fix refs

+BCL10 (B-cell lymphoma/leukemia 10) is a gene involved in apoptosis signaling and immune response regulation.

+Mutations in BCL10 have been implicated in the pathogenesis of various lymphomas, particularly mucosa-associated lymphoid tissue (MALT) lymphomas.

+They have also been reproducibly observed in a smaller proportion of DLBCLs with the frequency in non-MALT lymphomas under some debate.

+BCL10 mutations are a feature of the BN2 genetic subgroup, mutated in nearly 40% of BN2 cases.[@wrightProbabilisticClassificationTool2020; @phelanBCL10MutantsArchitects2022]

+

+## Experimental Evidence

+

+BCL10 missense mutations in the CARD domain and truncating mutations have distinct functions and different effects on BTK and MALT1 inhibitors. [@xiaBCL10MutationsDefine2022]

+| |1-EE[@xiaBCL10MutationsDefine2022] |high-confidence DLBCL gene[@morinFrequentMutationHistonemodifying2011] |

+|[BCL10](BCL10)|1-EE|[Morin et al](papers/morinFrequentMutationHistonemodifying2011)[@morinFrequentMutationHistonemodifying2011]|[@spinaGeneticsNodalMarginal2016b; @russler-germainMutationsAssociatedProgression2023b]|

+@article{phelanBCL10MutantsArchitects2022,

+ title = {{{BCL10 Mutants}}: {{Architects}} of {{Oncogenic Signaling Provide}} a {{Blueprint}} for {{Precision Medicine}}},

+ shorttitle = {{{BCL10 Mutants}}},

+ author = {Phelan, James D. and Oellerich, Thomas},

+ date = {2022-08-05},

+ journaltitle = {Cancer Discovery},

+ shortjournal = {Cancer Discov},

+ volume = {12},

+ number = {8},

+ eprint = {35929131},

+ eprinttype = {pmid},

+ pages = {1844--1846},

+ issn = {2159-8290},

+ doi = {10.1158/2159-8290.CD-22-0614},

+ abstract = {BCL10, a key activator of NF-κB downstream of oncogenic B-cell receptor signaling, is mutated in nearly 40\% of the BN2/C1 genetic subtype of diffuse large B-cell lymphoma, but how these mutations function to augment signaling and their relevance to targeted precision medicine agents remains unclear. In this issue of Cancer Discovery, Xia and colleagues demonstrate distinct mechanisms of oncogenic signaling regulation and therapeutic vulnerabilities among different recurrent BCL10 mutations. See related article by Xia et al., p. 1922 (1).},

+ langid = {english},

+ keywords = {B-Cell CLL-Lymphoma 10 Protein,Carcinogenesis,CARD Signaling Adaptor Proteins,Humans,Mutation,NF-kappa B,Precision Medicine,Signal Transduction},

+ file = {/Users/rmorin/Zotero/storage/US265RGF/Phelan and Oellerich - 2022 - BCL10 Mutants Architects of Oncogenic Signaling P.pdf}

+}

+

+@article{xiaBCL10MutationsDefine2022,

+ title = {{{BCL10 Mutations Define Distinct Dependencies Guiding Precision Therapy}} for {{DLBCL}}},

+ author = {Xia, Min and David, Liron and Teater, Matt and Gutierrez, Johana and Wang, Xiang and Meydan, Cem and Lytle, Andrew and Slack, Graham W. and Scott, David W. and Morin, Ryan D. and Onder, Ozlem and Elenitoba-Johnson, Kojo S. J. and Zamponi, Nahuel and Cerchietti, Leandro and Lu, Tianbao and Philippar, Ulrike and Fontan, Lorena and Wu, Hao and Melnick, Ari M.},

+ date = {2022-08-05},

+ journaltitle = {Cancer Discovery},

+ shortjournal = {Cancer Discov},

+ volume = {12},

+ number = {8},

+ eprint = {35658124},

+ eprinttype = {pmid},

+ pages = {1922--1941},

+ issn = {2159-8290},

+ doi = {10.1158/2159-8290.CD-21-1566},

+ abstract = {Activated B cell-like diffuse large B-cell lymphomas (ABC-DLBCL) have unfavorable outcomes and chronic activation of CARD11-BCL10-MALT1 (CBM) signal amplification complexes that form due to polymerization of BCL10 subunits, which is affected by recurrent somatic mutations in ABC-DLBCLs. Herein, we show that BCL10 mutants fall into at least two functionally distinct classes: missense mutations of the BCL10 CARD domain and truncation of its C-terminal tail. Truncating mutations abrogated a motif through which MALT1 inhibits BCL10 polymerization, trapping MALT1 in its activated filament-bound state. CARD missense mutations enhanced BCL10 filament formation, forming glutamine network structures that stabilize BCL10 filaments. Mutant forms of BCL10 were less dependent on upstream CARD11 activation and thus manifested resistance to BTK inhibitors, whereas BCL10 truncating but not CARD mutants were hypersensitive to MALT1 inhibitors. Therefore, BCL10 mutations are potential biomarkers for BTK inhibitor resistance in ABC-DLBCL, and further precision can be achieved by selecting therapy based on specific biochemical effects of distinct mutation classes. SIGNIFICANCE: ABC-DLBCLs feature frequent mutations of signaling mediators that converge on the CBM complex. We use structure-function approaches to reveal that BCL10 mutations fall into two distinct biochemical classes. Both classes confer resistance to BTK inhibitors, whereas BCL10 truncations confer hyperresponsiveness to MALT1 inhibitors, providing a road map for precision therapies in ABC-DLBCLs. See related commentary by Phelan and Oellerich, p. 1844. This article is highlighted in the In This Issue feature, p. 1825.},

+ langid = {english},

+ pmcid = {PMC9357155},

+ keywords = {B-Cell CLL-Lymphoma 10 Protein,CARD Signaling Adaptor Proteins,Guanylate Cyclase,Humans,Lymphoma Large B-Cell Diffuse,Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein,Mutation,Signal Transduction},

+ file = {/Users/rmorin/Zotero/storage/FMT36PXN/Xia et al. - 2022 - BCL10 Mutations Define Distinct Dependencies Guidi.pdf}

+}

+