Anaplastic Large Cell Lymphoma (ALK+/ALK−) - Revision history

Jennie.Thurston at 16:13, 2 February 2025

2025-02-02T16:13:33Z

← Older revision		Revision as of 11:13, 2 February 2025
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	==Primary Author(s)*==		==Primary Author(s)*==
	~~Put your text here~~		Jennie Thurston, PhD., FACMGG
	==WHO Classification of Disease<ref name=":0">Deckert, M, Ferry, JA, Paulus, W, et al. Anaplastic large cell lymphoma (ALK+/ALK−). In: WHO Classification of Tumours Editorial Board. Central nervous system tumours [Internet]. Lyon (France): International Agency for Research on Cancer; 2021 [cited 2025 02 2]. (WHO classification of tumours series, 5th ed.; vol. 6). Available from: <nowiki>https://tumourclassification.iarc.who.int/chapters/45</nowiki>.</ref>==		==WHO Classification of Disease<ref name=":0">Deckert, M, Ferry, JA, Paulus, W, et al. Anaplastic large cell lymphoma (ALK+/ALK−). In: WHO Classification of Tumours Editorial Board. Central nervous system tumours [Internet]. Lyon (France): International Agency for Research on Cancer; 2021 [cited 2025 02 2]. (WHO classification of tumours series, 5th ed.; vol. 6). Available from: <nowiki>https://tumourclassification.iarc.who.int/chapters/45</nowiki>.</ref>==
	{\| class="wikitable"		{\| class="wikitable"
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	==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 CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.		<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 CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
			<references />

Jennie.Thurston: /* Definition / Description of Disease */

2025-02-02T15:27:56Z

Definition / Description of Disease

Show changes

Jennie.Thurston: added additional information on definition and added references

2024-02-28T03:04:24Z

added additional information on definition and added references

← Older revision		Revision as of 22:04, 27 February 2024
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	\|}		\|}
	==Definition / Description of Disease==		==Definition / Description of Disease==
	Anaplastic large cell lymphoma (ALCL) is a distinctive CD30-positive peripheral T-cell lymphoma that is rare in the CNS and is separated into two distinct types: ALK-positive (ALK+ ALCL) and ALK-negative (ALK− ALCL).<ref name=":0" />		Primary central nervous system lymphoma (PCNSL) represents approximately 4% of all primary brain tumors and 1% to 2% of non-Hodgkin lymphoma.<ref>Villano JL, Koshy M, Shaikh H, et al. Age, gender, and racial differences in incidence and survival in primary CNS lymphoma. Br J Cancer. 2011;105:1414-1418.</ref> PCNSL is defined as a lymphoma confined to the brain, spinal cord, and/or eye. Diffuse large B-cell lymphomas make up more than 95% of PCNSL cases.<ref>Camilleri-Broët S, Martin A, Moreau A, et al. Primary central nervous system lymphomas in 72 immunocompetent patients: pathologic findings and clinical correlations. Am J Clin Pathol. 1998;110:607-612.</ref> Anaplastic large cell lymphoma (ALCL) is a distinctive CD30-positive peripheral T-cell lymphoma that is rare in the CNS and is separated into two distinct types: ALK-positive (ALK+ ALCL) and ALK-negative (ALK− ALCL).<ref name=":0" /><ref name=":2">ALK-negative anaplastic large cell lymphoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 12/13/2023, <nowiki>https://ccga.io/index.php/HAEM5:ALK-negative_anaplastic_large_cell_lymphoma</nowiki>.</ref><ref name=":3">ALK-positive anaplastic large cell lymphoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 12/13/2023, <nowiki>https://ccga.io/index.php/HAEM5:ALK-positive_anaplastic_large_cell_lymphoma</nowiki>.</ref>
	==Synonyms / Terminology==		==Synonyms / Terminology==
	None		None
	==Epidemiology / Prevalence==		==Epidemiology / Prevalence==
	ALK+ ALCL occurs from early childhood to young adulthood with a male preponderance.<ref name=":1">George, D.H.; Scheithauer, B.W.; Aker, F.V.; Kurtin, P.J.; Burger, P.C.; Cameselle-Teijeiro, J.; McLendon, R.E.; Parisi, J.E.; Paulus, W.; Roggendorf, W.; et al. Primary Anaplastic Large Cell Lymphoma of the Central Nervous System: Prognostic Effect of ALK-1 Expression. Am. J. Surg. Pathol. 2003, 27, 487–493</ref>		ALK+ ALCL occurs from early childhood to young adulthood with a male preponderance.<ref name=":1">George, D.H.; Scheithauer, B.W.; Aker, F.V.; Kurtin, P.J.; Burger, P.C.; Cameselle-Teijeiro, J.; McLendon, R.E.; Parisi, J.E.; Paulus, W.; Roggendorf, W.; et al. Primary Anaplastic Large Cell Lymphoma of the Central Nervous System: Prognostic Effect of ALK-1 Expression. Am. J. Surg. Pathol. 2003, 27, 487–493</ref><ref name=":3" />

	ALK− ALCL affects adults (median age: 65 years), also with a male preponderance.		ALK− ALCL affects adults (median age: 65 years), also with a male preponderance.<ref name=":2" />
	==Clinical Features==		==Clinical Features==
	{\| class="wikitable"		{\| class="wikitable"
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	\|-		\|-
	\|'''Laboratory Findings'''		\|'''Laboratory Findings'''
	\|~~EXAMPLE Cytopenias~~		\|None
	~~EXAMPLE Lymphocytosis (low level)~~
	\|}		\|}
	==Sites of Involvement==		==Sites of Involvement==
	ALK+ ALCL occurs as single or multiple supratentorial parenchymal lesions with or without infratentorial involvement, and rarely with spinal cord involvement. Extension to involve the meninges and (rarely) the skull can occur.<ref>Karikari, I.O.; Thomas, K.K.; Lagoo, A.; Cummings, T.J.; George, T.M. Primary Cerebral ALK-1-Positive Anaplastic Large Cell Lymphoma in a Child. Pediatr. Neurosurg. 2007, 43, 516–521. [CrossRef] [PubMed]</ref>		ALK+ ALCL occurs as single or multiple supratentorial parenchymal lesions with or without infratentorial involvement, and rarely with spinal cord involvement. Extension to involve the meninges and (rarely) the skull can occur.<ref>Karikari, I.O.; Thomas, K.K.; Lagoo, A.; Cummings, T.J.; George, T.M. Primary Cerebral ALK-1-Positive Anaplastic Large Cell Lymphoma in a Child. Pediatr. Neurosurg. 2007, 43, 516–521. [CrossRef] [PubMed]</ref><ref name=":0" />

	ALK− ALCL occurs as single or multiple lesions, usually supratentorial		ALK− ALCL occurs as single or multiple lesions, usually supratentorial<ref name=":0" />
	==Morphologic Features==		==Morphologic Features==
	ALK+ ALCL shows a diffuse proliferation of large atypical cells with abundant cytoplasm, including hallmark cells with bean-shaped nuclei and an eosinophilic paranuclear area<ref>Jaffe ES. Anaplastic large cell lymphoma: the shifting sands of diagnostic hematopathology. Modern Pathol. 2001;14:219-228.</ref>		ALK+ ALCL shows a diffuse proliferation of large atypical cells with abundant cytoplasm, including hallmark cells with bean-shaped nuclei and an eosinophilic paranuclear area<ref>Jaffe ES. Anaplastic large cell lymphoma: the shifting sands of diagnostic hematopathology. Modern Pathol. 2001;14:219-228.</ref>

	The cerebrospinal fluid may be involved. The large atypical neoplastic cells may have cytoplasmic azurophilic granules		The cerebrospinal fluid may be involved. The large atypical neoplastic cells may have cytoplasmic azurophilic granules<ref name=":0" />
	==Immunophenotype==		==Immunophenotype==
	Put your text here and fill in the table~~<ref>Kadin ME. Primary Ki-1-positive anaplastic large-cell lymphoma: a distinct clinicopathologic entity. Ann Oncol. 1994;5:S25-S30.</ref>~~		Put your text here and fill in the table
	{\| class="wikitable sortable"		{\| class="wikitable sortable"
	\|-		\|-
	!Finding!!Marker		!Finding!!Marker
	\|-		\|-
	\|Positive (universal)\|\|CD30+, ALK+, and EMA+, may express one or more T-cell antigens		\|Positive (universal)\|\|CD30+, ALK+, and EMA+, may express one or more T-cell antigens<ref>Kadin ME. Primary Ki-1-positive anaplastic large-cell lymphoma: a distinct clinicopathologic entity. Ann Oncol. 1994;5:S25-S30.</ref>
	\|-
	~~\|Positive (subset)\|\|EXAMPLE CD2~~
	\|-
	~~\|Negative (universal)\|\|EXAMPLE CD3~~
	\|-
	~~\|Negative (subset)\|\|EXAMPLE CD4~~
	\|}		\|}
	==Chromosomal Rearrangements (Gene Fusions) ALK+ ALCL==		==Chromosomal Rearrangements (Gene Fusions) ALK+ ALCL==
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	!Notes		!Notes
	\|-		\|-
	\|Complex Karyotype		\|Complex Karyotype<ref name=":0" />
	\|
	\|
	\|
	\|
	\|-
	~~\| +7 found in 20% of cases~~
	\|
	\|
	\|
	~~\|EXAMPLE~~:
	~~See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).~~
	\|-
	~~\|<nowiki>+9 in 5 to 10% of cases.</nowiki>~~
	\|
	\|
	\|
	\|
	\|-
	~~\|<nowiki>+X in 5 to 10% of cases.<~~/~~nowiki~~>
	\|
	\|		\|
	\|		\|
	\|		\|
			\|See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with anapestic large cell lymphoma<ref name=":0" />.
	\|}		\|}
	==Gene Mutations (SNV/INDEL)==		==Gene Mutations (SNV/INDEL)==
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	==References==		==References==
	<references />(use "Cite" icon at top of page)		<references />(use "Cite" icon at top of page)
	~~===<ref name=":1" />EXAMPLE Book===~~

	#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.

	==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 CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.		<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 CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.

Jennie.Thurston: /* WHO Classification of Disease */

2024-02-28T02:40:55Z

WHO Classification of Disease

← Older revision		Revision as of 21:40, 27 February 2024
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	==Primary Author(s)*==		==Primary Author(s)*==
	Put your text here		Put your text here
	==WHO Classification of Disease==		==WHO Classification of Disease<ref name=":0">Li, W. The 5th Edition of the World Health Organization Classification of Hematolymphoid Tumors. In Leukemia; Weijie, L., Ed.; Exon Publications: Brisbane, Australia, 2022; pp. 1–21, <nowiki>ISBN 978-0-645-33207-0</nowiki>.</ref>==
	{\| class="wikitable"		{\| class="wikitable"
	\|+		\|+
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	\|}		\|}
	==Definition / Description of Disease==		==Definition / Description of Disease==
	Anaplastic large cell lymphoma (ALCL) is a distinctive CD30-positive peripheral T-cell lymphoma that is rare in the CNS and is separated into two distinct types: ALK-positive (ALK+ ALCL) and ALK-negative (ALK− ALCL).		Anaplastic large cell lymphoma (ALCL) is a distinctive CD30-positive peripheral T-cell lymphoma that is rare in the CNS and is separated into two distinct types: ALK-positive (ALK+ ALCL) and ALK-negative (ALK− ALCL).<ref name=":0" />
	==Synonyms / Terminology==		==Synonyms / Terminology==
	None		None
	==Epidemiology / Prevalence==		==Epidemiology / Prevalence==
	ALK+ ALCL occurs from early childhood to young adulthood with a male preponderance.		ALK+ ALCL occurs from early childhood to young adulthood with a male preponderance.<ref name=":1">George, D.H.; Scheithauer, B.W.; Aker, F.V.; Kurtin, P.J.; Burger, P.C.; Cameselle-Teijeiro, J.; McLendon, R.E.; Parisi, J.E.; Paulus, W.; Roggendorf, W.; et al. Primary Anaplastic Large Cell Lymphoma of the Central Nervous System: Prognostic Effect of ALK-1 Expression. Am. J. Surg. Pathol. 2003, 27, 487–493</ref>

	ALK− ALCL affects adults (median age: 65 years), also with a male preponderance.		ALK− ALCL affects adults (median age: 65 years), also with a male preponderance.
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	\|}		\|}
	==Sites of Involvement==		==Sites of Involvement==
	ALK+ ALCL occurs as single or multiple supratentorial parenchymal lesions with or without infratentorial involvement, and rarely with spinal cord involvement. Extension to involve the meninges and (rarely) the skull can occur.		ALK+ ALCL occurs as single or multiple supratentorial parenchymal lesions with or without infratentorial involvement, and rarely with spinal cord involvement. Extension to involve the meninges and (rarely) the skull can occur.<ref>Karikari, I.O.; Thomas, K.K.; Lagoo, A.; Cummings, T.J.; George, T.M. Primary Cerebral ALK-1-Positive Anaplastic Large Cell Lymphoma in a Child. Pediatr. Neurosurg. 2007, 43, 516–521. [CrossRef] [PubMed]</ref>

	ALK− ALCL occurs as single or multiple lesions, usually supratentorial		ALK− ALCL occurs as single or multiple lesions, usually supratentorial
	==Morphologic Features==		==Morphologic Features==
	ALK+ ALCL shows a diffuse proliferation of large atypical cells with abundant cytoplasm, including hallmark cells with bean-shaped nuclei and an eosinophilic paranuclear area		ALK+ ALCL shows a diffuse proliferation of large atypical cells with abundant cytoplasm, including hallmark cells with bean-shaped nuclei and an eosinophilic paranuclear area<ref>Jaffe ES. Anaplastic large cell lymphoma: the shifting sands of diagnostic hematopathology. Modern Pathol. 2001;14:219-228.</ref>

	The cerebrospinal fluid may be involved. The large atypical neoplastic cells may have cytoplasmic azurophilic granules		The cerebrospinal fluid may be involved. The large atypical neoplastic cells may have cytoplasmic azurophilic granules
	==Immunophenotype==		==Immunophenotype==
	Put your text here and fill in the table		Put your text here and fill in the table<ref>Kadin ME. Primary Ki-1-positive anaplastic large-cell lymphoma: a distinct clinicopathologic entity. Ann Oncol. 1994;5:S25-S30.</ref>
	{\| class="wikitable sortable"		{\| class="wikitable sortable"
	\|-		\|-
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	\|-		\|-
	\|t(2;5)(p23;q35)\|\|''NPM1''::''ALK'' fusion		\|t(2;5)(p23;q35)\|\|''NPM1''::''ALK'' fusion
	\|5' NPM1::3' ALK on der(5). constitutive activation of the catalytic domain of ALK. Kinase function activated by oligomerization of NPM1::ALK mediated by the NPM1 portion\|\|~~EXAMPLE~~ 30 to 50% of ALCL		\|5' NPM1::3' ALK on der(5). constitutive activation of the catalytic domain of ALK. Kinase function activated by oligomerization of NPM1::ALK mediated by the NPM1 portion<ref>Geetha, N.; Sreelesh, K.P.; Nair, R.; Mathews, A. Anaplastic large cell lymphoma presenting as a cerebellar mass. Hematol. Oncol. Stem Cell Ther. 2014, 7, 157–161. </ref><ref>Benharroch D, Meguerian-Bedoyan Z, Lamant L, et al. ALK-positive lymphoma: a single disease with a broad spectrum of morphology. Blood. 1998;91:2076-2084.</ref>\|\|30 to 50% of ALCL<ref name=":0" />
	(~~COSMIC~~)		(COSF198)
	(~~add reference~~)		(<ref>John G Tate, Sally Bamford, Harry C Jubb, Zbyslaw Sondka, David M Beare, Nidhi Bindal, Harry Boutselakis, Charlotte G Cole, Celestino Creatore, Elisabeth Dawson, Peter Fish, Bhavana Harsha, Charlie Hathaway, Steve C Jupe, Chai Yin Kok, Kate Noble, Laura Ponting, Christopher C Ramshaw, Claire E Rye, Helen E Speedy, Ray Stefancsik, Sam L Thompson, Shicai Wang, Sari Ward, Peter J Campbell, Simon A Forbes, COSMIC: the Catalogue Of Somatic Mutations In Cancer, ''Nucleic Acids Research'', Volume 47, Issue D1, 08 January 2019, Pages D941–D947,</ref>)
	\|Yes		\|Yes
	\|Yes		\|Yes
	\|Yes		\|Yes
	\|~~EXAMPLE~~		\|Localized in both cytoplasm and nucleus.<ref name=":0" />
	~~The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference).~~


	Localized in both cytoplasm and nucleus.


	In translocations other than the t(2;5), i.e. in t(2;Var) involving various partners and ALK, the fusion protein has a cytoplasmic localization; they are therefore called "cytoplasm only" ALK+ ALCL.		In translocations other than the t(2;5), i.e. in t(2;Var) involving various partners and ALK, the fusion protein has a cytoplasmic localization; they are therefore called "cytoplasm only" ALK+ ALCL.<ref name=":0" />
	\|-		\|-
	\|t(X;2)(q11;p23)		\|t(X;2)(q11;p23)
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	\|		\|
	\|		\|
	\|For the t(X;2) translocation, localization is restricted to the membrane.		\|For the t(X;2) translocation, localization is restricted to the membrane.<ref name=":0" />
	\|-		\|-
	\|t(1;2)(q25;p23)		\|t(1;2)(q25;p23)
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	\|		\|
	\|		\|
	\|TPM3::ALK is constitutively activated		\|TPM3::ALK is constitutively activated<ref name=":0" />
	\|-		\|-
	\|inv(2)(p23q35)		\|inv(2)(p23q35)
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	\|		\|
	\|		\|
	\|ider(2)(q10)inv(2) has been found in some cases, carrying 2 additional copies of the ATIC::ALK hybrid gene; frequent complex karyotypes		\|ider(2)(q10)inv(2) has been found in some cases, carrying 2 additional copies of the ATIC::ALK hybrid gene; frequent complex karyotypes<ref name=":0" />
	\|-		\|-
	\|t(2;3)(p23;q21)		\|t(2;3)(p23;q21)
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	\|		\|
	\|		\|
	\|the localization is restricted to granules (vesicles) in the cytoplasm		\|the localization is restricted to granules (vesicles) in the cytoplasm<ref name=":0" />
	\|}		\|}
	==Individual Region Genomic Gain/Loss/LOH==		==Individual Region Genomic Gain/Loss/LOH==
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	==References==		==References==
	<references />(use "Cite" icon at top of page)		<references />(use "Cite" icon at top of page)
	===EXAMPLE Book===		===<ref name=":1" />EXAMPLE Book===

	#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.		#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.

Jennie.Thurston: /* Chromosomal Rearrangements (Gene Fusions) ALK+ ALCL */

2024-01-06T18:54:08Z

Chromosomal Rearrangements (Gene Fusions) ALK+ ALCL

← Older revision		Revision as of 13:54, 6 January 2024
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	{\| class="wikitable"		{\| class="wikitable"
	\|'''Signs and Symptoms'''		\|'''Signs and Symptoms'''
	\|Headache, seizures, nausea, fever, or a combination		\|Headache, seizures, nausea, fever, or a combination
	\|-		\|-
	\|'''Laboratory Findings'''		\|'''Laboratory Findings'''
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	\|Negative (subset)\|\|EXAMPLE CD4		\|Negative (subset)\|\|EXAMPLE CD4
	\|}		\|}
	==Chromosomal Rearrangements (Gene Fusions) ALK+ ALCL ==		==Chromosomal Rearrangements (Gene Fusions) ALK+ ALCL==
	Put your text here and fill in the table		Put your text here and fill in the table
	{\| class="wikitable sortable"		{\| class="wikitable sortable"
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	!Notes		!Notes
	\|-		\|-
	\|t(2;5)(p23;q35) \|\|''NPM1''::''ALK'' fusion		\|t(2;5)(p23;q35)\|\|''NPM1''::''ALK'' fusion
	\|5' NPM1::3' ALK on der(5). constitutive activation of the catalytic domain of ALK. Kinase function activated by oligomerization of NPM1::ALK mediated by the NPM1 portion\|\|EXAMPLE 30 to 50% of ALCL		\|5' NPM1::3' ALK on der(5). constitutive activation of the catalytic domain of ALK. Kinase function activated by oligomerization of NPM1::ALK mediated by the NPM1 portion\|\|EXAMPLE 30 to 50% of ALCL
	(COSMIC)		(COSMIC)
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	\|t(2;17)(p23;q23)		\|t(2;17)(p23;q23)
	\|		\|
	\|		\|5'CLTC::3'ALK
	\|		\|very rare, one case reported
	\|		\|
	\|		\|
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	\|		\|
	\|-		\|-
	\|t(2;19)(p23; p13.1)		\|t(2;19)(p23; p13.1)
	\|
	\|
	\|		\|
			\|5'TPM4::3'ALK
			\|very rare, one case reported
	\|		\|
	\|		\|
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	\|		\|
	\|-		\|-
	\| +7 found in 20% of cases		\| +7 found in 20% of cases
	\|		\|
	\|		\|

Jennie.Thurston: /* Cancer Sub-Classification / Subtype */

2024-01-06T18:50:20Z

Cancer Sub-Classification / Subtype

Show changes

Jennie.Thurston: /* WHO Classification of Disease */

2024-01-06T17:54:10Z

WHO Classification of Disease

← Older revision		Revision as of 12:54, 6 January 2024
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	\|-		\|-
	\|Type		\|Type
	\|~~anapestic~~ Large Cell Lymphoma (ALK+/~~ALk~~-)		\|Anaplastic Large Cell Lymphoma (ALK+/ALK-)
	\|-		\|-
	\|Subtype		\|Subtype

Jennie.Thurston: Added WHO classification Table

2024-01-06T17:53:08Z

Added WHO classification Table

← Older revision		Revision as of 12:53, 6 January 2024
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	\|-		\|-
	\|Book		\|Book
	\|Central Nervous System Tumours ~~WHO Classification of Tumours~~ 5th ~~edition, volume 6~~		\|WHO Classification of Tumours Central Nervous System Tumours (5th ed.)
	\|-		\|-
	\|Category		\|Category

Jennie.Thurston: Added WHO classification Table

2024-01-06T17:17:41Z

Added WHO classification Table

@@ Line 1: / Line 1: @@
 ==Primary Author(s)*==
 Put your text here
-==Cancer Category/Type==
+==WHO Classification of Disease==
-Put your text here
+{| class="wikitable"
 ==Cancer Sub-Classification / Subtype==
 Put your text here

Jennelleh: Created page with "==Primary Author(s)*== Put your text here ==Cancer Category/Type== Put your text here ==Cancer Sub-Classification / Subtype== Put your text here ==Definition / Description of..."

2023-07-02T14:15:29Z

Created page with "==Primary Author(s)*== Put your text here ==Cancer Category/Type== Put your text here ==Cancer Sub-Classification / Subtype== Put your text here ==Definition / Description of..."

New page

==Primary Author(s)*==
Put your text here
==Cancer Category/Type==
Put your text here
==Cancer Sub-Classification / Subtype==
Put your text here
==Definition / Description of Disease==
Put your text here
==Synonyms / Terminology==
Put your text here
==Epidemiology / Prevalence==
Put your text here
==Clinical Features==
Put your text here and fill in the table
{| class="wikitable"
|'''Signs and Symptoms'''
|EXAMPLE Asymptomatic (incidental finding on complete blood counts)
EXAMPLE B-symptoms (weight loss, fever, night sweats)

EXAMPLE Fatigue

EXAMPLE Lymphadenopathy (uncommon)
|-
|'''Laboratory Findings'''
|EXAMPLE Cytopenias
EXAMPLE Lymphocytosis (low level)
|}
==Sites of Involvement==
Put your text here
==Morphologic Features==
Put your text here
==Immunophenotype==
Put your text here and fill in the table
{| class="wikitable sortable"
|-
!Finding!!Marker
|-
|Positive (universal)||EXAMPLE CD1
|-
|Positive (subset)||EXAMPLE CD2
|-
|Negative (universal)||EXAMPLE CD3
|-
|Negative (subset)||EXAMPLE CD4
|}
==Chromosomal Rearrangements (Gene Fusions)==
Put your text here and fill in the table
{| class="wikitable sortable"
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|EXAMPLE t(9;22)(q34;q11.2)||EXAMPLE 3'ABL1 / 5'BCR||EXAMPLE der(22)||EXAMPLE 20% (COSMIC)
EXAMPLE 30% (add reference)
|Yes
|No
|Yes
|EXAMPLE
The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference).
|}
==Individual Region Genomic Gain/Loss/LOH==
Put your text here and fill in the table
{| class="wikitable sortable"
|-
!Chr #!!Gain / Loss / Amp / LOH!!Minimal Region Genomic Coordinates [Genome Build]!!Minimal Region Cytoband
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|EXAMPLE
7
|EXAMPLE Loss
|EXAMPLE
chr7:1- 159,335,973 [hg38]
|EXAMPLE
chr7
|Yes
|Yes
|No
|EXAMPLE
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add reference).
|-
|EXAMPLE
8
|EXAMPLE Gain
|EXAMPLE
chr8:1-145,138,636 [hg38]
|EXAMPLE
chr8
|No
|No
|No
|EXAMPLE
Common recurrent secondary finding for t(8;21) (add reference).
|}
==Characteristic Chromosomal Patterns==
Put your text here
{| class="wikitable sortable"
|-
!Chromosomal Pattern
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|EXAMPLE
Co-deletion of 1p and 18q
|Yes
|No
|No
|EXAMPLE:
See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).
|}
==Gene Mutations (SNV/INDEL)==
Put your text here and fill in the table
{| class="wikitable sortable"
|-
!Gene; Genetic Alteration!!'''Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other)'''!!'''Prevalence (COSMIC / TCGA / Other)'''!!'''Concomitant Mutations'''!!'''Mutually Exclusive Mutations'''
!'''Diagnostic Significance (Yes, No or Unknown)'''
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|EXAMPLE: TP53; Variable LOF mutations
EXAMPLE:

EGFR; Exon 20 mutations

EXAMPLE: BRAF; Activating mutations
|EXAMPLE: TSG
|EXAMPLE: 20% (COSMIC)
EXAMPLE: 30% (add Reference)
|EXAMPLE: IDH1 R123H
|EXAMPLE: EGFR amplification
|
|
|
|EXAMPLE: Excludes hairy cell leukemia (HCL) (add reference).
|}Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
==Epigenomic Alterations==
Put your text here
==Genes and Main Pathways Involved==
Put your text here and fill in the table
{| class="wikitable sortable"
|-
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
|-
|EXAMPLE: BRAF and MAP2K1; Activating mutations
|EXAMPLE: MAPK signaling
|EXAMPLE: Increased cell growth and proliferation
|-
|EXAMPLE: CDKN2A; Inactivating mutations
|EXAMPLE: Cell cycle regulation
|EXAMPLE: Unregulated cell division
|-
|EXAMPLE: KMT2C and ARID1A; Inactivating mutations
|EXAMPLE: Histone modification, chromatin remodeling
|EXAMPLE: Abnormal gene expression program
|}
==Genetic Diagnostic Testing Methods==
Put your text here
==Familial Forms==
Put your text here
==Additional Information==
Put your text here
==Links==
Put your text placeholder here (use "Link" icon at top of page)
==References==
<references />(use "Cite" icon at top of page)
===EXAMPLE Book===

#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.

==Notes==
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