HAEM5:EBV-positive diffuse large B-cell lymphoma - Revision history

Richard.Glen at 00:49, 26 February 2026

2026-02-26T00:49:12Z

← Older revision		Revision as of 19:49, 25 February 2026
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	# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420		# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420
	# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>		# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>
	# Mondello P, Ansell SM and Nowakowski GS (2022) Immune Epigenetic Crosstalk Between Malignant B Cells and the Tumor Microenvironment in B Cell Lymphoma. Front. Genet. 13:826594. doi: 10.3389/fgene.2022.826594 '''<u>(KMT2D) not able to create this citation</u>'''<references />		# Mondello P, Ansell SM and Nowakowski GS (2022) Immune Epigenetic Crosstalk Between Malignant B Cells and the Tumor Microenvironment in B Cell Lymphoma. Front. Genet. 13:826594. doi: 10.3389/fgene.2022.826594 '''<u>(KMT2D) not able to create this citation</u>'''
			<references />

	==Notes==		==Notes==

Richard.Glen at 00:36, 26 February 2026

2026-02-26T00:36:51Z

← Older revision		Revision as of 19:36, 25 February 2026
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	# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420		# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420
	# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>		# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>
	# Mondello P, Ansell SM and Nowakowski GS (2022) Immune Epigenetic Crosstalk Between Malignant B Cells and the Tumor Microenvironment in B Cell Lymphoma. Front. Genet. 13:826594. doi: 10.3389/fgene.2022.826594 '''<u>(KMT2D) not able to create this citation</u>'''		# Mondello P, Ansell SM and Nowakowski GS (2022) Immune Epigenetic Crosstalk Between Malignant B Cells and the Tumor Microenvironment in B Cell Lymphoma. Front. Genet. 13:826594. doi: 10.3389/fgene.2022.826594 '''<u>(KMT2D) not able to create this citation</u>'''<references />

	==Notes==		==Notes==

Fnu.Monika: /* Gene Mutations (SNV/INDEL) */

2025-12-05T00:51:00Z

Gene Mutations (SNV/INDEL)

← Older revision		Revision as of 19:51, 4 December 2025
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	\|D		\|D
	\|No		\|No
	\|Several tumor suppressor genes such as ''TNFAIP3'' and ''SOCS3'' also become silenced upon ''KMT2D'' loss of function ~~'''''~~<u>(doi:10.1038/nm.3943).</u>~~'''''~~ Targeting KDM5 demethylases counteracts ''KMT2D'' loss of function in DLBCL, which can open the opportunity for novel combination targeted therapies.		\|Several tumor suppressor genes such as ''TNFAIP3'' and ''SOCS3'' also become silenced upon ''KMT2D'' loss of function<ref>{{Cite journal\|last=Ortega-Molina\|first=Ana\|last2=Boss\|first2=Isaac W\|last3=Canela\|first3=Andres\|last4=Pan\|first4=Heng\|last5=Jiang\|first5=Yanwen\|last6=Zhao\|first6=Chunying\|last7=Jiang\|first7=Man\|last8=Hu\|first8=Deqing\|last9=Agirre\|first9=Xabier\|date=2015-10\|title=The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development\|url=https://www.nature.com/articles/nm.3943\|journal=Nature Medicine\|language=en\|volume=21\|issue=10\|pages=1199–1208\|doi=10.1038/nm.3943\|issn=1078-8956\|pmc=4676270\|pmid=26366710}}</ref>. Targeting KDM5 demethylases counteracts ''KMT2D'' loss of function in DLBCL, which can open the opportunity for novel combination targeted therapies.<ref>{{Cite journal\|last=Heward\|first=James\|last2=Koniali\|first2=Lola\|last3=D’Avola\|first3=Annalisa\|last4=Close\|first4=Karina\|last5=Yeomans\|first5=Alison\|last6=Philpott\|first6=Martin\|last7=Dunford\|first7=James\|last8=Rahim\|first8=Tahrima\|last9=Al Seraihi\|first9=Ahad F.\|date=2021-08-05\|title=KDM5 inhibition offers a novel therapeutic strategy for the treatment of KMT2D mutant lymphomas\|url=https://ashpublications.org/blood/article/138/5/370/475650/KDM5-inhibition-offers-a-novel-therapeutic\|journal=Blood\|language=en\|volume=138\|issue=5\|pages=370–381\|doi=10.1182/blood.2020008743\|issn=0006-4971\|pmc=8351530\|pmid=33786580}}</ref>
	\|-		\|-
	\|''CCR6''<ref name=":2" />		\|''CCR6''<ref name=":2" />

Fnu.Monika: /* Gene Mutations (SNV/INDEL) */

2025-12-05T00:47:12Z

Gene Mutations (SNV/INDEL)

← Older revision		Revision as of 19:47, 4 December 2025
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	\|-		\|-
	\|''KMT2D''<ref name=":1" /><ref name=":2" /><ref name=":5">{{Cite journal\|last=Zhou\|first=Yangying\|last2=Xu\|first2=Zhijie\|last3=Lin\|first3=Wei\|last4=Duan\|first4=Yumei\|last5=Lu\|first5=Can\|last6=Liu\|first6=Wei\|last7=Su\|first7=Weiping\|last8=Yan\|first8=Yuanliang\|last9=Liu\|first9=Huan\|date=2019-07-25\|title=Comprehensive Genomic Profiling of EBV-Positive Diffuse Large B-cell Lymphoma and the Expression and Clinicopathological Correlations of Some Related Genes\|url=https://www.frontiersin.org/article/10.3389/fonc.2019.00683/full\|journal=Frontiers in Oncology\|volume=9\|doi=10.3389/fonc.2019.00683\|issn=2234-943X\|pmc=6669985\|pmid=31403034}}</ref>		\|''KMT2D''<ref name=":1" /><ref name=":2" /><ref name=":5">{{Cite journal\|last=Zhou\|first=Yangying\|last2=Xu\|first2=Zhijie\|last3=Lin\|first3=Wei\|last4=Duan\|first4=Yumei\|last5=Lu\|first5=Can\|last6=Liu\|first6=Wei\|last7=Su\|first7=Weiping\|last8=Yan\|first8=Yuanliang\|last9=Liu\|first9=Huan\|date=2019-07-25\|title=Comprehensive Genomic Profiling of EBV-Positive Diffuse Large B-cell Lymphoma and the Expression and Clinicopathological Correlations of Some Related Genes\|url=https://www.frontiersin.org/article/10.3389/fonc.2019.00683/full\|journal=Frontiers in Oncology\|volume=9\|doi=10.3389/fonc.2019.00683\|issn=2234-943X\|pmc=6669985\|pmid=31403034}}</ref>
	\|		\|Inactivating mutations
	\|Tumor Suppressor Gene<ref>{{Cite journal\|title=OncoKB™ - MSK's Precision Oncology Knowledge Base\|url=https://www.oncokb.org/\|language=en}}</ref>		\|Tumor Suppressor Gene<ref>{{Cite journal\|title=OncoKB™ - MSK's Precision Oncology Knowledge Base\|url=https://www.oncokb.org/\|language=en}}</ref>
	\|Common<ref name=":1" /><ref name=":2" /><ref name=":5" />		\|Common<ref name=":1" /><ref name=":2" /><ref name=":5" />
	\|D		\|D
	\|No		\|No
	\|		\|Several tumor suppressor genes such as ''TNFAIP3'' and ''SOCS3'' also become silenced upon ''KMT2D'' loss of function '''''<u>(doi:10.1038/nm.3943).</u>''''' Targeting KDM5 demethylases counteracts ''KMT2D'' loss of function in DLBCL, which can open the opportunity for novel combination targeted therapies.
	\|-		\|-
	\|''CCR6''<ref name=":2" />		\|''CCR6''<ref name=":2" />
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	\|Abnormal and prolonged activation of the NF-κB pathway<ref name=":9" />		\|Abnormal and prolonged activation of the NF-κB pathway<ref name=":9" />
	\|-		\|-
	\|''KMT2D and KMT2C;''		\|''KMT2D and KMT2C;'' Loss of function mutations
	\|Histone methyltransferases involved in epigenetic regulation		\|Histone methyltransferases involved in epigenetic regulation; mediate H3K4 mono and demethylation (H4K3me1/2) primarily at gene enhancers (https://doi.org/10.3389/fgene.2022.826594)
			\|Aberrant repression of genes involved in immune signaling such as CD40, IL10-IL6, and NFkB signaling
			\|-
			\|
			\|
	\|		\|
	\|}		\|}
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	# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420		# Zhang XY, Xing TY, Hua W, Li Y, Kong YL, Pan BH, Zhang XY, Wu JZ, Shen HR, Yin H, Wang L, Li JY, Gao R, Liang JH, Xu W. Prognostic Role of SOCS1 Mutations in Diffuse Large B-Cell Lymphoma. Cancer Res Treat. ;0.0. doi: 10.4143/crt.2025.420
	# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>		# Carpenter, R. L., & Lo, H.-W. (2014). STAT3 Target Genes Relevant to Human Cancers. ''Cancers'', ''6''(2), 897-925. <nowiki>https://doi.org/10.3390/cancers6020897</nowiki>
			# Mondello P, Ansell SM and Nowakowski GS (2022) Immune Epigenetic Crosstalk Between Malignant B Cells and the Tumor Microenvironment in B Cell Lymphoma. Front. Genet. 13:826594. doi: 10.3389/fgene.2022.826594 '''<u>(KMT2D) not able to create this citation</u>'''

	==Notes==		==Notes==

Fnu.Monika: /* Genes and Main Pathways Involved */

2025-12-02T23:34:32Z

Genes and Main Pathways Involved

← Older revision		Revision as of 18:34, 2 December 2025
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	\|''STAT3 and STAT6''; Activating mutations<ref name=":1" /><ref name=":8">{{Cite journal\|last=Zeinalzadeh\|first=Elham\|last2=Valerievich Yumashev\|first2=Alexey\|last3=Rahman\|first3=Heshu Sulaiman\|last4=Marofi\|first4=Faroogh\|last5=Shomali\|first5=Navid\|last6=Kafil\|first6=Hossein Samadi\|last7=Solali\|first7=Saeed\|last8=Sajjadi-Dokht\|first8=Mehdi\|last9=Vakili-Samiani\|first9=Sajjad\|date=2021-12-21\|title=RETRACTED: The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics\|url=https://www.frontiersin.org/articles/10.3389/fgene.2021.703883/full\|journal=Frontiers in Genetics\|volume=12\|doi=10.3389/fgene.2021.703883\|issn=1664-8021\|pmc=8725977\|pmid=34992627}}</ref>		\|''STAT3 and STAT6''; Activating mutations<ref name=":1" /><ref name=":8">{{Cite journal\|last=Zeinalzadeh\|first=Elham\|last2=Valerievich Yumashev\|first2=Alexey\|last3=Rahman\|first3=Heshu Sulaiman\|last4=Marofi\|first4=Faroogh\|last5=Shomali\|first5=Navid\|last6=Kafil\|first6=Hossein Samadi\|last7=Solali\|first7=Saeed\|last8=Sajjadi-Dokht\|first8=Mehdi\|last9=Vakili-Samiani\|first9=Sajjad\|date=2021-12-21\|title=RETRACTED: The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics\|url=https://www.frontiersin.org/articles/10.3389/fgene.2021.703883/full\|journal=Frontiers in Genetics\|volume=12\|doi=10.3389/fgene.2021.703883\|issn=1664-8021\|pmc=8725977\|pmid=34992627}}</ref>
	\|Normal cellular events: Survival, proliferation, and differentiation<ref name=":8" />		\|Normal cellular events: Survival, proliferation, and differentiation<ref name=":8" />
	\|Tumor cell survival, proliferation, and invasion<ref name=":8" />		\|Tumor cell survival, proliferation, and invasion<ref name=":8" /><ref>{{Cite journal\|last=Kennedy\|first=Ruth\|last2=Klein\|first2=Ulf\|date=2018-10-30\|title=Aberrant Activation of NF-κB Signalling in Aggressive Lymphoid Malignancies\|url=https://www.mdpi.com/2073-4409/7/11/189\|journal=Cells\|language=en\|volume=7\|issue=11\|pages=189\|doi=10.3390/cells7110189\|issn=2073-4409\|pmc=6262606\|pmid=30380749}}</ref>
	\|-		\|-
	\|''TNFAIP3'' (A20) and ''MAP3K14'' (NIK); Inactivating mutations		\|''TNFAIP3'' (A20) and ''MAP3K14'' (NIK); Inactivating mutations
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	\|-		\|-
	\|''KMT2D and KMT2C;''		\|''KMT2D and KMT2C;''
	\|~~Epigenetic modifier~~		\|Histone methyltransferases involved in epigenetic regulation
	\|		\|
	\|}		\|}

Fnu.Monika: /* Gene Mutations (SNV/INDEL) */

2025-12-02T23:23:47Z

Gene Mutations (SNV/INDEL)

← Older revision		Revision as of 18:23, 2 December 2025
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	\|Abnormal and prolonged activation of the NF-κB pathway<ref name=":9" />		\|Abnormal and prolonged activation of the NF-κB pathway<ref name=":9" />
	\|-		\|-
	\|		\|''KMT2D and KMT2C;''
	\|		\|Epigenetic modifier
	\|		\|
	\|}		\|}

Fnu.Monika: /* Genes and Main Pathways Involved */

2025-12-02T23:20:47Z

Genes and Main Pathways Involved

← Older revision		Revision as of 18:20, 2 December 2025
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	\|-		\|-
	\|''TNFAIP3'' (A20) and ''MAP3K14'' (NIK); Inactivating mutations		\|''TNFAIP3'' (A20) and ''MAP3K14'' (NIK); Inactivating mutations
	\|<~~span class~~="~~blue-text~~">~~EXAMPLE~~:</~~span~~> ~~Histone modification, chromatin remodeling~~		\|Negative regulation of NF-κB pathway<ref name=":9">{{Cite journal\|last=Pasqualucci\|first=Laura\|last2=Dalla-Favera\|first2=Riccardo\|date=2018-05-24\|title=Genetics of diffuse large B-cell lymphoma\|url=https://ashpublications.org/blood/article/131/21/2307/37115/Genetics-of-diffuse-large-Bcell-lymphoma\|journal=Blood\|language=en\|volume=131\|issue=21\|pages=2307–2319\|doi=10.1182/blood-2017-11-764332\|issn=0006-4971\|pmc=5969374\|pmid=29666115}}</ref>
	\|<~~span class~~="~~blue-text~~"~~>EXAMPLE:<~~/~~span~~> ~~Abnormal gene expression program~~		\|Abnormal and prolonged activation of the NF-κB pathway<ref name=":9" />
	\|-		\|-
	\|		\|

Fnu.Monika: /* Genes and Main Pathways Involved */

2025-12-02T23:07:02Z

Genes and Main Pathways Involved

← Older revision		Revision as of 18:07, 2 December 2025
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	\|Tumor cell survival, proliferation, and invasion<ref name=":8" />		\|Tumor cell survival, proliferation, and invasion<ref name=":8" />
	\|-		\|-
	\|~~<span class="blue-text">EXAMPLE:</span>~~ ''~~KMT2C~~'' and ''~~ARID1A~~''; Inactivating mutations		\|''TNFAIP3'' (A20) and ''MAP3K14'' (NIK); Inactivating mutations
	\|<span class="blue-text">EXAMPLE:</span> Histone modification, chromatin remodeling		\|<span class="blue-text">EXAMPLE:</span> Histone modification, chromatin remodeling
	\|<span class="blue-text">EXAMPLE:</span> Abnormal gene expression program		\|<span class="blue-text">EXAMPLE:</span> Abnormal gene expression program

Fnu.Monika: /* Genes and Main Pathways Involved */

2025-12-02T22:57:47Z

Genes and Main Pathways Involved

← Older revision		Revision as of 17:57, 2 December 2025
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	!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome		!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
	\|-		\|-
	\|''SOCS1;'' ~~Activating~~ mutations<ref name=":1" />		\|''SOCS1;'' Inactivating mutations<ref name=":1" />
	\|JAK-STAT and interferon gamma (INFγ) signaling pathways		\|JAK-STAT and interferon gamma (INFγ) signaling pathways
	\|~~Negative regulator~~ of the JAK-STAT INFγ signaling pathways<ref name=":1" /><ref name=":7" />		\|Activation of the JAK-STAT INFγ signaling pathways<ref name=":1" /><ref name=":7" />
	\|-		\|-
	\|''STAT3 and STAT6''; Activating mutations<ref name=":1" /><ref>{{Cite journal\|last=Zeinalzadeh\|first=Elham\|last2=Valerievich Yumashev\|first2=Alexey\|last3=Rahman\|first3=Heshu Sulaiman\|last4=Marofi\|first4=Faroogh\|last5=Shomali\|first5=Navid\|last6=Kafil\|first6=Hossein Samadi\|last7=Solali\|first7=Saeed\|last8=Sajjadi-Dokht\|first8=Mehdi\|last9=Vakili-Samiani\|first9=Sajjad\|date=2021-12-21\|title=RETRACTED: The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics\|url=https://www.frontiersin.org/articles/10.3389/fgene.2021.703883/full\|journal=Frontiers in Genetics\|volume=12\|doi=10.3389/fgene.2021.703883\|issn=1664-8021\|pmc=8725977\|pmid=34992627}}</ref>		\|''STAT3 and STAT6''; Activating mutations<ref name=":1" /><ref name=":8">{{Cite journal\|last=Zeinalzadeh\|first=Elham\|last2=Valerievich Yumashev\|first2=Alexey\|last3=Rahman\|first3=Heshu Sulaiman\|last4=Marofi\|first4=Faroogh\|last5=Shomali\|first5=Navid\|last6=Kafil\|first6=Hossein Samadi\|last7=Solali\|first7=Saeed\|last8=Sajjadi-Dokht\|first8=Mehdi\|last9=Vakili-Samiani\|first9=Sajjad\|date=2021-12-21\|title=RETRACTED: The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics\|url=https://www.frontiersin.org/articles/10.3389/fgene.2021.703883/full\|journal=Frontiers in Genetics\|volume=12\|doi=10.3389/fgene.2021.703883\|issn=1664-8021\|pmc=8725977\|pmid=34992627}}</ref>
	\|<~~span class~~="~~blue-text~~"~~>EXAMPLE:<~~/~~span~~> ~~Cell cycle regulation~~		\|Normal cellular events: Survival, proliferation, and differentiation<ref name=":8" />
	\|<~~span class~~="~~blue-text~~"~~>EXAMPLE:<~~/~~span~~> ~~Unregulated cell division~~		\|Tumor cell survival, proliferation, and invasion<ref name=":8" />
	\|-		\|-
	\|<span class="blue-text">EXAMPLE:</span> ''KMT2C'' and ''ARID1A''; Inactivating mutations		\|<span class="blue-text">EXAMPLE:</span> ''KMT2C'' and ''ARID1A''; Inactivating mutations

Fnu.Monika: /* Genes and Main Pathways Involved */

2025-12-02T22:49:17Z

Genes and Main Pathways Involved

← Older revision		Revision as of 17:49, 2 December 2025
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	\|Negative regulator of the JAK-STAT INFγ signaling pathways<ref name=":1" /><ref name=":7" />		\|Negative regulator of the JAK-STAT INFγ signaling pathways<ref name=":1" /><ref name=":7" />
	\|-		\|-
	\|''STAT3 and STAT6''; Activating mutations<ref name=":1" />		\|''STAT3 and STAT6''; Activating mutations<ref name=":1" /><ref>{{Cite journal\|last=Zeinalzadeh\|first=Elham\|last2=Valerievich Yumashev\|first2=Alexey\|last3=Rahman\|first3=Heshu Sulaiman\|last4=Marofi\|first4=Faroogh\|last5=Shomali\|first5=Navid\|last6=Kafil\|first6=Hossein Samadi\|last7=Solali\|first7=Saeed\|last8=Sajjadi-Dokht\|first8=Mehdi\|last9=Vakili-Samiani\|first9=Sajjad\|date=2021-12-21\|title=RETRACTED: The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics\|url=https://www.frontiersin.org/articles/10.3389/fgene.2021.703883/full\|journal=Frontiers in Genetics\|volume=12\|doi=10.3389/fgene.2021.703883\|issn=1664-8021\|pmc=8725977\|pmid=34992627}}</ref>
	\|<span class="blue-text">EXAMPLE:</span> Cell cycle regulation		\|<span class="blue-text">EXAMPLE:</span> Cell cycle regulation
	\|<span class="blue-text">EXAMPLE:</span> Unregulated cell division		\|<span class="blue-text">EXAMPLE:</span> Unregulated cell division