HAEM5:B-lymphoblastic leukaemia/lymphoma with BCR::ABL1 fusion - Revision history

Bailey.Glen at 17:10, 3 July 2025

2025-07-03T17:10:14Z

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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 21:29, 25 May 2025

2025-05-25T21:29:37Z

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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 20:06, 25 May 2025

2025-05-25T20:06:01Z

← Older revision		Revision as of 15:06, 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
	\|		\|Philadelphia chromosome–positive (Ph+) B-ALL/LBL
	\|}		\|}

Bailey.Glen at 17:32, 24 March 2025

2025-03-24T17:32:47Z

← Older revision		Revision as of 12:32, 24 March 2025
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	{{DISPLAYTITLE:B-lymphoblastic leukaemia/lymphoma with BCR::ABL1 fusion}}		{{DISPLAYTITLE:B-lymphoblastic leukaemia/lymphoma with BCR::ABL1 fusion}}

	[[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)*==
	Afia Hasnain, MBBS, PhD; Yassmine Akkari, PhD, FACMG		Afia Hasnain, MBBS, PhD; Yassmine Akkari, PhD, FACMG

	~~__TOC__~~

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

Bailey.Glen: Removed old template contents

2025-02-11T15:20:51Z

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Bailey.Glen at 18:41, 10 February 2025

2025-02-10T18:41:09Z

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Bailey.Glen at 18:13, 10 February 2025

2025-02-10T18:13:06Z

← Older revision		Revision as of 13:13, 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>

	The presenting features are generally similar to those seen in patients with other B-ALLs. Most children with B-ALL with ''BCR-ABL1'' are considered to have high risk on the basis of age and white blood cell count (WBC). Patients tend to have a high WBC count at presentation, and although they may have organ involvement, lymphomatous presentations are rare.		The presenting features are generally similar to those seen in patients with other B-ALLs. Most children with B-ALL with ''BCR-ABL1'' are considered to have high risk on the basis of age and white blood cell count (WBC). Patients tend to have a high WBC count at presentation, and although they may have organ involvement, lymphomatous presentations are rare.

			<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>

	Put your text here and/or fill in the table		Put your text here and/or fill in the table
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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>

	The pediatric and adult Ph + B-ALL has been associated with the worst prognosis of the major cytogenetic subtypes of B- ALL. However, therapy with tyrosine kinase inhibitors (TKIs) has had a significantly favorable effect on outcome. A major molecular response is defined as a ≥3-log reduction in BCR-ABL1 transcript compared with the standardized baseline.		The pediatric and adult Ph + B-ALL has been associated with the worst prognosis of the major cytogenetic subtypes of B- ALL. However, therapy with tyrosine kinase inhibitors (TKIs) has had a significantly favorable effect on outcome. A major molecular response is defined as a ≥3-log reduction in BCR-ABL1 transcript compared with the standardized baseline.
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	The presence of IKZF1 deletion has been associated with poor outcome and high risk of re- lapse. <ref>{{Cite journal\|last=van der Veer\|first=Arian\|last2=Zaliova\|first2=Marketa\|last3=Mottadelli\|first3=Federica\|last4=De Lorenzo\|first4=Paola\|last5=Te Kronnie\|first5=Gertruuy\|last6=Harrison\|first6=Christine J.\|last7=Cavé\|first7=Hélène\|last8=Trka\|first8=Jan\|last9=Saha\|first9=Vaskar\|date=2014-03-13\|title=IKZF1 status as a prognostic feature in BCR-ABL1-positive childhood ALL\|url=https://pubmed.ncbi.nlm.nih.gov/24366361\|journal=Blood\|volume=123\|issue=11\|pages=1691–1698\|doi=10.1182/blood-2013-06-509794\|issn=1528-0020\|pmid=24366361}}</ref>		The presence of IKZF1 deletion has been associated with poor outcome and high risk of re- lapse. <ref>{{Cite journal\|last=van der Veer\|first=Arian\|last2=Zaliova\|first2=Marketa\|last3=Mottadelli\|first3=Federica\|last4=De Lorenzo\|first4=Paola\|last5=Te Kronnie\|first5=Gertruuy\|last6=Harrison\|first6=Christine J.\|last7=Cavé\|first7=Hélène\|last8=Trka\|first8=Jan\|last9=Saha\|first9=Vaskar\|date=2014-03-13\|title=IKZF1 status as a prognostic feature in BCR-ABL1-positive childhood ALL\|url=https://pubmed.ncbi.nlm.nih.gov/24366361\|journal=Blood\|volume=123\|issue=11\|pages=1691–1698\|doi=10.1182/blood-2013-06-509794\|issn=1528-0020\|pmid=24366361}}</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>

	The most common accompanying chromosomal abnormalities include monosomy 7 (including deletion of the IKZF1 gene) (18%), monosomy 9 or 9p deletion (9%), and gain of 1q (8%).		The most common accompanying chromosomal abnormalities include monosomy 7 (including deletion of the IKZF1 gene) (18%), monosomy 9 or 9p deletion (9%), and gain of 1q (8%).
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	\|}		\|}

			<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>

	The t(9;22) results in the production of a BCR-ABL1 fusion protein. The majority of pediatric and half of adult t(9;22) positive B-ALL involve the minor breakpoint cluster region (m-bcr) encoding a smaller p190 fusion protein in contrast to chronic myelogenous leukemia (CML), where it involves the major breakpoint cluster region (M-bcr). <ref>{{Cite journal\|last=Woo\|first=Jennifer S.\|last2=Alberti\|first2=Michael O.\|last3=Tirado\|first3=Carlos A.\|date=2014\|title=Childhood B-acute lymphoblastic leukemia: a genetic update\|url=https://pubmed.ncbi.nlm.nih.gov/24949228\|journal=Experimental Hematology & Oncology\|volume=3\|pages=16\|doi=10.1186/2162-3619-3-16\|issn=2162-3619\|pmc=4063430\|pmid=24949228}}</ref>		The t(9;22) results in the production of a BCR-ABL1 fusion protein. The majority of pediatric and half of adult t(9;22) positive B-ALL involve the minor breakpoint cluster region (m-bcr) encoding a smaller p190 fusion protein in contrast to chronic myelogenous leukemia (CML), where it involves the major breakpoint cluster region (M-bcr). <ref>{{Cite journal\|last=Woo\|first=Jennifer S.\|last2=Alberti\|first2=Michael O.\|last3=Tirado\|first3=Carlos A.\|date=2014\|title=Childhood B-acute lymphoblastic leukemia: a genetic update\|url=https://pubmed.ncbi.nlm.nih.gov/24949228\|journal=Experimental Hematology & Oncology\|volume=3\|pages=16\|doi=10.1186/2162-3619-3-16\|issn=2162-3619\|pmc=4063430\|pmid=24949228}}</ref>

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

	''BCR'' and ''ABL1''		''BCR'' and ''ABL1''

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

Bailey.Glen at 22:25, 6 September 2024

2024-09-06T22:25:41Z

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	__TOC__		__TOC__

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

	B-~~Lymphoblastic Leukemia/Lymphoma~~		{\| class="wikitable"
			!Structure
	~~==Cancer Sub~~-~~Classification~~ / Subtype==		!Disease
			\|-
	B-~~Lymphoblastic Leukemia~~/~~Lymphoma~~ with ~~t(9;22)(q34.1;q11.2); ''~~BCR-ABL1''		\|Book
			\|Haematolymphoid Tumours (5th ed.)
			\|-
			\|Category
			\|B-cell lymphoid proliferations and lymphomas
			\|-
			\|Family
			\|Precursor B-cell neoplasms
			\|-
			\|Type
			\|B-lymphoblastic leukaemias/lymphomas
			\|-
			\|Subtype(s)
			\|B-lymphoblastic leukaemia/lymphoma with BCR::ABL1 fusion
			\|}

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

Bailey.Glen at 21:51, 6 September 2024

2024-09-06T21:51:43Z

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Bailey.Glen: Undo revision 14826 by Bailey.Glen (talk)

2024-09-06T19:55:00Z

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