HAEM5:Kikuchi-Fujimoto disease - Revision history

Sumire.Kitahara: /* Notes */

2026-01-06T22:35:55Z

Notes

← Older revision		Revision as of 17:35, 6 January 2026
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	<references />		<references />
	==Notes==		==Notes==
	<nowiki>*</nowiki>~~Primary authors will typically be those that initially create and complete the content~~ of ~~a page~~. ~~If a subsequent user modifies the content and feels the effort put forth is~~ of ~~high enough significance to warrant listing in the authorship section~~, ~~please contact the [[Leadership\|''~~<u>~~Associate Editor~~</u>'']] or other CCGA representative. When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.		<nowiki>*</nowiki>''Citation of this Page'': Kitahara S. “Kikuchi-Fujimoto disease”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:Kikuchi-Fujimoto_disease</nowiki>.


	<nowiki>*</nowiki>~~''Citation~~ of ~~this Page'': “Kikuchi-Fujimoto disease”~~. ~~Compendium~~ of ~~Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}~~, <~~nowiki~~>~~https://ccga.io/index.php/HAEM5:Kikuchi-Fujimoto_disease~~</~~nowiki~~>.		<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the [[Leadership\|''<u>Associate Editor</u>'']] or other CCGA representative. When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.
	[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases K]]		[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases K]]

Jennelleh at 19:57, 10 December 2025

2025-12-10T19:57:33Z

← Older revision		Revision as of 14:57, 10 December 2025
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	==Gene Rearrangements==		==Gene Rearrangements==
	<big>Kikuchi-Fujimoto disease does ~~'''~~not have characteristic or recurrent genetic alterations~~'''~~.</big>		<big>Kikuchi-Fujimoto disease does not have characteristic or recurrent genetic alterations.</big>
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	==Individual Region Genomic Gain/Loss/LOH==		==Individual Region Genomic Gain/Loss/LOH==
	<big>Kikuchi-Fujimoto disease does ~~'''~~not have characteristic or recurrent genetic alterations~~'''~~.</big>		<big>Kikuchi-Fujimoto disease does not have characteristic or recurrent genetic alterations.</big>
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	==Characteristic Chromosomal or Other Global Mutational Patterns==		==Characteristic Chromosomal or Other Global Mutational Patterns==
	<big>Kikuchi-Fujimoto disease does ~~'''~~not have characteristic or recurrent genetic alterations~~'''~~.</big>		<big>Kikuchi-Fujimoto disease does not have characteristic or recurrent genetic alterations.</big>
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	==Gene Mutations (SNV/INDEL)==		==Gene Mutations (SNV/INDEL)==
	<big>Kikuchi-Fujimoto disease does ~~'''~~not have characteristic or recurrent genetic alterations~~'''~~.</big>		<big>Kikuchi-Fujimoto disease does not have characteristic or recurrent genetic alterations.</big>
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	==Epigenomic Alterations==		==Epigenomic Alterations==
	NA		N/A
	==Genes and Main Pathways Involved==		==Genes and Main Pathways Involved==
	<big>~~Kikuchi-Fujimoto disease (~~KFD) does ~~'''~~not have characteristic or recurrent genetic alterations~~'''.~~</big>		<big>While KFD does not have characteristic or recurrent genetic alterations, a</big> <big>study using exome and transcriptome sequencing of lymph node tissue samples from KFD patients found fourteen</big> <big>SNPs</big> <big>as possible candidate markers for the disease and hundreds of genes with altered expression involving immune system, chromatin remodeling, and transcription pathways.</big><ref>{{Cite journal\|last=Anuntakarun\|first=Songtham\|last2=Larbcharoensub\|first2=Noppadol\|last3=Payungporn\|first3=Sunchai\|last4=Reamtong\|first4=Onrapak\|date=2021-06\|title=Identification of genes associated with Kikuchi-Fujimoto disease using RNA and exome sequencing\|url=https://pubmed.ncbi.nlm.nih.gov/33819568\|journal=Molecular and Cellular Probes\|volume=57\|pages=101728\|doi=10.1016/j.mcp.2021.101728\|issn=1096-1194\|pmid=33819568}}</ref>

	<big>~~However, a~~ study using exome and transcriptome sequencing of lymph node tissue samples from KFD patients found fourteen ~~'''single nucleotide polymorphisms'''~~ as possible candidate markers for the disease and hundreds of genes with altered expression involving immune system, chromatin remodeling, transcription pathways.</big><ref>{{Cite journal\|last=Anuntakarun\|first=Songtham\|last2=Larbcharoensub\|first2=Noppadol\|last3=Payungporn\|first3=Sunchai\|last4=Reamtong\|first4=Onrapak\|date=2021-06\|title=Identification of genes associated with Kikuchi-Fujimoto disease using RNA and exome sequencing\|url=https://pubmed.ncbi.nlm.nih.gov/33819568\|journal=Molecular and Cellular Probes\|volume=57\|pages=101728\|doi=10.1016/j.mcp.2021.101728\|issn=1096-1194\|pmid=33819568}}</ref>
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	==Familial Forms==		==Familial Forms==
	<big>Some reports describe ~~'''~~HLA class II associations~~'''~~ (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)</big><ref>{{Cite journal\|last=Tanaka\|first=T.\|last2=Ohmori\|first2=M.\|last3=Yasunaga\|first3=S.\|last4=Ohshima\|first4=K.\|last5=Kikuchi\|first5=M.\|last6=Sasazuki\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility</big> <big>and rare reports in siblings suggest familial susceptibility</big><big>.</big><ref>{{Cite journal\|last=Isoda\|first=Atsushi\|last2=Tahara\|first2=Kenichi\|last3=Ide\|first3=Munenori\|date=2023-12\|title=Kikuchi-Fujimoto Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility\|url=https://pubmed.ncbi.nlm.nih.gov/38264372\|journal=Cureus\|volume=15\|issue=12\|pages=e51010\|doi=10.7759/cureus.51010\|issn=2168-8184\|pmc=10803893\|pmid=38264372}}</ref>		<big>Some reports describe HLA class II associations (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)</big><ref>{{Cite journal\|last=Tanaka\|first=T.\|last2=Ohmori\|first2=M.\|last3=Yasunaga\|first3=S.\|last4=Ohshima\|first4=K.\|last5=Kikuchi\|first5=M.\|last6=Sasazuki\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility</big> <big>and rare reports in siblings suggest familial susceptibility</big><big>.</big><ref>{{Cite journal\|last=Isoda\|first=Atsushi\|last2=Tahara\|first2=Kenichi\|last3=Ide\|first3=Munenori\|date=2023-12\|title=Kikuchi-Fujimoto Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility\|url=https://pubmed.ncbi.nlm.nih.gov/38264372\|journal=Cureus\|volume=15\|issue=12\|pages=e51010\|doi=10.7759/cureus.51010\|issn=2168-8184\|pmc=10803893\|pmid=38264372}}</ref>

	==Additional Information==		==Additional Information==
	<big>Most published studies indicate a ~~'''~~reactive, immune-mediated process~~'''~~ rather than a neoplastic one.</big><ref>{{Cite journal\|last=Li\|first=Elizabeth Y.\|last2=Xu\|first2=Jason\|last3=Nelson\|first3=Nya D.\|last4=Teachey\|first4=David T.\|last5=Tan\|first5=Kai\|last6=Romberg\|first6=Neil\|last7=Behrens\|first7=Ed\|last8=Pillai\|first8=Vinodh\|date=2022-04\|title=Kikuchi-Fujimoto disease is mediated by an aberrant type I interferon response\|url=https://pubmed.ncbi.nlm.nih.gov/34952944\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=35\|issue=4\|pages=462–469\|doi=10.1038/s41379-021-00992-7\|issn=1530-0285\|pmid=34952944}}</ref>		<big>Most published studies indicate a reactive, immune-mediated process rather than a neoplastic one.</big><ref>{{Cite journal\|last=Li\|first=Elizabeth Y.\|last2=Xu\|first2=Jason\|last3=Nelson\|first3=Nya D.\|last4=Teachey\|first4=David T.\|last5=Tan\|first5=Kai\|last6=Romberg\|first6=Neil\|last7=Behrens\|first7=Ed\|last8=Pillai\|first8=Vinodh\|date=2022-04\|title=Kikuchi-Fujimoto disease is mediated by an aberrant type I interferon response\|url=https://pubmed.ncbi.nlm.nih.gov/34952944\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=35\|issue=4\|pages=462–469\|doi=10.1038/s41379-021-00992-7\|issn=1530-0285\|pmid=34952944}}</ref>

	==Links==		==Links==

	<big>NA</big>		<big>N/A</big>

	==References==		==References==

Jennelleh at 19:38, 10 December 2025

2025-12-10T19:38:46Z

← Older revision		Revision as of 14:38, 10 December 2025
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	!Clinical Relevance Details/Other Notes		!Clinical Relevance Details/Other Notes
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	==Individual Region Genomic Gain/Loss/LOH==		==Individual Region Genomic Gain/Loss/LOH==
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	!Clinical Relevance Details/Other Notes		!Clinical Relevance Details/Other Notes
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	==Characteristic Chromosomal or Other Global Mutational Patterns==		==Characteristic Chromosomal or Other Global Mutational Patterns==
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	!Clinical Relevance Details/Other Notes		!Clinical Relevance Details/Other Notes
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	==Gene Mutations (SNV/INDEL)==		==Gene Mutations (SNV/INDEL)==
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	!Clinical Relevance Details/Other Notes		!Clinical Relevance Details/Other Notes
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	==Epigenomic Alterations==		==Epigenomic Alterations==
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	!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome		!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
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	==Genetic Diagnostic Testing Methods==		==Genetic Diagnostic Testing Methods==

Sumire.Kitahara: /* References */

2025-11-07T01:01:20Z

References

← Older revision		Revision as of 20:01, 6 November 2025
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	==References==		==References==
			<references />
	==Notes==		==Notes==
	<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the [[Leadership\|''<u>Associate Editor</u>'']] or other CCGA representative. When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.		<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the [[Leadership\|''<u>Associate Editor</u>'']] or other CCGA representative. When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.

Sumire.Kitahara: /* Additional Information */

2025-11-07T01:00:12Z

Additional Information

← Older revision		Revision as of 20:00, 6 November 2025
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	NA		NA
	==Genes and Main Pathways Involved==		==Genes and Main Pathways Involved==
	<big>Kikuchi-Fujimoto disease does '''not have characteristic or recurrent genetic alterations'''.</big>		<big>Kikuchi-Fujimoto disease (KFD) does '''not have characteristic or recurrent genetic alterations'''.</big>

	<big>However, in a study using exome and transcriptome sequencing of lymph node tissue samples from KFD patients, fourteen '''single nucleotide polymorphisms''' ~~were identified~~ as candidate markers for the disease and ~~found~~ hundreds of genes with altered expression involving immune system, chromatin remodeling, transcription pathways.</big>		<big>However, a study using exome and transcriptome sequencing of lymph node tissue samples from KFD patients found fourteen '''single nucleotide polymorphisms''' as possible candidate markers for the disease and hundreds of genes with altered expression involving immune system, chromatin remodeling, transcription pathways.</big><ref>{{Cite journal\|last=Anuntakarun\|first=Songtham\|last2=Larbcharoensub\|first2=Noppadol\|last3=Payungporn\|first3=Sunchai\|last4=Reamtong\|first4=Onrapak\|date=2021-06\|title=Identification of genes associated with Kikuchi-Fujimoto disease using RNA and exome sequencing\|url=https://pubmed.ncbi.nlm.nih.gov/33819568\|journal=Molecular and Cellular Probes\|volume=57\|pages=101728\|doi=10.1016/j.mcp.2021.101728\|issn=1096-1194\|pmid=33819568}}</ref>
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	==Familial Forms==		==Familial Forms==
	NA		<big>Some reports describe '''HLA class II associations''' (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)</big><ref>{{Cite journal\|last=Tanaka\|first=T.\|last2=Ohmori\|first2=M.\|last3=Yasunaga\|first3=S.\|last4=Ohshima\|first4=K.\|last5=Kikuchi\|first5=M.\|last6=Sasazuki\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility</big> <big>and rare reports in siblings suggest familial susceptibility</big><big>.</big><ref>{{Cite journal\|last=Isoda\|first=Atsushi\|last2=Tahara\|first2=Kenichi\|last3=Ide\|first3=Munenori\|date=2023-12\|title=Kikuchi-Fujimoto Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility\|url=https://pubmed.ncbi.nlm.nih.gov/38264372\|journal=Cureus\|volume=15\|issue=12\|pages=e51010\|doi=10.7759/cureus.51010\|issn=2168-8184\|pmc=10803893\|pmid=38264372}}</ref>

	==Additional Information==		==Additional Information==
	<big>Most published studies indicate a '''reactive, immune-mediated process''' rather than a neoplastic one. ~~Some reports describe '''HLA class II associations''' (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)~~</big><ref>{{Cite journal\|last=~~Tanaka~~\|first=T.\|last2=~~Ohmori~~\|first2=M.\|last3=~~Yasunaga~~\|first3=S.\|last4=~~Ohshima~~\|first4=K.\|last5=~~Kikuchi~~\|first5=M.\|last6=~~Sasazuki~~\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility.</big><ref>{{Cite journal\|~~last~~=~~Isoda~~\|~~first~~=~~Atsushi~~\|~~last2~~=~~Tahara~~\|~~first2~~=~~Kenichi\|last3=Ide\|first3=Munenori~~\|date=~~2023~~-12\|title=Kikuchi-Fujimoto ~~Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility~~\|url=https://pubmed.ncbi.nlm.nih.gov/~~38264372~~\|journal=~~Cureus~~\|volume=15\|issue=12\|pages=~~e51010~~\|doi=10.~~7759~~/~~cureus.51010~~\|issn=~~2168~~-~~8184\|pmc=10803893~~\|pmid=~~38264372~~}}</ref>		<big>Most published studies indicate a '''reactive, immune-mediated process''' rather than a neoplastic one.</big><ref>{{Cite journal\|last=Li\|first=Elizabeth Y.\|last2=Xu\|first2=Jason\|last3=Nelson\|first3=Nya D.\|last4=Teachey\|first4=David T.\|last5=Tan\|first5=Kai\|last6=Romberg\|first6=Neil\|last7=Behrens\|first7=Ed\|last8=Pillai\|first8=Vinodh\|date=2022-04\|title=Kikuchi-Fujimoto disease is mediated by an aberrant type I interferon response\|url=https://pubmed.ncbi.nlm.nih.gov/34952944\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=35\|issue=4\|pages=462–469\|doi=10.1038/s41379-021-00992-7\|issn=1530-0285\|pmid=34952944}}</ref>

	Exomes and transcriptomes of lymph node tissue samples from KFD patients were analyzed by DNA sequencing. Fourteen single nucleotide polymorphisms (SNPs) were identified as candidate KFD markers and found hundreds of genes with altered expression (238 up, 1,519 down) involving immune system, chromatin remodeling, transcription pathways.

	==Links==		==Links==

Sumire.Kitahara: /* Additional Information */

2025-11-07T00:54:16Z

Additional Information

← Older revision		Revision as of 19:54, 6 November 2025
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	NA		NA
	==Genes and Main Pathways Involved==		==Genes and Main Pathways Involved==
	<big>Kikuchi-Fujimoto disease does '''not have characteristic or recurrent genetic alterations'''.</big>		<big>Kikuchi-Fujimoto disease does '''not have characteristic or recurrent genetic alterations'''.</big>

			<big>However, in a study using exome and transcriptome sequencing of lymph node tissue samples from KFD patients, fourteen '''single nucleotide polymorphisms''' were identified as candidate markers for the disease and found hundreds of genes with altered expression involving immune system, chromatin remodeling, transcription pathways.</big>
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	==Additional Information==		==Additional Information==
	<big>Most published studies indicate a '''reactive, immune-mediated process''' rather than a neoplastic one. Some reports describe '''HLA class II associations''' (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)</big><ref>{{Cite journal\|last=Tanaka\|first=T.\|last2=Ohmori\|first2=M.\|last3=Yasunaga\|first3=S.\|last4=Ohshima\|first4=K.\|last5=Kikuchi\|first5=M.\|last6=Sasazuki\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility.</big><ref>{{Cite journal\|last=Isoda\|first=Atsushi\|last2=Tahara\|first2=Kenichi\|last3=Ide\|first3=Munenori\|date=2023-12\|title=Kikuchi-Fujimoto Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility\|url=https://pubmed.ncbi.nlm.nih.gov/38264372\|journal=Cureus\|volume=15\|issue=12\|pages=e51010\|doi=10.7759/cureus.51010\|issn=2168-8184\|pmc=10803893\|pmid=38264372}}</ref>		<big>Most published studies indicate a '''reactive, immune-mediated process''' rather than a neoplastic one. Some reports describe '''HLA class II associations''' (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)</big><ref>{{Cite journal\|last=Tanaka\|first=T.\|last2=Ohmori\|first2=M.\|last3=Yasunaga\|first3=S.\|last4=Ohshima\|first4=K.\|last5=Kikuchi\|first5=M.\|last6=Sasazuki\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility.</big><ref>{{Cite journal\|last=Isoda\|first=Atsushi\|last2=Tahara\|first2=Kenichi\|last3=Ide\|first3=Munenori\|date=2023-12\|title=Kikuchi-Fujimoto Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility\|url=https://pubmed.ncbi.nlm.nih.gov/38264372\|journal=Cureus\|volume=15\|issue=12\|pages=e51010\|doi=10.7759/cureus.51010\|issn=2168-8184\|pmc=10803893\|pmid=38264372}}</ref>

			Exomes and transcriptomes of lymph node tissue samples from KFD patients were analyzed by DNA sequencing. Fourteen single nucleotide polymorphisms (SNPs) were identified as candidate KFD markers and found hundreds of genes with altered expression (238 up, 1,519 down) involving immune system, chromatin remodeling, transcription pathways.

	==Links==		==Links==

Sumire.Kitahara: /* Genetic Diagnostic Testing Methods */

2025-11-07T00:44:40Z

Genetic Diagnostic Testing Methods

← Older revision		Revision as of 19:44, 6 November 2025
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	==Genetic Diagnostic Testing Methods==		==Genetic Diagnostic Testing Methods==
	<big>Genetic testing is non-contributory to rule-in a diagnosis of Kikuchi-Fujimoto disease. T-cell receptor gene rearrangement and/or NGS studies may play a role ~~when morphology and immunophenotype raise concern for lymphoma~~.</big>		<big>Genetic testing is non-contributory to rule-in a diagnosis of Kikuchi-Fujimoto disease. If the morphology and immunophenotype raise concern for lymphoma, particularly of T-lineage, genetic testing (e.g. T-cell receptor gene rearrangement, cytogenetic and/or NGS studies) may play a role.</big>

	==Familial Forms==		==Familial Forms==

Sumire.Kitahara: /* Additional Information */

2025-11-07T00:42:13Z

Additional Information

← Older revision		Revision as of 19:42, 6 November 2025
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	==Additional Information==		==Additional Information==
	<big>Most published studies indicate a '''reactive, immune-mediated process''' rather than a neoplastic one. Some reports describe '''HLA class II associations''' (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms<ref ~~name~~=~~":0">~~Tanaka T, Ohmori M, Yasunaga S, Ohshima K, Kikuchi M, Sasazuki T. DNA typing of HLA class II genes (~~HLA-DR~~, ~~-DQ~~ and ~~-DP~~) in Japanese patients with histiocytic necrotizing lymphadenitis (~~Kikuchi's~~ disease). ''Tissue Antigens~~''. 1999;~~54(3~~):246-253.~~ doi:10.1034/j.1399-0039.1999.540305.x</ref>) in certain populations</big~~><ref name=":0" /~~><big>, suggesting a genetic susceptibility.</big>		<big>Most published studies indicate a '''reactive, immune-mediated process''' rather than a neoplastic one. Some reports describe '''HLA class II associations''' (e.g., HLA-DPA1 and HLA-DPB1 polymorphisms)</big><ref>{{Cite journal\|last=Tanaka\|first=T.\|last2=Ohmori\|first2=M.\|last3=Yasunaga\|first3=S.\|last4=Ohshima\|first4=K.\|last5=Kikuchi\|first5=M.\|last6=Sasazuki\|first6=T.\|date=1999-09\|title=DNA typing of HLA class II genes (HLA‐DR, ‐DQ and ‐DP) in Japanese patients with histiocytic necrotizing lymphadenitis (Kikuchi’s disease)\|url=https://onlinelibrary.wiley.com/doi/10.1034/j.1399-0039.1999.540305.x\|journal=Tissue Antigens\|language=en\|volume=54\|issue=3\|pages=246–253\|doi=10.1034/j.1399-0039.1999.540305.x\|issn=0001-2815}}</ref> <big>in certain populations</big><big>, suggesting a genetic susceptibility.</big><ref>{{Cite journal\|last=Isoda\|first=Atsushi\|last2=Tahara\|first2=Kenichi\|last3=Ide\|first3=Munenori\|date=2023-12\|title=Kikuchi-Fujimoto Disease in Human Leukocyte Antigen Partially Matched Siblings: A Case Study of Familial Susceptibility\|url=https://pubmed.ncbi.nlm.nih.gov/38264372\|journal=Cureus\|volume=15\|issue=12\|pages=e51010\|doi=10.7759/cureus.51010\|issn=2168-8184\|pmc=10803893\|pmid=38264372}}</ref>

	==Links==		==Links==
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	==References==		==References==
	(use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''Instructions: Add each reference into the text above by clicking where you want to insert the reference, selecting the “Cite” icon at the top of the wiki page, and using the “Automatic” tab option to search by PMID to select the reference to insert. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference. To insert the same reference again later in the page, select the “Cite” icon and “Re-use” to find the reference; DO NOT insert the same reference twice using the “Automatic” tab as it will be treated as two separate references. The reference list in this section will be automatically generated and sorted''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">)</span>

	==Notes==		==Notes==

Sumire.Kitahara at 00:34, 7 November 2025

2025-11-07T00:34:14Z

Show changes

Bailey.Glen at 17:19, 3 July 2025

2025-07-03T17:19:15Z

← Older revision		Revision as of 12:19, 3 July 2025
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	\|}		\|}

	~~==WHO Essential and Desirable Genetic Diagnostic Criteria==~~
	<span style="color:#0070C0">(''Instructions: The table will have the diagnostic criteria from the WHO book <u>autocompleted</u>; remove any <u>non</u>-genetics related criteria. If applicable, add text about other classification'' ''systems that define this entity and specify how the genetics-related criteria differ.'')</span>
	~~{\| class="wikitable"~~
	\|+
	\|WHO Essential Criteria (Genetics)*
	\|
	\|-
	\|WHO Desirable Criteria (Genetics)*
	\|
	\|-
	~~\|Other Classification~~
	\|
	\|}
	<nowiki>*</nowiki>Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the [https://tumourclassification.iarc.who.int/home <u>WHO Classification of Tumours</u>].
	==Related Terminology==		==Related Terminology==