EBF1.md
... ...
@@ -3,6 +3,7 @@
3 3
## Overview
4 4
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.<sup>1</sup> Mutations in EBF1 can impair BCR signaling pathways, affecting B-cell survival and proliferation.<sup>1</sup> 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*.
5 5
6
+
6 7
## History
7 8
8 9
```mermaid
... ...
@@ -75,11 +76,13 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/E
75 76
76 77
![](images/proteinpaint/EBF1.svg)
77 78
78
-## References
79
-1. *Györy I, Boller S, Nechanitzky R, Mandel E, Pott S, Liu E, Grosschedl R. Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferation, and survival of B cells. Genes Dev. 2012 Apr 1;26(7):668-82. doi: 10.1101/gad.187328.112. Epub 2012 Mar 19. PMID: 22431510; PMCID: PMC3323878.*
80 79
## EBF1 Expression
81 80
![](images/gene_expression/EBF1_by_pathology.svg)
82 81
<!-- ORIGIN: bohleRoleEarlyBcell2013 -->
83 82
<!-- BL: thomasGeneticSubgroupsInform2023 -->
84 83
<!-- PMBL: reichelFlowSortingExome2015a -->
85 84
<!-- DLBCL: bohleRoleEarlyBcell2013 -->
85
+
86
+## References
87
+1. *Györy I, Boller S, Nechanitzky R, Mandel E, Pott S, Liu E, Grosschedl R. Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferation, and survival of B cells. Genes Dev. 2012 Apr 1;26(7):668-82. doi: 10.1101/gad.18$
88
+
ETS1.md
... ...
@@ -1,7 +1,10 @@
1 1
# ETS1
2 2
3 3
## Overview
4
-ETS1 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). The mutation pattern in DLBCL implies the preferential accumulation of *inactivating mutations*.
4
+ETS1 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.
5
+This gene has some recurrent sites of mutations (hot spots).
6
+The mutation pattern in DLBCL implies the preferential accumulation of *inactivating mutations*.
7
+
5 8
## History
6 9
```mermaid
7 10
%%{init: { 'logLevel': 'debug', 'theme': 'dark' } }%%
ETV6.md
... ...
@@ -1,7 +1,12 @@
1 1
# ETV6
2 2
3 3
## Overview
4
-ETV6 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. The prevalence of mutations in DLBCL has varied across different studies and may occur in as many as 10% of patients. This gene has some recurrent sites of mutations (hot spots) including multiple mutations predicted to affect splicing of ETV6 pre-mRNA. The mutation pattern in DLBCL mplies the preferential accumulation of *inactivating mutations*. Coding and non-coding mutations in this gene are associated with the MCD genetic subgroup of DLBCL.
4
+ETV6 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.
5
+The prevalence of mutations in DLBCL has varied across different studies and may occur in as many as 10% of patients.
6
+This gene has some recurrent sites of mutations (hot spots) including multiple mutations predicted to affect splicing of ETV6 pre-mRNA.
7
+The mutation pattern in DLBCL mplies the preferential accumulation of *inactivating mutations*.
8
+Coding and non-coding mutations in this gene are associated with the MCD genetic subgroup of DLBCL.
9
+
5 10
## History
6 11
7 12
```mermaid
EZH2.md
... ...
@@ -1,7 +1,11 @@
1 1
# EZH2
2 2
3 3
## Overview
4
-EZH2 encodes a histone methyltransferase that is a component of the polycomb repressive complex 2 (PRC2). This gene is recurrently mutated in both FL and DLBCL and has a common mutation hot spot (Y646) that affects the SET domain.<sup>1</sup> Mutations of this residue and some of the less common hotspots lead to enhanced methylation by PRC2.<sup>2,3</sup> Pharmacologic inhibitors of this activity such as tazemetostat have shown benefit in FL.<sup>3</sup> EZH2 mutations are one of the defining features of the EZB genetic subgroup of DLBCL. Although mutations in EZH2 have been described in some BL patients, they are extremely rare in most studies.<sup>4</sup>
4
+EZH2 encodes a histone methyltransferase that is a component of the polycomb repressive complex 2 (PRC2).
5
+This gene is recurrently mutated in both FL and DLBCL and has a common mutation hot spot (Y646) that affects the SET domain.<sup>1</sup> Mutations of this residue and some of the less common hotspots lead to enhanced methylation by PRC2.<sup>2,3</sup>
6
+Pharmacologic inhibitors of this activity such as tazemetostat have shown benefit in FL.<sup>3</sup> EZH2 mutations are one of the defining features of the EZB genetic subgroup of DLBCL.
7
+Although mutations in EZH2 have been described in some BL patients, they are extremely rare in most studies.<sup>4</sup>
8
+
5 9
## History
6 10
```mermaid
7 11
%%{init: { 'logLevel': 'debug', 'theme': 'dark' } }%%
FAS.md
... ...
@@ -1,7 +1,12 @@
1 1
# FAS
2 2
3 3
## Overview
4
-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.<sup>1,2</sup> Mutations also occur in FL at a lower rate.<sup>3</sup> Although reported in one BL study,<sup>4</sup> overall the evidence for FAS mutations in BL remains sparse. Mutations in FAS often lead to a loss of function, making lymphoma cells resistant to Fas ligand-induced apoptosis, thereby allowing malignant cells to evade immune surveillance.<sup>5</sup> In mouse models, Fas mutations led to a significantly shorter lymphoma-specific survival and reduced sensitivity to chemotherapy.<sup>5</sup>
4
+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.<sup>1,2</sup>
5
+Mutations also occur in FL at a lower rate.<sup>3</sup> Although reported in one BL study,<sup>4</sup> overall the evidence for FAS mutations in BL remains sparse.
6
+Mutations in FAS often lead to a loss of function, making lymphoma cells resistant to Fas ligand-induced apoptosis,
7
+thereby allowing malignant cells to evade immune surveillance.<sup>5</sup>
8
+In mouse models, Fas mutations led to a significantly shorter lymphoma-specific survival and reduced sensitivity to chemotherapy.<sup>5</sup>
9
+
5 10
## History
6 11
```mermaid
7 12
%%{init: { 'logLevel': 'debug', 'theme': 'dark' } }%%
... ...
@@ -50,6 +55,9 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/F
50 55
51 56
![](images/proteinpaint/FAS.svg)
52 57
58
+## FAS Expression
59
+![](images/gene_expression/FAS_by_pathology.svg)
60
+
53 61
## References
54 62
55 63
1. *Wohlfart, S., Sebinger, D., Gruber, P., Buch, J., Polgar, D., Krupitza, G., Rosner, M., Hengstschläger, M., Raderer, M., Chott, A., & Müllauer, L. (2004). FAS (CD95) mutations are rare in gastric MALT lymphoma but occur more frequently in primary gastric diffuse large B-cell lymphoma.. The American journal of pathology, 164 3, 1081-9 . https://doi.org/10.1016/S0002-9440(10)63195-1.*
... ...
@@ -57,8 +65,6 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/F
57 65
3. *Morin RD, Mendez-Lago M, Mungall AJ, Goya R, Mungall KL, Corbett RD, Johnson NA, Severson TM, Chiu R, Field M, Jackman S, Krzywinski M, Scott DW, Trinh DL, Tamura-Wells J, Li S, Firme MR, Rogic S, Griffith M, Chan S, Yakovenko O, Meyer IM, Zhao EY, Smailus D, Moksa M, Chittaranjan S, Rimsza L, Brooks-Wilson A, Spinelli JJ, Ben-Neriah S, Meissner B, Woolcock B, Boyle M, McDonald H, Tam A, Zhao Y, Delaney A, Zeng T, Tse K, Butterfield Y, Birol I, Holt R, Schein J, Horsman DE, Moore R, Jones SJ, Connors JM, Hirst M, Gascoyne RD, Marra MA. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma. Nature. 2011 Jul 27;476(7360):298-303. doi: 10.1038/nature10351. PMID: 21796119; PMCID: PMC3210554.*
58 66
4. *Panea RI, Love CL, Shingleton JR, Reddy A, Bailey JA, Moormann AM, Otieno JA, Ong'echa JM, Oduor CI, Schroeder KMS, Masalu N, Chao NJ, Agajanian M, Major MB, Fedoriw Y, Richards KL, Rymkiewicz G, Miles RR, Alobeid B, Bhagat G, Flowers CR, Ondrejka SL, Hsi ED, Choi WWL, Au-Yeung RKH, Hartmann W, Lenz G, Meyerson H, Lin YY, Zhuang Y, Luftig MA, Waldrop A, Dave T, Thakkar D, Sahay H, Li G, Palus BC, Seshadri V, Kim SY, Gascoyne RD, Levy S, Mukhopadyay M, Dunson DB, Dave SS. The whole-genome landscape of Burkitt lymphoma subtypes. Blood. 2019 Nov 7;134(19):1598-1607. doi: 10.1182/blood.2019001880. Erratum in: Blood. 2022 Feb 24;139(8):1256. Erratum in: Blood. 2023 Sep 7;142(10):940. PMID: 31558468; PMCID: PMC6871305.*
59 67
5. *Rys, R., Venkataraman, M., Zeng, J., Mann, K., & Johnson, N. (2019). Fas Mutations in Non-Hodgkin's Lymphoma (NHL): Implications for Disease Progression and Therapeutic Resistance. Blood. https://doi.org/10.1182/blood-2019-130602.*
60
-## FAS Expression
61
-![](images/gene_expression/FAS_by_pathology.svg)
62 68
<!-- ORIGIN: schollMutationsRegionFAS2007 -->
63 69
<!-- DLBCL: schollMutationsRegionFAS2007 -->
64 70
<!-- MZL: spinaGeneticsNodalMarginal2016b -->
FBXO11.md
... ...
@@ -1,7 +1,9 @@
1 1
# FBXO11
2 2
3 3
## Overview
4
-Somatic mutations in FBXO11 are common in BL<sup>1,2</sup> and appear in a small number of DLBCLs.<sup>3</sup> This gene has some recurrent sites of mutations (hot spots). Mutations lead to stabilization of BCL6, an important transcriptional repressor involved in lymphomagenesis.<sup>4</sup> These mutations present a potential novel target for therapeutic intervention, particularly through strategies aimed at degrading BCL6 or inhibiting its function.<sup>4</sup>
4
+Somatic mutations in FBXO11 are common in BL<sup>1,2</sup> and appear in a small number of DLBCLs.<sup>3</sup>
5
+This gene has some recurrent sites of mutations (hot spots). Mutations lead to stabilization of BCL6, an important transcriptional repressor involved in lymphomagenesis.<sup>4</sup>
6
+These mutations present a potential novel target for therapeutic intervention, particularly through strategies aimed at degrading BCL6 or inhibiting its function.<sup>4</sup>
5 7
6 8
## History
7 9
Mutations in this gene were first described in BL in 2015 by Pighi et al<sup>4</sup> and in DLBCL by Hübschmann et al.<sup>5</sup>
... ...
@@ -73,14 +75,15 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/F
73 75
74 76
![](images/proteinpaint/FBXO11.svg)
75 77
78
+## FBXO11 Expression
79
+![](images/gene_expression/FBXO11_by_pathology.svg)
80
+
76 81
## References
77 82
1. *Pighi, C., Compagno, M., Wang, Q., Cheong, T., Poggio, T., Langellotto, F., Celle, P., Zamó, A., & Chiarle, R. (2015). FBXO11, a Regulator of BCL6 Stability, Is Recurrently Mutated in Burkitt Lymphoma. Blood, 126, 3673-3673. https://doi.org/10.1182/BLOOD.V126.23.3673.3673.*
78 83
2. *Grande BM, Gerhard DS, Jiang A, Griner NB, Abramson JS, Alexander TB, Allen H, Ayers LW, Bethony JM, Bhatia K, Bowen J, Casper C, Choi JK, Culibrk L, Davidsen TM, Dyer MA, Gastier-Foster JM, Gesuwan P, Greiner TC, Gross TG, Hanf B, Harris NL, He Y, Irvin JD, Jaffe ES, Jones SJM, Kerchan P, Knoetze N, Leal FE, Lichtenberg TM, Ma Y, Martin JP, Martin MR, Mbulaiteye SM, Mullighan CG, Mungall AJ, Namirembe C, Novik K, Noy A, Ogwang MD, Omoding A, Orem J, Reynolds SJ, Rushton CK, Sandlund JT, Schmitz R, Taylor C, Wilson WH, Wright GW, Zhao EY, Marra MA, Morin RD, Staudt LM. Genome-wide discovery of somatic coding and noncoding mutations in pediatric endemic and sporadic Burkitt lymphoma. Blood. 2019 Mar 21;133(12):1313-1324. doi: 10.1182/blood-2018-09-871418. Epub 2019 Jan 7. PMID: 30617194; PMCID: PMC6428665.*
79 84
3. *Thomas N, Dreval K, Gerhard DS, Hilton LK, Abramson JS, Ambinder RF, Barta S, Bartlett NL, Bethony J, Bhatia K, Bowen J, Bryan AC, Cesarman E, Casper C, Chadburn A, Cruz M, Dittmer DP, Dyer MA, Farinha P, Gastier-Foster JM, Gerrie AS, Grande BM, Greiner T, Griner NB, Gross TG, Harris NL, Irvin JD, Jaffe ES, Henry D, Huppi R, Leal FE, Lee MS, Martin JP, Martin MR, Mbulaiteye SM, Mitsuyasu R, Morris V, Mullighan CG, Mungall AJ, Mungall K, Mutyaba I, Nokta M, Namirembe C, Noy A, Ogwang MD, Omoding A, Orem J, Ott G, Petrello H, Pittaluga S, Phelan JD, Ramos JC, Ratner L, Reynolds SJ, Rubinstein PG, Sissolak G, Slack G, Soudi S, Swerdlow SH, Traverse-Glehen A, Wilson WH, Wong J, Yarchoan R, ZenKlusen JC, Marra MA, Staudt LM, Scott DW, Morin RD. Genetic subgroups inform on pathobiology in adult and pediatric Burkitt lymphoma. Blood. 2023 Feb 23;141(8):904-916. doi: 10.1182/blood.2022016534. PMID: 36201743; PMCID: PMC10023728.*
80 85
4. *Pighi, C., Cheong, T., Compagno, M., Patrucco, E., Arigoni, M., Olivero, M., Wang, Q., López, C., Bernhart, S., Grande, B., Poggio, T., Langellotto, F., Bonello, L., Dall’Olio, R., Martínez-Martín, S., Molinaro, L., Celle, P., Whitfield, J., Soucek, L., Voena, C., Calogero, R., Morin, R., Staudt, L., Siebert, R., Zamó, A., & Chiarle, R. (2021). Frequent mutations of FBXO11 highlight BCL6 as a therapeutic target in Burkitt lymphoma.. Blood advances. https://doi.org/10.1182/bloodadvances.2021005682.*
81 86
5. *Hübschmann D, Kleinheinz K, Wagener R, Bernhart SH, López C, Toprak UH, Sungalee S, Ishaque N, Kretzmer H, Kreuz M, Waszak SM, Paramasivam N, Ammerpohl O, Aukema SM, Beekman R, Bergmann AK, Bieg M, Binder H, Borkhardt A, Borst C, Brors B, Bruns P, Carrillo de Santa Pau E, Claviez A, Doose G, Haake A, Karsch D, Haas S, Hansmann ML, Hoell JI, Hovestadt V, Huang B, Hummel M, Jäger-Schmidt C, Kerssemakers JNA, Korbel JO, Kube D, Lawerenz C, Lenze D, Martens JHA, Ott G, Radlwimmer B, Reisinger E, Richter J, Rico D, Rosenstiel P, Rosenwald A, Schillhabel M, Stilgenbauer S, Stadler PF, Martín-Subero JI, Szczepanowski M, Warsow G, Weniger MA, Zapatka M, Valencia A, Stunnenberg HG, Lichter P, Möller P, Loeffler M, Eils R, Klapper W, Hoffmann S, Trümper L; ICGC MMML-Seq consortium; ICGC DE-Mining consortium; BLUEPRINT consortium; Küppers R, Schlesner M, Siebert R. Mutational mechanisms shaping the coding and noncoding genome of germinal center derived B-cell lymphomas. Leukemia. 2021 Jul;35(7):2002-2016. doi: 10.1038/s41375-021-01251-z. Epub 2021 May 5. PMID: 33953289; PMCID: PMC8257491.*
82
-## FBXO11 Expression
83
-![](images/gene_expression/FBXO11_by_pathology.svg)
84 87
<!-- ORIGIN: parryWholeExomeSequencing2013 -->
85 88
<!-- BL: richterRecurrentMutationID32012a -->
86 89
<!-- MZL: parryWholeExomeSequencing2013 -->
FBXW7.md
... ...
@@ -1,7 +1,11 @@
1 1
# FBXW7
2 2
3 3
## Overview
4
-FBXW7 mutations are found in a range of lymphoid malignancies, including B-cell lymphomas. These mutations often include missense mutations, deletions, frameshift mutations and splice-site mutations. Overall, these mutations are relatively rare in DLBCL and occur more frequently in other solid tumors as well as T-cell acute lymphocytic leukemia.<sup>1</sup> The most commonly observed mutations in those cancers are the hot spots R465 and R479.<sup>1</sup> In leukemias, FBXW7 mutations enhance the activity of leukemia-initiating cells by stabilizing oncogenic MYC.<sup>2</sup> Whether they have this role in DLBCL remains to be determined.
4
+FBXW7 mutations are found in a range of lymphoid malignancies, including B-cell lymphomas. These mutations often include missense mutations, deletions, frameshift mutations and splice-site mutations.
5
+Overall, these mutations are relatively rare in DLBCL and occur more frequently in other solid tumors as well as T-cell acute lymphocytic leukemia.<sup>1</sup>
6
+The most commonly observed mutations in those cancers are the hot spots R465 and R479.<sup>1</sup>
7
+In leukemias, FBXW7 mutations enhance the activity of leukemia-initiating cells by stabilizing oncogenic MYC.<sup>2</sup> Whether they have this role in DLBCL remains to be determined.
8
+
5 9
## History
6 10
```mermaid
7 11
%%{init: { 'logLevel': 'debug', 'theme': 'dark' } }%%
... ...
@@ -43,10 +47,11 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/F
43 47
44 48
![](images/proteinpaint/FBXW7.svg)
45 49
50
+## FBXW7 Expression
51
+![](images/gene_expression/FBXW7_by_pathology.svg)
52
+
46 53
## References
47 54
1. *Akhoondi, S., Sun, D., Lehr, N., Apostolidou, S., Klotz, K., Maljukova, A., Cepeda, D., Fiegl, H., Dafou, D., Marth, C., Mueller-Holzner, E., Corcoran, M., Dagnell, M., Nejad, S., Nayer, B., Zali, M., Hansson, J., Egyhazi, S., Petersson, F., Sangfelt, P., Nordgren, H., Grandér, D., Reed, S., Widschwendter, M., Sangfelt, O., & Spruck, C. (2007). FBXW7/hCDC4 is a general tumor suppressor in human cancer.. Cancer research, 67 19, 9006-12 . https://doi.org/10.1158/0008-5472.CAN-07-1320.*
48 55
2. *King, B., Trimarchi, T., Reavie, L., Xu, L., Mullenders, J., Ntziachristos, P., Aranda-Orgilles, B., Pérez-García, A., Shi, J., Vakoc, C., Sandy, P., Shen, S., Ferrando, A., & Aifantis, I. (2013). The Ubiquitin Ligase FBXW7 Modulates Leukemia-Initiating Cell Activity by Regulating MYC Stability. Cell, 153, 1552-1566. https://doi.org/10.1016/j.cell.2013.05.041.*
49
-## FBXW7 Expression
50
-![](images/gene_expression/FBXW7_by_pathology.svg)
51 56
<!-- ORIGIN: zhangGeneticHeterogeneityDiffuse2013 -->
52 57
<!-- DLBCL: zhangGeneticHeterogeneityDiffuse2013 -->
FOXO1.md
... ...
@@ -90,11 +90,6 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/F
90 90
![](images/gene_expression/FOXO1_by_pathology.svg)
91 91
92 92
## References
93
-1. *Trinh, D., Scott, D., Morin, R., Méndez-Lago, M., An, J., Jones, S., Mungall, A., Zhao, Y., Schein, J., Steidl, C., Connors, J., Gascoyne, R., & Marra, M. (2013). Analysis of FOXO1 mutations in diffuse large B-cell lymphoma.. Blood, 121 18, 3666-74 . https://doi.org/10.1182/blood-2013-01-479865.*
94
-2. *Zhou, P., Blain, A., Newman, A., Zaka, M., Chagaluka, G., Adlar, F., Offor, U., Broadbent, C., Chaytor, L., Whitehead, A., Hall, A., O'Connor, H., Noorden, S., Lampert, I., Bailey, S., Molyneux, E., Bacon, C., Bomken, S., & Rand, V. (2019). Sporadic and endemic Burkitt lymphoma have frequent FOXO1 mutations but distinct hotspots in the AKT recognition motif.. Blood advances, 3 14, 2118-2127 . https://doi.org/10.1182/bloodadvances.2018029546.*
95
-3. *Grande BM, Gerhard DS, Jiang A, Griner NB, Abramson JS, Alexander TB, Allen H, Ayers LW, Bethony JM, Bhatia K, Bowen J, Casper C, Choi JK, Culibrk L, Davidsen TM, Dyer MA, Gastier-Foster JM, Gesuwan P, Greiner TC, Gross TG, Hanf B, Harris NL, He Y, Irvin JD, Jaffe ES, Jones SJM, Kerchan P, Knoetze N, Leal FE, Lichtenberg TM, Ma Y, Martin JP, Martin MR, Mbulaiteye SM, Mullighan CG, Mungall AJ, Namirembe C, Novik K, Noy A, Ogwang MD, Omoding A, Orem J, Reynolds SJ, Rushton CK, Sandlund JT, Schmitz R, Taylor C, Wilson WH, Wright GW, Zhao EY, Marra MA, Morin RD, Staudt LM. Genome-wide discovery of somatic coding and noncoding mutations in pediatric endemic and sporadic Burkitt lymphoma. Blood. 2019 Mar 21;133(12):1313-1324. doi: 10.1182/blood-2018-09-871418. Epub 2019 Jan 7. PMID: 30617194; PMCID: PMC6428665.*
96
-4. *Pyrzynska B, Dwojak M, Zerrouqi A, Morlino G, Zapala P, Miazek N, Zagozdzon A, Bojarczuk K, Bobrowicz M, Siernicka M, Machnicki MM, Gobessi S, Barankiewicz J, Lech-Maranda E, Efremov DG, Juszczynski P, Calado D, Golab J, Winiarska M. FOXO1 promotes resistance of non-Hodgkin lymphomas to anti-CD20-based therapy. Oncoimmunology. 2018 Jan 25;7(5):e1423183. doi: 10.1080/2162402X.2017.1423183. PMID: 29721381; PMCID: PMC5927521.*
97
-5. *Morin RD, Mendez-Lago M, Mungall AJ, Goya R, Mungall KL, Corbett RD, Johnson NA, Severson TM, Chiu R, Field M, Jackman S, Krzywinski M, Scott DW, Trinh DL, Tamura-Wells J, Li S, Firme MR, Rogic S, Griffith M, Chan S, Yakovenko O, Meyer IM, Zhao EY, Smailus D, Moksa M, Chittaranjan S, Rimsza L, Brooks-Wilson A, Spinelli JJ, Ben-Neriah S, Meissner B, Woolcock B, Boyle M, McDonald H, Tam A, Zhao Y, Delaney A, Zeng T, Tse K, Butterfield Y, Birol I, Holt R, Schein J, Horsman DE, Moore R, Jones SJ, Connors JM, Hirst M, Gascoyne RD, Marra MA. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma. Nature. 2011 Jul 27;476(7360):298-303. doi: 10.1038/nature10351. PMID: 21796119; PMCID: PMC3210554.*
98 93
99 94
<!-- ORIGIN: morinFrequentMutationHistonemodifying2011 -->
100 95
<!-- BL: schmitzBurkittLymphomaPathogenesis2012 -->
GNA13.md
... ...
@@ -81,8 +81,3 @@ View all variants in GenomePaint [hg19](https://morinlab.github.io/LLMPP/GAMBL/G
81 81
<!-- DLBCL: morinFrequentMutationHistonemodifying2011 -->
82 82
83 83
## References
84
-1. *Morin RD, Mendez-Lago M, Mungall AJ, Goya R, Mungall KL, Corbett RD, Johnson NA, Severson TM, Chiu R, Field M, Jackman S, Krzywinski M, Scott DW, Trinh DL, Tamura-Wells J, Li S, Firme MR, Rogic S, Griffith M, Chan S, Yakovenko O, Meyer IM, Zhao EY, Smailus D, Moksa M, Chittaranjan S, Rimsza L, Brooks-Wilson A, Spinelli JJ, Ben-Neriah S, Meissner B, Woolcock B, Boyle M, McDonald H, Tam A, Zhao Y, Delaney A, Zeng T, Tse K, Butterfield Y, Birol I, Holt R, Schein J, Horsman DE, Moore R, Jones SJM, Connors JM, Hirst M, Gascoyne RD, Marra MA. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma. Nature. 2011 Jul 27;476(7360):298–303. PMCID: PMC3210554*
85
-2. *Muppidi JR, Schmitz R, Green JA, Xiao W, Larsen AB, Braun SE, An J, Xu Y, Rosenwald A, Ott G, Gascoyne RD, Rimsza LM, Campo E, Jaffe ES, Delabie J, Smeland EB, Braziel RM, Tubbs RR, Cook JR, Weisenburger DD, Chan WC, Vaidehi N, Staudt LM, Cyster JG. Loss of signalling via Gα13 in germinal centre B-cell-derived lymphoma. Nature. 2014 Dec 11;516(7530):254-8. doi: 10.1038/nature13765. Epub 2014 Sep 28. PMID: 25274307; PMCID: PMC4267955.*
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