fix refs

-||2|relevance in MZL not firmly established[@spinaGeneticsNodalMarginal2016b]|

-||2|relevance in PMBL/cHL/GZL not firmly established[@sarkozyMutationalLandscapeGray2021a]|

-| |2 |relevance in FL not firmly established[@russler-germainMutationsAssociatedProgression2023b]|

-ACTB is one of [a number of genes](https://github.com/morinlab/LLMPP/wiki/ashm) affected by aberrant somatic hypermutation in B-cell lymphomas. The function of mutations in ACTB and ACTG1 have not yet been determined.[@witjesPrevalenceCytoplasmicActin2020b]

-||1|high-confidence PMBL/cHL/GZL gene[@wienandGenomicAnalysesFlowsorted2019b]|

-| |1 |high-confidence DLBCL gene, hypermutated[@lohrDiscoveryPrioritizationSomatic2012a]|

-ACTG1 is one of [a number of genes](https://github.com/morinlab/LLMPP/wiki/ashm) affected by aberrant somatic hypermutation in B-cell lymphomas. The function of mutations in ACTB and ACTG1 have not yet been determined.[@witjesPrevalenceCytoplasmicActin2020b]

-||2|relevance in MZL not firmly established[@spinaGeneticsNodalMarginal2016b]|

-||2|relevance in FL not firmly established[@hubschmannMutationalMechanismsShaping2021b]|

-| |1 | aSHM target and high-confidence DLBCL gene[@hubschmannMutationalMechanismsShaping2021b] |

-| |2 |relevance in DLBCL not firmly established[@hubschmannMutationalMechanismsShaping2021b]|

-| |2 |relevance in BL not firmly established[@burkhardtClinicalRelevanceMolecular2022b]|

-||2|relevance in MZL not firmly established[@spinaGeneticsNodalMarginal2016b]|

-| |2 |relevance in BL not firmly established[@burkhardtClinicalRelevanceMolecular2022b]|

-| |2 |relevance in BL not firmly established[@burkhardtClinicalRelevanceMolecular2022b]|

-||2|relevance in PMBL/cHL/GZL not firmly established[@tiacciPervasiveMutationsJAKSTAT2018b]|

-||2|relevance in MZL not firmly established[@spinaGeneticsNodalMarginal2016b]|

-| |2 |relevance in DLBCL not firmly established[@hubschmannMutationalMechanismsShaping2021b]|

-||2|relevance in MZL not firmly established[@spinaGeneticsNodalMarginal2016b]|

-| |2 |relevance in BL not firmly established[@muppidiLossSignalingGa132014b]|

-Overall, components of SWI/SNF have been identified as an emerging theme in germinal centre-derived B-cell lymphomas but their role has not been thoroughly elucidated.[@lunningMutationChromatinModifiers2015b]

-||2|relevance in PMBL/cHL/GZL not firmly established[@reichelFlowSortingExome2015a]|

-| |1 |high-confidence FL gene[@okosunRecurrentMTORC1activatingRRAGC2016a]|

-| |2 |relevance in FL not firmly established[@hubschmannMutationalMechanismsShaping2021b]|

-| |1 |high-confidence FL gene[@okosunRecurrentMTORC1activatingRRAGC2016a]|

-B2M mutations in B-cell lymphomas, particularly in DLBCL and PMBCL, lead to reduced MHC class I expression, enabling tumor cells to evade immune detection and destruction by cytotoxic T cells. This is often accompanied by mutations in the β2-Microglobulin gene, which further aids in immune evasion.[@challa-malladiCombinedGeneticInactivationa]

-||1-EE |high-confidence PMBL/cHL/GZL gene[@reichelFlowSortingExome2015a]|

-||2|relevance in PMBL/cHL/GZL not firmly established[@sarkozyMutationalLandscapeGray2021a]|

-| |2 |relevance in BL not firmly established[@burkhardtClinicalRelevanceMolecular2022b]|

-BCL7A protein interacts with components of the SWI/SNF chromatin remodeling complex, implicating it in chromatin remodeling processes essential for normal cellular function.[@reichelFlowSortingExome2015a] Mutations in the BCL7A gene have been identified in diffuse large B-cell lymphoma (DLBCL) and other B-cell lymphomas, implicating this gene in the pathogenesis of these cancers. Importantly, BCL7A is one of [a number of genes](https://github.com/morinlab/LLMPP/wiki/ashm) affected by aberrant somatic hypermutation in B-cell lymphomas, which complicates the interpretation of mutations at this locus. Due to the presence of some loss-of-function mutations, BCL7A has been described as a tumour-suppressor gene in DLBCL.[@balinas-gaviraFrequentMutationsAminoterminal2020b]

-||2|relevance in PMBL/cHL/GZL not firmly established[@reichelFlowSortingExome2015a]|

-| |1-EE[@balinas-gaviraFrequentMutationsAminoterminal2020b] | high-confidence DLBCL gene[@morinFrequentMutationHistonemodifying2011; @zhangGeneticHeterogeneityDiffuse2013; @arthurGenomewideDiscoverySomatic2018] |

-| |1 | high-confidence FL gene [@krysiakRecurrentSomaticMutations2017b] |

-@article{abateDistinctViralMutational2015a,

- title = {Distinct {{Viral}} and {{Mutational Spectrum}} of {{Endemic Burkitt Lymphoma}}},

- author = {Abate, F. and Ambrosio, M. and Mundo, L. and Laginestra, M. and Fuligni, F. and Rossi, M. and Zairis, Sakellarios and Gazaneo, Sara and Falco, G. De and Lazzi, S. and Bellan, C. and Rocca, B. J. and Amato, T. and Marasco, E. and Etebari, Maryam and Ogwang, M. and Calbi, V. and Ndede, I. and Patel, K. and Chumba, D. and Piccaluga, P. and Pileri, S. and Leoncini, L. and Rabadán, R.},

- date = {2015},

- journaltitle = {PLoS Pathogens},

- shortjournal = {PLoS Pathogens},

- volume = {11},

- doi = {10.1371/journal.ppat.1005158},

- file = {/Users/rmorin/Zotero/storage/8CUFAQ4L/Abate et al. - 2015 - Distinct Viral and Mutational Spectrum of Endemic .pdf}

-}

-

-@article{albuquerqueEnhancingKnowledgeDiscovery2017a,

- title = {Enhancing Knowledge Discovery from Cancer Genomics Data with {{Galaxy}}},

- author = {Albuquerque, Marco A. and Grande, Bruno M. and Ritch, Elie J. and Pararajalingam, Prasath and Jessa, Selin and Krzywinski, Martin and Grewal, Jasleen K. and Shah, Sohrab P. and Boutros, Paul C. and Morin, Ryan D.},

- date = {2017-05-01},

- journaltitle = {GigaScience},

- shortjournal = {Gigascience},

- volume = {6},

- number = {5},

- eprint = {28327945},

- eprinttype = {pmid},

- pages = {1--13},

- issn = {2047-217X},

- doi = {10.1093/gigascience/gix015},

- abstract = {The field of cancer genomics has demonstrated the power of massively parallel sequencing techniques to inform on the genes and specific alterations that drive tumor onset and progression. Although large comprehensive sequence data sets continue to be made increasingly available, data analysis remains an ongoing challenge, particularly for laboratories lacking dedicated resources and bioinformatics expertise. To address this, we have produced a collection of Galaxy tools that represent many popular algorithms for detecting somatic genetic alterations from cancer genome and exome data. We developed new methods for parallelization of these tools within Galaxy to accelerate runtime and have demonstrated their usability and summarized their runtimes on multiple cloud service providers. Some tools represent extensions or refinement of existing toolkits to yield visualizations suited to cohort-wide cancer genomic analysis. For example, we present Oncocircos and Oncoprintplus, which generate data-rich summaries of exome-derived somatic mutation. Workflows that integrate these to achieve data integration and visualizations are demonstrated on a cohort of 96 diffuse large B-cell lymphomas and enabled the discovery of multiple candidate lymphoma-related genes. Our toolkit is available from our GitHub repository as Galaxy tool and dependency definitions and has been deployed using virtualization on multiple platforms including Docker.},

- langid = {english},

- pmcid = {PMC5437943},

- keywords = {Algorithms,Cancer,Cloud,Driver,Genome,Genomics,Humans,Internet,Lymphoma,Lymphoma Large B-Cell Diffuse,Mutation,Pipeline,Software,Tool,Workflow},

- file = {/Users/rmorin/Zotero/storage/SCLMAU55/Albuquerque et al. - 2017 - Enhancing knowledge discovery from cancer genomics.pdf}

-}

-