f1a18d7c49a52abeddd712a8cd87359b791e2b3f
BL_genes.md
| ... | ... | @@ -39,7 +39,7 @@ link-citations: true |
| 39 | 39 | |[SMARCA4](SMARCA4)|Tier 1 GE[@richterRecurrentMutationID32012a], FE[@dengSMARCA4HaploinsufficientCell2024]|[Richter et al](papers/richterRecurrentMutationID32012a)|[@krysiakRecurrentSomaticMutations2017b; @nadeuGenomicEpigenomicInsights2020b; @reddyGeneticFunctionalDrivers2017]|| |
| 40 | 40 | |[TCF3](TCF3)|Tier 1 GE[@schmitzBurkittLymphomaPathogenesis2012], FE[@schmitzBurkittLymphomaPathogenesis2012]|[Schmitz et al](papers/schmitzBurkittLymphomaPathogenesis2012)||| |
| 41 | 41 | |[TCL1A](TCL1A)|Tier 1 GE[@grandeGenomewideDiscoverySomatic2019]|[Grande et al](papers/grandeGenomewideDiscoverySomatic2019)|[@reddyGeneticFunctionalDrivers2017]|| |
| 42 | -|[TFAP4](TFAP4)|Tier 1 GE[@grandeGenomewideDiscoverySomatic2019]|[Grande et al](papers/grandeGenomewideDiscoverySomatic2019)||| |
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| 42 | +|[TFAP4](TFAP4)|Tier 1 GE[@grandeGenomewideDiscoverySomatic2019], FE[@toncUnexpectedSuppressionTumorigenesis2021]|[Grande et al](papers/grandeGenomewideDiscoverySomatic2019)||| |
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| 43 | 43 | |[TP53](TP53)|Tier 1 GE[@wildaInactivationARFMDM2p53Pathway2004], FE[@rowhTp53DeletionLineage2011]|[Wilda et al](papers/wildaInactivationARFMDM2p53Pathway2004)|[@beaLandscapeSomaticMutations2013; @lohrDiscoveryPrioritizationSomatic2012a; @morinFrequentMutationHistonemodifying2011; @rossiCodingGenomeSplenic2012c; @tiacciPervasiveMutationsJAKSTAT2018b]|| |
| 44 | 44 | |[USP7](USP7)|Tier 1 GE[@grandeGenomewideDiscoverySomatic2019]|[Grande et al](papers/grandeGenomewideDiscoverySomatic2019)|[@arthurGenomewideDiscoverySomatic2018]|| |
| 45 | 45 | |[WNK1](WNK1)|Tier 1 GE[@thomasGeneticSubgroupsInform2023]|[Thomas et al](papers/thomasGeneticSubgroupsInform2023)|[@hubschmannMutationalMechanismsShaping2021b; @jalladesExomeSequencingIdentifies2017]|| |
morinlab.bib
| ... | ... | @@ -1,3 +1,23 @@ |
| 1 | +@article{toncUnexpectedSuppressionTumorigenesis2021, |
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| 2 | + title = {Unexpected Suppression of Tumorigenesis by C-{{MYC}} via {{TFAP4-dependent}} Restriction of Stemness in {{B}} Lymphocytes}, |
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| 3 | + author = {Tonc, Elena and Takeuchi, Yoshiko and Chou, Chun and Xia, Yu and Holmgren, Melanie and Fujii, Chika and Raju, Saravanan and Chang, Gue Su and Iwamoto, Masahiro and Egawa, Takeshi}, |
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| 4 | + date = {2021-12-16}, |
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| 5 | + journaltitle = {Blood}, |
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| 6 | + shortjournal = {Blood}, |
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| 7 | + volume = {138}, |
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| 8 | + number = {24}, |
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| 9 | + eprint = {34283887}, |
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| 10 | + eprinttype = {pmid}, |
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| 11 | + pages = {2526--2538}, |
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| 12 | + issn = {1528-0020}, |
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| 13 | + doi = {10.1182/blood.2021011711}, |
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| 14 | + abstract = {The proliferative burst of B lymphocytes is essential for antigen receptor repertoire diversification during the development and selective expansion of antigen-specific clones during immune responses. High proliferative activity inevitably promotes oncogenesis, the risk of which is further elevated in B lymphocytes by endogenous gene rearrangement and somatic mutations. However, B-cell-derived cancers are rare, perhaps owing to putative intrinsic tumor-suppressive mechanisms. We show that c-MYC facilitates B-cell proliferation as a protumorigenic driver and unexpectedly coengages counteracting tumor suppression through its downstream factor TFAP4. TFAP4 is mutated in human lymphoid malignancies, particularly in {$>$}10\% of Burkitt lymphomas, and reduced TFAP4 expression was associated with poor survival of patients with MYC-high B-cell acute lymphoblastic leukemia. In mice, insufficient TFAP4 expression accelerated c-MYC-driven transformation of B cells. Mechanistically, c-MYC suppresses the stemness of developing B cells by inducing TFAP4 and restricting self-renewal of proliferating B cells. Thus, the pursuant transcription factor cascade functions as a tumor suppressor module that safeguards against the transformation of developing B cells.}, |
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| 15 | + langid = {english}, |
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| 16 | + pmcid = {PMC8678995}, |
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| 17 | + keywords = {Animals,B-Lymphocytes,Carcinogenesis,Cell Transformation Neoplastic,DNA-Binding Proteins,Gene Expression Regulation Neoplastic,Genes Tumor Suppressor,Humans,Leukemia Lymphoid,Lymphoma B-Cell,Mice,Mice Inbred C57BL,Mutation,Proto-Oncogene Proteins c-myc,Transcription Factors,Tumor Cells Cultured}, |
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| 18 | + file = {/Users/rmorin/Zotero/storage/LFPCKSN7/Tonc et al. - 2021 - Unexpected suppression of tumorigenesis by c-MYC v.pdf} |
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| 19 | +} |
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| 20 | + |
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| 1 | 21 | @article{ohayreInactivatingMutationsGNA132016, |
| 2 | 22 | title = {Inactivating Mutations in {{GNA13}} and {{RHOA}} in {{Burkitt}}'s Lymphoma and Diffuse Large {{B-cell}} Lymphoma: A Tumor Suppressor Function for the {{Gα13}}/{{RhoA}} Axis in {{B}} Cells}, |
| 3 | 23 | shorttitle = {Inactivating Mutations in {{GNA13}} and {{RHOA}} in {{Burkitt}}'s Lymphoma and Diffuse Large {{B-cell}} Lymphoma}, |