In text citation formatting (removing superscripts and citing with citation keys)

-Mutations were first described in DLBCL in 2013 by Morin et al.¹ Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-Mutations in this gene were first described in DLBCL in 2021 by Hübschmann et al.¹

-Mutations in this gene were first described in DLBCL in 2021 by Hübschmann et al.¹

-Mutations in this gene were first described in MZL by Braggio et al,^{[@braggioGenomicAnalysisMarginal2012]} then in MCL by Bea et al.^{[@beaLandscapeSomaticMutations2013]} ATM mutations were later described in DLBCL by Reddy et al.^{[@reddyGeneticFunctionalDrivers2017]}

-Mutations in this gene were first described in DLBCL in 2021 by Hübschmann et al.^{[@hubschmannMutationalMechanismsShaping2021]}

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.^{[@reddyGeneticFunctionalDrivers2017]} Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-BCOR acts as a co-repressor of BCL6, and mutations in BCOR could impair its binding affinity to BCL6 and other partners. Overall, protein-altering mutations in BCOR seem to be rare in DLBCL and MCL.^{[@jalladesExomeSequencingIdentifies2017],[@nadeuGenomicEpigenomicInsights2020]} One study reported a much higher prevalence of a hot spot mutation in BCOR but this result has not been reproduced.^{[@jalladesExomeSequencingIdentifies2017]}

-BIRC6, as a negative regulator of non-canonical NF-κB signaling, is implicated in lymphomagenesis. Mutations in the BIRC6 have been found in DLBCL and grey zone lymphoma (GZL).^{[@sarkozyMutationalLandscapeGray2021],[@reddyGeneticFunctionalDrivers2017]}

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.^{[@reddyGeneticFunctionalDrivers2017]} Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-*Q36H* Conditional knock-in mouse models expressing the BTG1 Q36H mutation in B cells have shown that these mutations lead to earlier onset of lymphoma, shorter survival, and dysplastic B cell infiltration into non-lymphoid organs. These findings reinforce the role of BTG1 mutations in enhancing lymphoma aggressiveness.³

-*L26P, G66D, and I115V* Have each been shown to be unable to rescue wild-type BTG1 activity in a xenotransplantation model, suggesting that they impair BTG1 function.²

-One study reported BTK mutations in approximately 7% of FL and 11% of transformed FL cases.^{[@krysiakRecurrentSomaticMutations2017]} Another showed these mutations were more common, and typically co-occur in tumours with BCL2 translocations. Despite the known role of certain BTK mutations in acquired resistance to BTK inhibitors, these mutations were found in BTK inhibitor-naïve patients.^{[@albuquerqueEnhancingKnowledgeDiscovery2017]} These mutations often occur in treatment-naive patients and lead to inactivation of the BTK protein through destabilization or by altering key residues involved in enzymatic activity.^{[@krysiakRecurrentSomaticMutations2017]} The mutation pattern in DLBCL and FL implies the preferential accumulation of *inactivating mutations*^{[@huFollicularLymphomaassociatedBTK2021; @schejbelInactivatingBTKMutations2022]}. No notable hot spots have been described in this gene in the context of the cancers listed below.

-Mutations in this gene were first described in DLBCL in 2021 by Hübschmann et al.¹

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.¹

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.¹ Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.¹ Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-CD36 is a transmembrane glycoprotein involved in fatty acid metabolism, glucose intolerance, and immune responses. It is expressed on various cell types, including platelets, monocytes, and some lymphocytes. One study showed higher rates of CD36 mutations in FL relative to DLBCLs.¹

-Mutations at Y196 enhance B-cell receptor (BCR) signaling by preventing the negative regulatory feedback provided by Lyn kinase, a feedback inhibitor of BCR signaling. This results in continuous activation of the NF-κB pathway, promoting tumor cell survival and proliferation.^{[@kimCD79BMYD88Mutations2014]}

-Mutations in this gene were first described in DLBCL in 2013 by Morin et al^{[@morinMutationalStructuralAnalysis2013]}, in BL in 2019 by Panea et al^{[@paneaWholeGenomeLandscape2019]} and in FL in 2023 by Russler-Germain et al.^{[@russler-germainMutationsAssociatedProgression2023]}

-Mutations in this gene were first described in FL in 2021 by Hübschmann et al.^{[@hubschmannMutationalMechanismsShaping2021]}

-Mutations in this gene were first described in BL in 2012 by Love et al¹ and subsequently in DLBCL by Reddy et al.² Subsequent exome and genome-wide studies of DLBCL and BL did not reproduce these observations.

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.¹ Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.¹ Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-CIITA encodes the major histocompatibility complex (MHC) class II transactivator. CIITA mutations are frequent in PMBCL. These mutations often include structural genomic rearrangements, missense, nonsense, and frameshift mutations. In PMBCL, these mutations are thought to contribute to loss of MHC expression.¹ Although loss of CIITA and MHC Class II Expression is commonly observed in DLBCL, the role of mutations and methylation affecting this locus remains unclear.² CIITA 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.

-Mutations in this gene were first described in DLBCL in 2021 by Hübschmann et al.¹

-Mutations in this gene were first described in DLBCL in 2013 by Morin et al.¹

-Mutations in this gene were first described in FL in 2021 by Hübschmann et al.¹

-### BL

-This gene has some recurrent sites of mutations (hot spots). The mutation pattern in DLBCL and FL implies the preferential accumulation of *inactivating mutations* however the pattern is notable. These mutations often result in truncations affecting the DAZAP1 C-terminus, which are predicted to alter protein sub-cellular localization and disrupt protein-protein interactions.¹

-Mutations in this gene were first described in DLBCL in 2017 by Reddy et al.¹ Subsequent exome and genome-wide studies of DLBCL did not reproduce this observation.

-Mutations in this gene were first described in FL in 2021 by Hübschmann et al.¹

-Mutations in this gene were first described in DLBCL in 2021 by Hübschmann et al.¹

-Mutations in this gene were first described in DLBCL and FL in 2021 by Hübschmann et al.¹

-EBF1 is a critical transcription factor in early B-cell development, regulating the expression of key genes involved in B-cell differentiation, survival, and function. EBF1 is essential for proper B-cell receptor (BCR) signaling.^{[@gyoryTranscriptionFactorEbf12012]} Mutations in EBF1 can impair BCR signaling pathways, affecting B-cell survival and proliferation.¹ EBF1 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. This gene has some recurrent sites of mutations (hot spots) but the mutation pattern in DLBCL and FL implies the preferential accumulation of *inactivating mutations*.

-### BL²

-FAS encodes a cell surface receptor involved in the induction of apoptosis. FAS mutations are common in DLBCL and may be more frequent in primary gastric DLBCL.^{[@wohlfartFASCD95Mutations2004],[@schollMutationsRegionFAS2007]}

-Mutations also occur in FL at a lower rate.^{[@morinFrequentMutationHistonemodifying2011]} Although reported in one BL study,^{[[@paneaWholeGenomeLandscape2019]} overall the evidence for FAS mutations in BL remains sparse.

-thereby allowing malignant cells to evade immune surveillance.^{[@rysFasMutationsNonHodgkins2019]}

-In mouse models, Fas mutations led to a significantly shorter lymphoma-specific survival and reduced sensitivity to chemotherapy.^{[@rysFasMutationsNonHodgkins2019]}

-Overall, these mutations are relatively rare in DLBCL and occur more frequently in other solid tumors as well as T-cell acute lymphocytic leukemia.^{[@akhoondiFBXW7HCDC4General2007]}

-The most commonly observed mutations in those cancers are the hot spots R465 and R479.^{[@akhoondiFBXW7HCDC4General2007]}

-In leukemias, FBXW7 mutations enhance the activity of leukemia-initiating cells by stabilizing oncogenic MYC.^{[@kingUbiquitinLigaseFBXW72013]} Whether they have this role in DLBCL remains to be determined.