HAEM5:Acute myeloid leukaemia with minimal differentiation - Revision history

Malini.Sathanoori at 22:00, 7 September 2025

2025-09-07T22:00:05Z

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	{{DISPLAYTITLE:Acute myeloid leukaemia with minimal differentiation}}		{{DISPLAYTITLE:Acute myeloid leukaemia with minimal differentiation}}

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

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

	~~Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine~~


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	Prior Author(s):		Prior Author(s):

			Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine

Bailey.Glen at 17:07, 3 July 2025

2025-07-03T17:07:13Z

← Older revision		Revision as of 12:07, 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==

Bailey.Glen at 21:26, 25 May 2025

2025-05-25T21:26:38Z

← Older revision		Revision as of 16:26, 25 May 2025
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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 20:03, 25 May 2025

2025-05-25T20:03:01Z

← Older revision		Revision as of 15:03, 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
	\|		\|N/A
	\|-		\|-
	\|Not Recommended		\|Not Recommended
	\|		\|Acute myeloid leukaemia, M0
	\|}		\|}

Bailey.Glen at 17:30, 24 March 2025

2025-03-24T17:30:37Z

← Older revision		Revision as of 12:30, 24 March 2025
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	{{DISPLAYTITLE:Acute myeloid leukaemia with minimal differentiation}}		{{DISPLAYTITLE:Acute myeloid leukaemia with minimal differentiation}}

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

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	Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine		Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine



	~~__TOC__~~

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

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2025-02-11T13:52:53Z

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Bailey.Glen at 18:38, 10 February 2025

2025-02-10T18:38:12Z

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Bailey.Glen at 18:10, 10 February 2025

2025-02-10T18:10:07Z

← 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 present with evidence of bone marrow failure		• Patients present with evidence of bone marrow failure
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	• Some patients present with leukocytosis and numerous circulating blasts		• Some patients present with leukocytosis and numerous circulating blasts

			<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:Immunophenotype\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Immunophenotype\|The content below was from the old template. Please incorporate above.}}</blockquote>

	POSITIVE		POSITIVE
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	• Pediatric cases: Negative for TdT, CD34 and CD13 (weak)		• Pediatric cases: Negative for TdT, CD34 and CD13 (weak)

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Chromosomal Rearrangements (Gene Fusions)==		==Chromosomal Rearrangements (Gene Fusions)==
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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>

	There is no recurrent rearrangements in this entity.		There is no recurrent rearrangements in this entity.
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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>

	• Adverse outcome in children. May relate to a lack of more favorable AML cytogenetic abnormalities, such as t(8;21) and inv 16 and presence of high-risk abnormalities (i.e. chromosome 5)<ref name=":6" />.		• Adverse outcome in children. May relate to a lack of more favorable AML cytogenetic abnormalities, such as t(8;21) and inv 16 and presence of high-risk abnormalities (i.e. chromosome 5)<ref name=":6" />.
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	• MDR1/p-170 protein is positive in blasts and mediates multidrug resistance in adults. This protein functions as a barrier, reducing intracellular concentrations of chemotherapeutics<ref>{{Cite journal\|last=Campos\|first=L.\|last2=Guyotat\|first2=D.\|last3=Jaffar\|first3=C.\|last4=Solary\|first4=E.\|last5=Archimbaud\|first5=E.\|last6=Treille\|first6=D.\|date=1992\|title=Correlation of MDR1/P-170 expression with daunorubicin uptake and sensitivity of leukemic progenitors in acute myeloid leukemia\|url=https://www.ncbi.nlm.nih.gov/pubmed/1353726\|journal=European Journal of Haematology\|volume=48\|issue=5\|pages=254–258\|doi=10.1111/j.1600-0609.1992.tb01803.x\|issn=0902-4441\|pmid=1353726}}</ref><ref>{{Cite journal\|last=Wuchter\|first=C.\|last2=Karawajew\|first2=L.\|last3=Ruppert\|first3=V.\|last4=Büchner\|first4=T.\|last5=Schoch\|first5=C.\|last6=Haferlach\|first6=T.\|last7=Ratei\|first7=R.\|last8=Dörken\|first8=B.\|last9=Ludwig\|first9=W. D.\|date=1999\|title=Clinical significance of CD95, Bcl-2 and Bax expression and CD95 function in adult de novo acute myeloid leukemia in context of P-glycoprotein function, maturation stage, and cytogenetics\|url=https://www.ncbi.nlm.nih.gov/pubmed/10602414\|journal=Leukemia\|volume=13\|issue=12\|pages=1943–1953\|doi=10.1038/sj.leu.2401605\|issn=0887-6924\|pmid=10602414}}</ref>.		• MDR1/p-170 protein is positive in blasts and mediates multidrug resistance in adults. This protein functions as a barrier, reducing intracellular concentrations of chemotherapeutics<ref>{{Cite journal\|last=Campos\|first=L.\|last2=Guyotat\|first2=D.\|last3=Jaffar\|first3=C.\|last4=Solary\|first4=E.\|last5=Archimbaud\|first5=E.\|last6=Treille\|first6=D.\|date=1992\|title=Correlation of MDR1/P-170 expression with daunorubicin uptake and sensitivity of leukemic progenitors in acute myeloid leukemia\|url=https://www.ncbi.nlm.nih.gov/pubmed/1353726\|journal=European Journal of Haematology\|volume=48\|issue=5\|pages=254–258\|doi=10.1111/j.1600-0609.1992.tb01803.x\|issn=0902-4441\|pmid=1353726}}</ref><ref>{{Cite journal\|last=Wuchter\|first=C.\|last2=Karawajew\|first2=L.\|last3=Ruppert\|first3=V.\|last4=Büchner\|first4=T.\|last5=Schoch\|first5=C.\|last6=Haferlach\|first6=T.\|last7=Ratei\|first7=R.\|last8=Dörken\|first8=B.\|last9=Ludwig\|first9=W. D.\|date=1999\|title=Clinical significance of CD95, Bcl-2 and Bax expression and CD95 function in adult de novo acute myeloid leukemia in context of P-glycoprotein function, maturation stage, and cytogenetics\|url=https://www.ncbi.nlm.nih.gov/pubmed/10602414\|journal=Leukemia\|volume=13\|issue=12\|pages=1943–1953\|doi=10.1038/sj.leu.2401605\|issn=0887-6924\|pmid=10602414}}</ref>.

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Individual Region Genomic Gain / Loss / LOH==		==Individual Region Genomic Gain / Loss / LOH==
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	\|}		\|}

	<blockquote class='blockedit'>{{Box-round\|title=v4:Genomic Gain/Loss/LOH\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Genomic Gain/Loss/LOH\|The content below was from the old template. Please incorporate above.}}</blockquote>
	• +4 sole; intermediate/poor prognosis		• +4 sole; intermediate/poor prognosis

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	• Loss and haploinsufficiency of ''ETV6'' through deletion may be a leukemogenic step in AML-M0<ref name=":2" />		• Loss and haploinsufficiency of ''ETV6'' through deletion may be a leukemogenic step in AML-M0<ref name=":2" />

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

	• No specific chromosomal abnormality is identified		• No specific chromosomal abnormality is identified
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	• Pediatric: Chromosome 5 aberrations, trisomy 21 and hypodiploidy more common in AML M0 than non-M0 counterparts<ref name=":6">{{Cite journal\|last=Barbaric\|first=Draga\|last2=Alonzo\|first2=Todd A.\|last3=Gerbing\|first3=Robert B.\|last4=Meshinchi\|first4=Soheil\|last5=Heerema\|first5=Nyla A.\|last6=Barnard\|first6=Dorothy R.\|last7=Lange\|first7=Beverly J.\|last8=Woods\|first8=William G.\|last9=Arceci\|first9=Robert J.\|date=2007\|title=Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961\|url=https://www.ncbi.nlm.nih.gov/pubmed/17158236\|journal=Blood\|volume=109\|issue=6\|pages=2314–2321\|doi=10.1182/blood-2005-11-025536\|issn=0006-4971\|pmc=1852193\|pmid=17158236}}</ref>		• Pediatric: Chromosome 5 aberrations, trisomy 21 and hypodiploidy more common in AML M0 than non-M0 counterparts<ref name=":6">{{Cite journal\|last=Barbaric\|first=Draga\|last2=Alonzo\|first2=Todd A.\|last3=Gerbing\|first3=Robert B.\|last4=Meshinchi\|first4=Soheil\|last5=Heerema\|first5=Nyla A.\|last6=Barnard\|first6=Dorothy R.\|last7=Lange\|first7=Beverly J.\|last8=Woods\|first8=William G.\|last9=Arceci\|first9=Robert J.\|date=2007\|title=Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961\|url=https://www.ncbi.nlm.nih.gov/pubmed/17158236\|journal=Blood\|volume=109\|issue=6\|pages=2314–2321\|doi=10.1182/blood-2005-11-025536\|issn=0006-4971\|pmc=1852193\|pmid=17158236}}</ref>

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Gene Mutations (SNV / INDEL)==		==Gene Mutations (SNV / INDEL)==
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	• Co-existence of gene mutations is common		• Co-existence of gene mutations is common
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	• Mutations of ''RUNX1'' occur in ~30% of cases<ref name=":7" />, and correlates with the presence of trisomy 13 and increased ''FLT3'' expression. ''De novo'' cases with RUNX1 mutations are now classified as the provisional entity of AML with mutated RUNX1 in the 2017 WHO<ref name=":0" />.		• Mutations of ''RUNX1'' occur in ~30% of cases<ref name=":7" />, and correlates with the presence of trisomy 13 and increased ''FLT3'' expression. ''De novo'' cases with RUNX1 mutations are now classified as the provisional entity of AML with mutated RUNX1 in the 2017 WHO<ref name=":0" />.

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

Bailey.Glen at 22:19, 6 September 2024

2024-09-06T22:19:37Z

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	__TOC__		__TOC__

	==~~Cancer Category / Type~~==		==WHO Classification of Disease==

	~~[[AML~~\|~~Acute~~ Myeloid ~~Leukemia]]~~		{\| class="wikitable"
			!Structure
	~~==Cancer Sub~~-~~Classification / Subtype==~~		!Disease
			\|-
	Acute ~~Myeloid Leukemia~~ (~~AML~~) with minimal differentiation		\|Book
			\|Haematolymphoid Tumours (5th ed.)
			\|-
			\|Category
			\|Myeloid proliferations and neoplasms
			\|-
			\|Family
			\|Acute myeloid leukaemia
			\|-
			\|Type
			\|Acute myeloid leukaemia, defined by differentiation
			\|-
			\|Subtype(s)
			\|Acute myeloid leukaemia with minimal differentiation
			\|}

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

Bailey.Glen at 21:48, 6 September 2024

2024-09-06T21:48:45Z

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