fix refs

+|[SMARCA4](SMARCA4)|1-EE|[Richter et al](papers/richterRecurrentMutationID32012a)[@richterRecurrentMutationID32012a]|[@lohrDiscoveryPrioritizationSomatic2012a; @krysiakRecurrentSomaticMutations2017b; @nadeuGenomicEpigenomicInsights2020b]|

+| |1-EE[@dengSMARCA4HaploinsufficientCell2024] |high-confidence BL gene [@richterRecurrentMutationID32012a]|

+| |1-EE[@dengSMARCA4HaploinsufficientCell2024] |high-confidence DLBCL gene[@lohrDiscoveryPrioritizationSomatic2012a]|

+@article{dengSMARCA4HaploinsufficientCell2024,

+ title = {{{SMARCA4}} Is a Haploinsufficient {{B}} Cell Lymphoma Tumor Suppressor That Fine-Tunes Centrocyte Cell Fate Decisions},

+ author = {Deng, Qing and Lakra, Priya and Gou, Panhong and Yang, Haopeng and Meydan, Cem and Teater, Matthew and Chin, Christopher and Zhang, Wenchao and Dinh, Tommy and Hussein, Usama and Li, Xubin and Rojas, Estela and Liu, Weiguang and Reville, Patrick K. and Kizhakeyil, Atish and Barisic, Darko and Parsons, Sydney and Wilson, Ashley and Henderson, Jared and Scull, Brooks and Gurumurthy, Channabasavaiah and Vega, Francisco and Chadburn, Amy and Cuglievan, Branko and El-Mallawany, Nader Kim and Allen, Carl and Mason, Christopher and Melnick, Ari and Green, Michael R.},

+ date = {2024-04-08},

+ journaltitle = {Cancer Cell},

+ shortjournal = {Cancer Cell},

+ volume = {42},

+ number = {4},

+ eprint = {38458188},

+ eprinttype = {pmid},

+ pages = {605-622.e11},

+ issn = {1878-3686},

+ doi = {10.1016/j.ccell.2024.02.011},

+ abstract = {SMARCA4 encodes one of two mutually exclusive ATPase subunits in the BRG/BRM associated factor (BAF) complex that is recruited by transcription factors (TFs) to drive chromatin accessibility and transcriptional activation. SMARCA4 is among the most recurrently mutated genes in human cancer, including ∼30\% of germinal center (GC)-derived Burkitt lymphomas. In mice, GC-specific Smarca4 haploinsufficiency cooperated with MYC over-expression to drive lymphomagenesis. Furthermore, monoallelic Smarca4 deletion drove GC hyperplasia with centroblast polarization via significantly increased rates of centrocyte recycling to the dark zone. Mechanistically, Smarca4 loss reduced the activity of TFs that are activated in centrocytes to drive GC-exit, including SPI1 (PU.1), IRF family, and NF-κB. Loss of activity for these factors phenocopied aberrant BCL6 activity within murine centrocytes and human Burkitt lymphoma cells. SMARCA4 therefore facilitates chromatin accessibility for TFs that shape centrocyte trajectories, and loss of fine-control of these programs biases toward centroblast cell-fate, GC hyperplasia and lymphoma.},

+ langid = {english},

+ pmcid = {PMC11003852},

+ keywords = {Animals,B-cell,BAF,Chromatin,DNA Helicases,epigenetics,germinal center,Haploinsufficiency,Humans,Hyperplasia,immunology,lymphoma,Lymphoma B-Cell,Mice,Nuclear Proteins,SMARCA4,SWI/SNF,transcription,Transcription Factors},

+ file = {/Users/rmorin/Zotero/storage/FGVKXYYU/Deng et al. - 2024 - SMARCA4 is a haploinsufficient B cell lymphoma tum.pdf}

+}

+

+@article{challa-malladiCombinedGeneticInactivationa,

+ title = {Combined {{Genetic Inactivation}} of \β2-{{Microglobulin}} and {{CD58 Reveals Frequent Escape}} from {{Immune Recognition}} in {{Diffuse Large B Cell Lymphoma}}},

+ author = {Challa-Malladi, Madhavi and Lieu, Yen K and Califano, Olivia and Holmes, Antony B and Bhagat, Govind and Murty, Vundavalli V and Dominguez-Sola, David and Pasqualucci, Laura and Dalla-Favera, Riccardo},

+ journaltitle = {Cancer Cell},

+ pages = {1--13},

+ keywords = {nosource}

+}

+