HAEM5:Acute myeloid leukaemia with KMT2A rearrangement - Revision history

Bailey.Glen at 17:07, 3 July 2025

2025-07-03T17:07:07Z

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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==

Bailey.Glen at 21:26, 25 May 2025

2025-05-25T21:26:32Z

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	{\| class="wikitable sortable"		{\| class="wikitable sortable"
	\|-		\|-
	!Chr #!!~~'''~~Gain, Loss, Amp, LOH~~'''~~!!~~'''~~Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size]~~'''~~!!~~'''~~Relevant Gene(s)~~'''~~		!Chr #!!Gain, Loss, Amp, LOH!!Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size]!!Relevant Gene(s)
	!~~'''~~Diagnostic, Prognostic, and Therapeutic Significance - D, P, T~~'''~~		!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
	!~~'''~~Established Clinical Significance Per Guidelines - Yes or No (Source)~~'''~~		!Established Clinical Significance Per Guidelines - Yes or No (Source)
	!~~'''~~Clinical Relevance Details/Other Notes~~'''~~		!Clinical Relevance Details/Other Notes
	\|-		\|-
	\|<span class="blue-text">EXAMPLE:</span>		\|<span class="blue-text">EXAMPLE:</span>
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	!Chromosomal Pattern		!Chromosomal Pattern
	!Molecular Pathogenesis		!Molecular Pathogenesis
	!~~'''~~Prevalence -~~'''~~		!Prevalence -
	~~'''~~Common >20%, Recurrent 5-20% or Rare <5% (Disease)~~'''~~		Common >20%, Recurrent 5-20% or Rare <5% (Disease)
	!~~'''~~Diagnostic, Prognostic, and Therapeutic Significance - D, P, T~~'''~~		!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
	!~~'''~~Established Clinical Significance Per Guidelines - Yes or No (Source)~~'''~~		!Established Clinical Significance Per Guidelines - Yes or No (Source)
	!~~'''~~Clinical Relevance Details/Other Notes~~'''~~		!Clinical Relevance Details/Other Notes
	\|-		\|-
	\|<span class="blue-text">EXAMPLE:</span>		\|<span class="blue-text">EXAMPLE:</span>
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	{\| class="wikitable sortable"		{\| class="wikitable sortable"
	\|-		\|-
	!Gene!!~~'''~~Genetic Alteration~~'''~~!!~~'''~~Tumor Suppressor Gene, Oncogene, Other~~'''~~!!~~'''~~Prevalence -~~'''~~		!Gene!!Genetic Alteration!!Tumor Suppressor Gene, Oncogene, Other!!Prevalence -
	~~'''~~Common >20%, Recurrent 5-20% or Rare <5% (Disease)~~'''~~		Common >20%, Recurrent 5-20% or Rare <5% (Disease)
	!~~'''~~Diagnostic, Prognostic, and Therapeutic Significance - D, P, T ~~'''~~		!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
	!~~'''~~Established Clinical Significance Per Guidelines - Yes or No (Source)~~'''~~		!Established Clinical Significance Per Guidelines - Yes or No (Source)
	!~~'''~~Clinical Relevance Details/Other Notes~~'''~~		!Clinical Relevance Details/Other Notes
	\|-		\|-
	\|<span class="blue-text">EXAMPLE:</span>''EGFR''		\|<span class="blue-text">EXAMPLE:</span>''EGFR''

Bailey.Glen at 20:02, 25 May 2025

2025-05-25T20:02:56Z

← Older revision		Revision as of 15:02, 25 May 2025
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	<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>].		<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==
	~~<span style="color:#0070C0">(''Instructions: The table will have the related terminology from the WHO <u>autocompleted</u>.)''</span>~~
	{\| class="wikitable"		{\| class="wikitable"
	\|+		\|+
	\|Acceptable		\|Acceptable
	\|		\|Acute myeloid leukaemia with KMT2A::MLLT3 or other exact fusion; acute myeloid leukaemia with t(9;11)(p21.3;q23.3) or other exact balanced translocation
	\|-		\|-
	\|Not Recommended		\|Not Recommended
	\|		\|Acute myeloid leukaemia with MLL rearrangement
	\|}		\|}

Bailey.Glen at 17:30, 24 March 2025

2025-03-24T17:30:30Z

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	{{DISPLAYTITLE:Acute myeloid leukaemia with KMT2A rearrangement}}		{{DISPLAYTITLE:Acute myeloid leukaemia with KMT2A rearrangement}}

	[[HAEM5:Table_of_Contents\|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]		[[HAEM5:Table_of_Contents\|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]

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	Megan Piazza, Ph.D., Yiming Zhong, Ph.D., Shashi Shetty, Ph.D.		Megan Piazza, Ph.D., Yiming Zhong, Ph.D., Shashi Shetty, Ph.D.

	~~__TOC__~~

	==WHO Classification of Disease==		==WHO Classification of Disease==

Bailey.Glen: Removed old template contents

2025-02-11T13:44:21Z

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Bailey.Glen at 18:38, 10 February 2025

2025-02-10T18:38:05Z

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Bailey.Glen at 18:10, 10 February 2025

2025-02-10T18:10:02Z

← Older revision		Revision as of 13:10, 10 February 2025
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	<blockquote class='blockedit'>{{Box-round\|title=v4:Clinical Features\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Clinical Features\|The content below was from the old template. Please incorporate above.}}</blockquote>

	Patients may present with disseminated intravascular coagulation (DIC), extramedullary myeloid (monocytic) sarcomas, and/or tissue infiltration involving the gingiva and skin<ref name=":0" />.		Patients may present with disseminated intravascular coagulation (DIC), extramedullary myeloid (monocytic) sarcomas, and/or tissue infiltration involving the gingiva and skin<ref name=":0" />.

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Sites of Involvement==		==Sites of Involvement==
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	<blockquote class='blockedit'>{{Box-round\|title=v4:Chromosomal Rearrangements (Gene Fusions)\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Chromosomal Rearrangements (Gene Fusions)\|The content below was from the old template. Please incorporate above.}}</blockquote>

	This AML subtype is classified based on the translocation between chromosomes 9 and 11, specifically t(9;11)(p21.3;q23.3). This translocation leads to the fusion of the 5’ portion of ''KMT2A'' at 11q23.3 and the 3’ portion of ''MLLT3'' at 9p21.3. Both reciprocal fusions are expressed, however, the KMT2A-MLLT3 fusion on the derivative chromosome 11 is the candidate oncoprotein as it contains the putative functional domains of both proteins<ref name=":0" /><ref name=":1" /><ref name=":3">{{Cite journal\|last=Mrózek\|first=K.\|last2=Heinonen\|first2=K.\|last3=Lawrence\|first3=D.\|last4=Carroll\|first4=A. J.\|last5=Koduru\|first5=P. R.\|last6=Rao\|first6=K. W.\|last7=Strout\|first7=M. P.\|last8=Hutchison\|first8=R. E.\|last9=Moore\|first9=J. O.\|date=1997\|title=Adult patients with de novo acute myeloid leukemia and t(9; 11)(p22; q23) have a superior outcome to patients with other translocations involving band 11q23: a cancer and leukemia group B study\|url=https://www.ncbi.nlm.nih.gov/pubmed/9373264\|journal=Blood\|volume=90\|issue=11\|pages=4532–4538\|issn=0006-4971\|pmid=9373264}}</ref>.		This AML subtype is classified based on the translocation between chromosomes 9 and 11, specifically t(9;11)(p21.3;q23.3). This translocation leads to the fusion of the 5’ portion of ''KMT2A'' at 11q23.3 and the 3’ portion of ''MLLT3'' at 9p21.3. Both reciprocal fusions are expressed, however, the KMT2A-MLLT3 fusion on the derivative chromosome 11 is the candidate oncoprotein as it contains the putative functional domains of both proteins<ref name=":0" /><ref name=":1" /><ref name=":3">{{Cite journal\|last=Mrózek\|first=K.\|last2=Heinonen\|first2=K.\|last3=Lawrence\|first3=D.\|last4=Carroll\|first4=A. J.\|last5=Koduru\|first5=P. R.\|last6=Rao\|first6=K. W.\|last7=Strout\|first7=M. P.\|last8=Hutchison\|first8=R. E.\|last9=Moore\|first9=J. O.\|date=1997\|title=Adult patients with de novo acute myeloid leukemia and t(9; 11)(p22; q23) have a superior outcome to patients with other translocations involving band 11q23: a cancer and leukemia group B study\|url=https://www.ncbi.nlm.nih.gov/pubmed/9373264\|journal=Blood\|volume=90\|issue=11\|pages=4532–4538\|issn=0006-4971\|pmid=9373264}}</ref>.
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	\|}		\|}

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>

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	* Individual Region Genomic Gain/Loss/LOH		* Individual Region Genomic Gain/Loss/LOH
	* Characteristic Chromosomal Patterns		* Characteristic Chromosomal Patterns
	* Gene Mutations (SNV/INDEL)}}		* Gene Mutations (SNV/INDEL)}}</blockquote>

	Patients with t(9;11) resulting in a fusion between ''KMT2A'' and ''MLLT3'' and ≥20% blasts are diagnosed with AML with t(9;11). AML with t(9;11)(p21.3;q23.3) has an intermediate survival, which is superior to AML with other 11q23 translocations<ref name=":3" /><ref>{{Cite journal\|last=Rubnitz\|first=Jeffrey E.\|last2=Raimondi\|first2=Susana C.\|last3=Tong\|first3=Xin\|last4=Srivastava\|first4=Deo Kumar\|last5=Razzouk\|first5=Bassem I.\|last6=Shurtleff\|first6=Sheila A.\|last7=Downing\|first7=James R.\|last8=Pui\|first8=Ching-Hon\|last9=Ribeiro\|first9=Raul C.\|date=2002\|title=Favorable impact of the t(9;11) in childhood acute myeloid leukemia\|url=https://www.ncbi.nlm.nih.gov/pubmed/11981001\|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology\|volume=20\|issue=9\|pages=2302–2309\|doi=10.1200/JCO.2002.08.023\|issn=0732-183X\|pmid=11981001}}</ref>. There have been over 50 ''KMT2A'' translocation partners identified<ref>{{Cite journal\|last=Meyer\|first=C.\|last2=Schneider\|first2=B.\|last3=Jakob\|first3=S.\|last4=Strehl\|first4=S.\|last5=Attarbaschi\|first5=A.\|last6=Schnittger\|first6=S.\|last7=Schoch\|first7=C.\|last8=Jansen\|first8=M. W. J. C.\|last9=van Dongen\|first9=J. J. M.\|date=2006\|title=The MLL recombinome of acute leukemias\|url=https://www.ncbi.nlm.nih.gov/pubmed/16511515\|journal=Leukemia\|volume=20\|issue=5\|pages=777–784\|doi=10.1038/sj.leu.2404150\|issn=0887-6924\|pmid=16511515}}</ref><ref>{{Cite journal\|last=Shih\|first=L.-Y.\|last2=Liang\|first2=D.-C.\|last3=Fu\|first3=J.-F.\|last4=Wu\|first4=J.-H.\|last5=Wang\|first5=P.-N.\|last6=Lin\|first6=T.-L.\|last7=Dunn\|first7=P.\|last8=Kuo\|first8=M.-C.\|last9=Tang\|first9=T.-C.\|date=2006\|title=Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement\|url=https://www.ncbi.nlm.nih.gov/pubmed/16341046\|journal=Leukemia\|volume=20\|issue=2\|pages=218–223\|doi=10.1038/sj.leu.2404024\|issn=0887-6924\|pmid=16341046}}</ref> and one of the most common partners is ''MLLT3''<ref name=":0" />.		Patients with t(9;11) resulting in a fusion between ''KMT2A'' and ''MLLT3'' and ≥20% blasts are diagnosed with AML with t(9;11). AML with t(9;11)(p21.3;q23.3) has an intermediate survival, which is superior to AML with other 11q23 translocations<ref name=":3" /><ref>{{Cite journal\|last=Rubnitz\|first=Jeffrey E.\|last2=Raimondi\|first2=Susana C.\|last3=Tong\|first3=Xin\|last4=Srivastava\|first4=Deo Kumar\|last5=Razzouk\|first5=Bassem I.\|last6=Shurtleff\|first6=Sheila A.\|last7=Downing\|first7=James R.\|last8=Pui\|first8=Ching-Hon\|last9=Ribeiro\|first9=Raul C.\|date=2002\|title=Favorable impact of the t(9;11) in childhood acute myeloid leukemia\|url=https://www.ncbi.nlm.nih.gov/pubmed/11981001\|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology\|volume=20\|issue=9\|pages=2302–2309\|doi=10.1200/JCO.2002.08.023\|issn=0732-183X\|pmid=11981001}}</ref>. There have been over 50 ''KMT2A'' translocation partners identified<ref>{{Cite journal\|last=Meyer\|first=C.\|last2=Schneider\|first2=B.\|last3=Jakob\|first3=S.\|last4=Strehl\|first4=S.\|last5=Attarbaschi\|first5=A.\|last6=Schnittger\|first6=S.\|last7=Schoch\|first7=C.\|last8=Jansen\|first8=M. W. J. C.\|last9=van Dongen\|first9=J. J. M.\|date=2006\|title=The MLL recombinome of acute leukemias\|url=https://www.ncbi.nlm.nih.gov/pubmed/16511515\|journal=Leukemia\|volume=20\|issue=5\|pages=777–784\|doi=10.1038/sj.leu.2404150\|issn=0887-6924\|pmid=16511515}}</ref><ref>{{Cite journal\|last=Shih\|first=L.-Y.\|last2=Liang\|first2=D.-C.\|last3=Fu\|first3=J.-F.\|last4=Wu\|first4=J.-H.\|last5=Wang\|first5=P.-N.\|last6=Lin\|first6=T.-L.\|last7=Dunn\|first7=P.\|last8=Kuo\|first8=M.-C.\|last9=Tang\|first9=T.-C.\|date=2006\|title=Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement\|url=https://www.ncbi.nlm.nih.gov/pubmed/16341046\|journal=Leukemia\|volume=20\|issue=2\|pages=218–223\|doi=10.1038/sj.leu.2404024\|issn=0887-6924\|pmid=16341046}}</ref> and one of the most common partners is ''MLLT3''<ref name=":0" />.
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	Patients presenting with t(9;11)(p22;q23) and <20% blasts should be monitored closely for more definite evidence of AML.		Patients presenting with t(9;11)(p22;q23) and <20% blasts should be monitored closely for more definite evidence of AML.

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
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	</blockquote>		</blockquote>
	==Individual Region Genomic Gain / Loss / LOH==		==Individual Region Genomic Gain / Loss / LOH==
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	The t(9;11)( p21.3;q23.3) can present with secondary abnormalities, most frequently trisomy of chromosome 8<ref name=":1" /><ref name=":3" />.		The t(9;11)( p21.3;q23.3) can present with secondary abnormalities, most frequently trisomy of chromosome 8<ref name=":1" /><ref name=":3" />.
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			<center><span style="color:Maroon">'''End of V4 Section'''</span>
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	==Characteristic Chromosomal Patterns==		==Characteristic Chromosomal Patterns==
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	<blockquote class='blockedit'>{{Box-round\|title=v4:Characteristic Chromosomal Aberrations / Patterns\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Characteristic Chromosomal Aberrations / Patterns\|The content below was from the old template. Please incorporate above.}}</blockquote>

	Not applicable		Not applicable

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			<center><span style="color:Maroon">'''End of V4 Section'''</span>
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	==Gene Mutations (SNV / INDEL)==		==Gene Mutations (SNV / INDEL)==
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	NA		NA

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	NA		NA

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			<center><span style="color:Maroon">'''End of V4 Section'''</span>
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	==Epigenomic Alterations==		==Epigenomic Alterations==
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	<blockquote class='blockedit'>{{Box-round\|title=v4:Genes and Main Pathways Involved\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Genes and Main Pathways Involved\|The content below was from the old template. Please incorporate above.}}</blockquote>

	The ''KMT2A'' (Lysine Methyltransferase 2A) gene encodes a protein that complexes with other proteins and functions to regulate gene transcription through chromatin remodeling. This protein plays a vital role in regulating gene expressing during early development and hematopoiesis. The ''MLLT3'' (Super Elongation Complex Subunit) gene encodes a protein that is an element of the super elongation complex (SEC). The SEC is a complex that plays an essential role in regulating the activity of RNA polymerase II transcription. The fusion protein created, KMT2A-MLLT3, leads to the promotion of transcriptional elongation, activation of genes that would typically be silenced, and thus inhibits hematopoietic cells from properly maturing<ref>{{Cite journal\|last=Mueller\|first=Dorothee\|last2=García-Cuéllar\|first2=María-Paz\|last3=Bach\|first3=Christian\|last4=Buhl\|first4=Sebastian\|last5=Maethner\|first5=Emanuel\|last6=Slany\|first6=Robert K.\|date=2009\|title=Misguided transcriptional elongation causes mixed lineage leukemia\|url=https://www.ncbi.nlm.nih.gov/pubmed/19956800\|journal=PLoS biology\|volume=7\|issue=11\|pages=e1000249\|doi=10.1371/journal.pbio.1000249\|issn=1545-7885\|pmc=2774266\|pmid=19956800}}</ref>.		The ''KMT2A'' (Lysine Methyltransferase 2A) gene encodes a protein that complexes with other proteins and functions to regulate gene transcription through chromatin remodeling. This protein plays a vital role in regulating gene expressing during early development and hematopoiesis. The ''MLLT3'' (Super Elongation Complex Subunit) gene encodes a protein that is an element of the super elongation complex (SEC). The SEC is a complex that plays an essential role in regulating the activity of RNA polymerase II transcription. The fusion protein created, KMT2A-MLLT3, leads to the promotion of transcriptional elongation, activation of genes that would typically be silenced, and thus inhibits hematopoietic cells from properly maturing<ref>{{Cite journal\|last=Mueller\|first=Dorothee\|last2=García-Cuéllar\|first2=María-Paz\|last3=Bach\|first3=Christian\|last4=Buhl\|first4=Sebastian\|last5=Maethner\|first5=Emanuel\|last6=Slany\|first6=Robert K.\|date=2009\|title=Misguided transcriptional elongation causes mixed lineage leukemia\|url=https://www.ncbi.nlm.nih.gov/pubmed/19956800\|journal=PLoS biology\|volume=7\|issue=11\|pages=e1000249\|doi=10.1371/journal.pbio.1000249\|issn=1545-7885\|pmc=2774266\|pmid=19956800}}</ref>.

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			<center><span style="color:Maroon">'''End of V4 Section'''</span>
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	==Genetic Diagnostic Testing Methods==		==Genetic Diagnostic Testing Methods==

Bailey.Glen at 22:18, 6 September 2024

2024-09-06T22:18:42Z

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	__TOC__		__TOC__

	==~~Cancer Category / Type~~==		==WHO Classification of Disease==
	~~Acute Myeloid Leukemia~~

	=~~=Cancer Sub~~-~~Classification / Subtype==~~		{\| class="wikitable"
			!Structure
	Acute myeloid ~~leukemia~~ with t(~~9;11~~)~~(p21.3;q23.3) resulting in~~ KMT2A~~(MLL)-MLLT3(AF9) fusion~~		!Disease
			\|-
			\|Book
			\|Haematolymphoid Tumours (5th ed.)
			\|-
			\|Category
			\|Myeloid proliferations and neoplasms
			\|-
			\|Family
			\|Acute myeloid leukaemia
			\|-
			\|Type
			\|Acute myeloid leukaemia with defining genetic abnormalities
			\|-
			\|Subtype(s)
			\|Acute myeloid leukaemia with KMT2A rearrangement
			\|}

	==Definition / Description of Disease==		==Definition / Description of Disease==

Bailey.Glen at 21:48, 6 September 2024

2024-09-06T21:48:37Z

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Bailey.Glen at 19:17, 13 December 2023

2023-12-13T19:17:03Z

← Older revision		Revision as of 14:17, 13 December 2023
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	<blockquote class='blockedit'>{{Box-round\|title=HAEM5 Conversion Notes\|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Acute Myeloid Leukemia (AML) with t(9;11)(p21.3;q23.3); KMT2A-MLLT3]].		<blockquote class='blockedit'>{{Box-round\|title=HAEM5 Conversion Notes\|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Acute Myeloid Leukemia (AML) with t(9;11)(p21.3;q23.3); KMT2A-MLLT3]].
	}}</blockquote>		}}</blockquote>

			<span style="color:#0070C0">(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ HGVS-based nomenclature for variants], as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples). Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see </span><u>[[Author_Instructions]]</u><span style="color:#0070C0"> and [[Frequently Asked Questions (FAQs)\|<u>FAQs</u>]] as well as contact your [[Leadership\|<u>Associate Editor</u>]] or [mailto:CCGA@cancergenomics.org <u>Technical Support</u>])</span>

	==Primary Author(s)*==		==Primary Author(s)*==