fix refs

+| |1-EE[@mlynarczykBTG1MutationYields2023b; @delageBTG1InactivationDrives2023a] | aSHM target and high-confidence DLBCL gene [@morinFrequentMutationHistonemodifying2011]|

+| |1 | aSHM target and high-confidence FL gene |

+| |2 | aSHM target; Although recurrent, the relevance of mutations in BL is tenuous [@burkhardtClinicalRelevanceMolecular2022b]|

+|[BCL7A](BCL7A)|1-EE|[Arthur et al](papers/arthurGenomewideDiscoverySomatic2018)[@arthurGenomewideDiscoverySomatic2018]|[@krysiakRecurrentSomaticMutations2017b; @grandeGenomewideDiscoverySomatic2019; @reichelFlowSortingExome2015a]|

+|[BTG1](BTG1)|1-EE|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)[@morinFrequentMutationHistonemodifying2011]|[@sarkozyMutationalLandscapeGray2021a; @burkhardtClinicalRelevanceMolecular2022b]|

+@article{delageBTG1InactivationDrives2023a,

+ title = {{{BTG1}} Inactivation Drives Lymphomagenesis and Promotes Lymphoma Dissemination through Activation of {{BCAR1}}},

+ author = {Delage, Lorric and Lambert, Mireille and Bardel, Émilie and Kundlacz, Cindy and Chartoire, Dimitri and Conchon, Axel and Peugnet, Anne-Laure and Gorka, Lucas and Auberger, Patrick and Jacquel, Arnaud and Soussain, Carole and Destaing, Olivier and Delecluse, Henri-Jacques and Delecluse, Susanne and Merabet, Samir and Traverse-Glehen, Alexandra and Salles, Gilles and Bachy, Emmanuel and Billaud, Marc and Ghesquières, Hervé and Genestier, Laurent and Rouault, Jean-Pierre and Sujobert, Pierre},

+ date = {2023-03-09},

+ journaltitle = {Blood},

+ shortjournal = {Blood},

+ volume = {141},

+ number = {10},

+ eprint = {36375119},

+ eprinttype = {pmid},

+ pages = {1209--1220},

+ issn = {1528-0020},

+ doi = {10.1182/blood.2022016943},

+ abstract = {Understanding the functional role of mutated genes in cancer is required to translate the findings of cancer genomics into therapeutic improvement. BTG1 is recurrently mutated in the MCD/C5 subtype of diffuse large B-cell lymphoma (DLBCL), which is associated with extranodal dissemination. Here, we provide evidence that Btg1 knock out accelerates the development of a lethal lymphoproliferative disease driven by Bcl2 overexpression. Furthermore, we show that the scaffolding protein BCAR1 is a BTG1 partner. Moreover, after BTG1 deletion or expression of BTG1 mutations observed in patients with DLBCL, the overactivation of the BCAR1-RAC1 pathway confers increased migration ability in~vitro and in~vivo. These modifications are targetable with the SRC inhibitor dasatinib, which opens novel therapeutic opportunities in BTG1 mutated DLBCL.},

+ langid = {english},

+ keywords = {Crk-Associated Substrate Protein,Genes cdc,Humans,Lymphoma Large B-Cell Diffuse,Mutation,Neoplasm Proteins},

+ file = {/Users/rmorin/Zotero/storage/55PFVYIT/Delage et al. - 2023 - BTG1 inactivation drives lymphomagenesis and promo.pdf}

+}

+

+@article{mlynarczykBTG1MutationYields2023b,

+ title = {{{BTG1}} Mutation Yields Supercompetitive {{B}} Cells Primed for Malignant Transformation},

+ author = {Mlynarczyk, Coraline and Teater, Matt and Pae, Juhee and Chin, Christopher R. and Wang, Ling and Arulraj, Theinmozhi and Barisic, D. and Papin, A. and Hoehn, Kenneth B. and Kots, E. and Ersching, Jonatan and Bandyopadhyay, A. and Barin, Ersilia and Poh, Hui Xian and Evans, Chiara M. and Chadburn, A. and Chen, Zhengming and Shen, Hao and Isles, H. and Pelzer, Benedikt W. and Tsialta, Ioanna and Doane, A. and Geng, H. and Rehman, Muhammad Hassan and Melnick, Jonah and Morgan, Wyatt and Nguyen, D. and Elemento, O. and Kharas, Michael G. and Jaffrey, S. and Scott, D. and Khelashvili, G. and Meyer-Hermann, M. and Victora, G. and Melnick, A.},

+ date = {2023},

+ journaltitle = {Science},

+ shortjournal = {Science},

+ volume = {379},

+ doi = {10.1126/science.abj7412}

+}

+