEK293 Cells,Humans,Lymphoma Large B-Cell Diffuse,Mice,Neoplasm Proteins,Oxidative Phosphorylation,Proteolysis,RNA Small Interfering,Signal Transduction,Ubiquitin,Xenograft Model Antitumor Assays}, |
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| 18 | + file = {/Users/rmorin/Zotero/storage/5KJ466DP/Saffie et al. - 2020 - FBXW7 Triggers Degradation of KMT2D to Favor Growt.pdf} |
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| 19 | +} |
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| 20 | + |
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| 1 | 21 | @article{schneiderFBXO11InactivationLeads2016b, |
| 2 | 22 | title = {{{FBXO11}} Inactivation Leads to Abnormal Germinal-Center Formation and Lymphoproliferative Disease}, |
| 3 | 23 | 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}, |