BL_genes.md
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@@ -11,17 +11,16 @@ link-citations: true
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## Tier 1 BL genes
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-### *29 total*
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+### *28 total*
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|Gene|Summary| First BL study | Other entities | QC result |
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|:-:|:-:|:-:|:-|:-|
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-|[ARID1A](ARID1A)|Tier 1 GE[@loveGeneticLandscapeMutations2012]|[Love et al](papers/loveGeneticLandscapeMutations2012)|[@krysiakRecurrentSomaticMutations2017b; @rossiCodingGenomeSplenic2012c; @wienandGenomicAnalysesFlowsorted2019b; @zhangGeneticHeterogeneityDiffuse2013]||
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+|[ARID1A](ARID1A)|Tier 1 GE[@loveGeneticLandscapeMutations2012], FE[@barisicARID1AOrchestratesSWI2024]|[Love et al](papers/loveGeneticLandscapeMutations2012)|[@krysiakRecurrentSomaticMutations2017b; @rossiCodingGenomeSplenic2012c; @wienandGenomicAnalysesFlowsorted2019b; @zhangGeneticHeterogeneityDiffuse2013]||
19 19
|[BCL7A](BCL7A)|Tier 1 GE[@grandeGenomewideDiscoverySomatic2019], FE[@balinas-gaviraFrequentMutationsAminoterminal2020b]|[Grande et al](papers/grandeGenomewideDiscoverySomatic2019)|[@krysiakRecurrentSomaticMutations2017b; @morinFrequentMutationHistonemodifying2011; @reichelFlowSortingExome2015a]||
20 20
|[BMP7](BMP7)|Tier 1 GE[@paneaWholeGenomeLandscape2019]|[Panea et al](papers/paneaWholeGenomeLandscape2019)|||
21 21
|[CCND3](CCND3)|Tier 1 GE[@richterRecurrentMutationID32012a], FE[@schmitzBurkittLymphomaPathogenesis2012]|[Richter et al](papers/richterRecurrentMutationID32012a)|[@deschGenotypingCirculatingTumor2020; @jalladesExomeSequencingIdentifies2017; @morinFrequentMutationHistonemodifying2011]||
22 22
|[CHD8](CHD8)|Tier 1 GE[@grandeGenomewideDiscoverySomatic2019]|[Grande et al](papers/grandeGenomewideDiscoverySomatic2019)|||
23 23
|[DDX3X](DDX3X)|Tier 1 GE[@schmitzBurkittLymphomaPathogenesis2012], FE[@gongSequentialInverseDysregulation2021], CE[@kizhakeyilDDX3XLossAdverse2021]|[Schmitz et al](papers/schmitzBurkittLymphomaPathogenesis2012)|[@mottokIntegrativeGenomicAnalysis2019b; @reddyGeneticFunctionalDrivers2017]||
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-|[EIF4A1](EIF4A1)|Tier 1 GE[@paneaWholeGenomeLandscape2019]|[Panea et al](papers/paneaWholeGenomeLandscape2019)|||
25 24
|[EPPK1](EPPK1)|Tier 1 GE[@paneaWholeGenomeLandscape2019]|[Panea et al](papers/paneaWholeGenomeLandscape2019)|||
26 25
|[FBXO11](FBXO11)|Tier 1 GE[@richterRecurrentMutationID32012a], FE[@schneiderFBXO11InactivationLeads2016b]|[Richter et al](papers/richterRecurrentMutationID32012a)|[@hubschmannMutationalMechanismsShaping2021b; @parryWholeExomeSequencing2013]||
27 26
|[FOXO1](FOXO1)|Tier 1 GE[@schmitzBurkittLymphomaPathogenesis2012], FE[@trinhAnalysisFOXO1Mutations], CE[@trinhAnalysisFOXO1Mutations]|[Schmitz et al](papers/schmitzBurkittLymphomaPathogenesis2012)|[@dunsCharacterizationDLBCLPMBL2021b; @morinFrequentMutationHistonemodifying2011]||
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@@ -47,7 +46,7 @@ link-citations: true
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## Tier 2 BL genes
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-### *75 total*
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+### *76 total*
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|Gene|Summary| First BL study | Other entities | QC result |
53 52
|:-:|:-:|:-:|:-|:-|
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|[EBF1](EBF1)|Tier 2 GE[@thomasGeneticSubgroupsInform2023]|[Thomas et al](papers/thomasGeneticSubgroupsInform2023)|[@bohleRoleEarlyBcell2013; @reichelFlowSortingExome2015a]||
77 76
|[EDNRB](EDNRB)|Tier 2 GE[@burkhardtClinicalRelevanceMolecular2022b]|[Burkhardt et al](papers/burkhardtClinicalRelevanceMolecular2022b)|||
78 77
|[EHD1](EHD1)|Tier 2 GE[@thomasGeneticSubgroupsInform2023]|[Thomas et al](papers/thomasGeneticSubgroupsInform2023)|||
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+|[EIF4A1](EIF4A1)|Tier 2 GE[@paneaWholeGenomeLandscape2019]|[Panea et al](papers/paneaWholeGenomeLandscape2019)|||
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|[ELP2](ELP2)|Tier 2 GE[@schmitzBurkittLymphomaPathogenesis2012]|[Schmitz et al](papers/schmitzBurkittLymphomaPathogenesis2012)|||
80 80
|[ERAP1](ERAP1)|Tier 2 GE[@burkhardtClinicalRelevanceMolecular2022b]|[Burkhardt et al](papers/burkhardtClinicalRelevanceMolecular2022b)|||
81 81
|[EXOSC6](EXOSC6)|Tier 2 GE[@schmitzBurkittLymphomaPathogenesis2012]|[Schmitz et al](papers/schmitzBurkittLymphomaPathogenesis2012)|||
morinlab.bib
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1
+@article{barisicARID1AOrchestratesSWI2024,
2
+ title = {{{ARID1A}} Orchestrates {{SWI}}/{{SNF-mediated}} Sequential Binding of Transcription Factors with {{ARID1A}} Loss Driving Pre-Memory {{B}} Cell Fate and Lymphomagenesis},
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+ author = {Barisic, Darko and Chin, Christopher R. and Meydan, Cem and Teater, Matt and Tsialta, Ioanna and Mlynarczyk, Coraline and Chadburn, Amy and Wang, Xuehai and Sarkozy, Margot and Xia, Min and Carson, Sandra E. and Raggiri, Santo and Debek, Sonia and Pelzer, Benedikt and Durmaz, Ceyda and Deng, Qing and Lakra, Priya and Rivas, Martin and Steidl, Christian and Scott, David W. and Weng, Andrew P. and Mason, Christopher E. and Green, Michael R. and Melnick, Ari},
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+ date = {2024-04-08},
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+ journaltitle = {Cancer Cell},
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+ shortjournal = {Cancer Cell},
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+ volume = {42},
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+ number = {4},
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+ eprint = {38458187},
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+ eprinttype = {pmid},
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+ pages = {583-604.e11},
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+ issn = {1878-3686},
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+ doi = {10.1016/j.ccell.2024.02.010},
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+ abstract = {ARID1A, a subunit of the canonical BAF nucleosome remodeling complex, is commonly mutated in lymphomas. We show that ARID1A orchestrates B cell fate during the germinal center (GC) response, facilitating cooperative and sequential binding of PU.1 and NF-kB at crucial genes for cytokine and CD40 signaling. The absence of ARID1A tilts GC cell fate toward immature IgM+CD80-PD-L2- memory B cells, known for their potential to re-enter new GCs. When combined with BCL2 oncogene, ARID1A haploinsufficiency hastens the progression of aggressive follicular lymphomas (FLs) in mice. Patients with FL with ARID1A-inactivating mutations preferentially display an immature memory B cell-like state with increased transformation risk to aggressive disease. These observations offer mechanistic understanding into the emergence of both indolent and aggressive ARID1A-mutant lymphomas through the formation of immature memory-like clonal precursors. Lastly, we demonstrate that ARID1A mutation induces synthetic lethality to SMARCA2/4 inhibition, paving the way for potential precision therapy for high-risk patients.},
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+ langid = {english},
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+ keywords = {Animals,BAF complex,chromatin,chromatin remodeling,clonal precursor cells,DNA-Binding Proteins,epigenetics,Humans,humoral immunity,lymphoma,Lymphoma,Memory B Cells,Mice,Mutation,Nuclear Proteins,pioneer transcription factors,plasticity,precision therapy,Transcription Factors}
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+}
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+
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@article{dobashiTP53OSBPL10Alterations2018b,
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title = {{{TP53}} and {{OSBPL10}} Alterations in Diffuse Large {{B-cell}} Lymphoma: Prognostic Markers Identified via Exome Analysis of Cases with Extreme Prognosis},
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shorttitle = {{{TP53}} and {{OSBPL10}} Alterations in Diffuse Large {{B-cell}} Lymphoma},