STBT5:NTRK-rearranged spindle cell neoplasm (emerging) - Revision history

Kathleen.Schieffer at 18:48, 26 February 2026

2026-02-26T18:48:36Z

← Older revision		Revision as of 13:48, 26 February 2026
Line 130:		Line 130:
	\|}		\|}
	==Genetic Diagnostic Testing Methods==		==Genetic Diagnostic Testing Methods==
	'~~'Immunohistochemistry:'' Antibodies have been developed for detection of~~ ''~~NTRK'' fusions and are being used in clinical laboratories.~~ Immunohistochemistry has a fast turnaround time, but sensitivity and specificity for detection of ''NTRK'' fusions are lower than other methods listed here. In sarcomas in particular, false positives can be seen in neural-derived tumors and in tumors harboring ''~~BCOR~~'' alterations<ref name=":1" /><ref>{{Cite journal\|last=Solomon\|first=James P.\|last2=Linkov\|first2=Irina\|last3=Rosado\|first3=Andrea\|last4=Mullaney\|first4=Kerry\|last5=Rosen\|first5=Ezra Y.\|last6=Frosina\|first6=Denise\|last7=Jungbluth\|first7=Achim A.\|last8=Zehir\|first8=Ahmet\|last9=Benayed\|first9=Ryma\|date=2020-01\|title=NTRK fusion detection across multiple assays and 33,997 cases: diagnostic implications and pitfalls\|url=https://pubmed.ncbi.nlm.nih.gov/31375766\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=33\|issue=1\|pages=38–46\|doi=10.1038/s41379-019-0324-7\|issn=1530-0285\|pmc=7437403\|pmid=31375766}}</ref><ref>{{Cite journal\|last=Hung\|first=Yin P.\|last2=Fletcher\|first2=Christopher D. M.\|last3=Hornick\|first3=Jason L.\|date=2018-10\|title=Evaluation of pan-TRK immunohistochemistry in infantile fibrosarcoma, lipofibromatosis-like neural tumour and histological mimics\|url=https://pubmed.ncbi.nlm.nih.gov/29863809\|journal=Histopathology\|volume=73\|issue=4\|pages=634–644\|doi=10.1111/his.13666\|issn=1365-2559\|pmid=29863809}}</ref><ref>{{Cite journal\|last=Kao\|first=Yu-Chien\|last2=Sung\|first2=Yun-Shao\|last3=Argani\|first3=Pedram\|last4=Swanson\|first4=David\|last5=Alaggio\|first5=Rita\|last6=Tap\|first6=William\|last7=Wexler\|first7=Leonard\|last8=Dickson\|first8=Brendan C.\|last9=Antonescu\|first9=Cristina R.\|date=2020-07\|title=NTRK3 overexpression in undifferentiated sarcomas with YWHAE and BCOR genetic alterations\|url=https://pubmed.ncbi.nlm.nih.gov/32034283\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=33\|issue=7\|pages=1341–1349\|doi=10.1038/s41379-020-0495-2\|issn=1530-0285\|pmc=7329614\|pmid=32034283}}</ref>. Confirmatory testing with other molecular-based methods is recommended.		'''Immunohistochemistry'''

			* Antibodies have been developed for detection of ''NTRK'' fusions and are being used in clinical laboratories.
			* Immunohistochemistry has a fast turnaround time, but sensitivity and specificity for detection of ''NTRK'' fusions are lower than other methods listed here.
			* In sarcomas in particular, false positives can be seen in neural-derived tumors and in tumors harboring ''BCOR'' alterations<ref name=":1" /><ref>{{Cite journal\|last=Solomon\|first=James P.\|last2=Linkov\|first2=Irina\|last3=Rosado\|first3=Andrea\|last4=Mullaney\|first4=Kerry\|last5=Rosen\|first5=Ezra Y.\|last6=Frosina\|first6=Denise\|last7=Jungbluth\|first7=Achim A.\|last8=Zehir\|first8=Ahmet\|last9=Benayed\|first9=Ryma\|date=2020-01\|title=NTRK fusion detection across multiple assays and 33,997 cases: diagnostic implications and pitfalls\|url=https://pubmed.ncbi.nlm.nih.gov/31375766\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=33\|issue=1\|pages=38–46\|doi=10.1038/s41379-019-0324-7\|issn=1530-0285\|pmc=7437403\|pmid=31375766}}</ref><ref>{{Cite journal\|last=Hung\|first=Yin P.\|last2=Fletcher\|first2=Christopher D. M.\|last3=Hornick\|first3=Jason L.\|date=2018-10\|title=Evaluation of pan-TRK immunohistochemistry in infantile fibrosarcoma, lipofibromatosis-like neural tumour and histological mimics\|url=https://pubmed.ncbi.nlm.nih.gov/29863809\|journal=Histopathology\|volume=73\|issue=4\|pages=634–644\|doi=10.1111/his.13666\|issn=1365-2559\|pmid=29863809}}</ref><ref>{{Cite journal\|last=Kao\|first=Yu-Chien\|last2=Sung\|first2=Yun-Shao\|last3=Argani\|first3=Pedram\|last4=Swanson\|first4=David\|last5=Alaggio\|first5=Rita\|last6=Tap\|first6=William\|last7=Wexler\|first7=Leonard\|last8=Dickson\|first8=Brendan C.\|last9=Antonescu\|first9=Cristina R.\|date=2020-07\|title=NTRK3 overexpression in undifferentiated sarcomas with YWHAE and BCOR genetic alterations\|url=https://pubmed.ncbi.nlm.nih.gov/32034283\|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc\|volume=33\|issue=7\|pages=1341–1349\|doi=10.1038/s41379-020-0495-2\|issn=1530-0285\|pmc=7329614\|pmid=32034283}}</ref>. Confirmatory testing with other molecular-based methods is recommended.

	''Fluorescent in situ hybridization (FISH)'': Breakapart probes for ''NTRK1, NTRK2,'' and ''NTRK3'' can identify breaks in these genes, although the probes not widely available in clinical laboratories. Benefits of this approach include high sensitivity, particularly in samples with low tumor content, fast turnaround time, and only require a few unstained slides. This approach does not allow for identification of the fusion partner nor for a detailed evaluation of oncogenicity.

	''~~Reverse transcriptase polymerase chain reaction (RT-PCR)~~'' ~~can only identify specific fusion pairs~~ (~~e.g. '~~'~~ETV6::NTRK3~~''~~), such that alternate pairings will be missed.~~ '' ~~''With the availability of RNA-based sequencing, this technique is now rarely used clinically.~~		'''''Fluorescent in situ hybridization (FISH)'''''

			* Breakapart probes for ''NTRK1, NTRK2,'' and ''NTRK3'' can identify breaks in these genes, although the probes not widely available in clinical laboratories.
			* Benefits of this approach include high sensitivity, particularly in samples with low tumor content, fast turnaround time, and only require a few unstained slides.
			* This approach does not allow for identification of the fusion partner nor for a detailed evaluation of oncogenicity.'

	''RNA-based sequencing'' ~~is becoming~~ widely used for comprehensive fusion detection. It is often performed as a comprehensive panel, so ''NTRK'' fusions can be assessed at the same time as many other sarcoma-associated fusions. A platform that supports fusion detection in a partner agnostic manner such as anchored multiplex PCR or hybridization capture methods is preferred<ref>{{Cite journal\|last=Amatu\|first=A.\|last2=Sartore-Bianchi\|first2=A.\|last3=Bencardino\|first3=K.\|last4=Pizzutilo\|first4=E. G.\|last5=Tosi\|first5=F.\|last6=Siena\|first6=S.\|date=2019-11-01\|title=Tropomyosin receptor kinase (TRK) biology and the role of NTRK gene fusions in cancer\|url=https://pubmed.ncbi.nlm.nih.gov/31738427\|journal=Annals of Oncology: Official Journal of the European Society for Medical Oncology\|volume=30\|issue=Suppl_8\|pages=viii5–viii15\|doi=10.1093/annonc/mdz383\|issn=1569-8041\|pmc=6859819\|pmid=31738427}}</ref>. A systematic approach should be used to assess oncogenicity of ''NTRK'' fusions including stranding and directionality, inclusion of the kinase domain, and review of the literature<ref>{{Cite journal\|last=Saliba\|first=Jason\|last2=Church\|first2=Alanna J.\|last3=Rao\|first3=Shruti\|last4=Danos\|first4=Arpad\|last5=Furtado\|first5=Larissa V.\|last6=Laetsch\|first6=Theodore\|last7=Zhang\|first7=Liying\|last8=Nardi\|first8=Valentina\|last9=Lin\|first9=Wan-Hsin\|date=2022-06\|title=Standardized evidence-based approach for assessment of oncogenic and clinical significance of NTRK fusions\|url=https://pubmed.ncbi.nlm.nih.gov/35366592\|journal=Cancer Genetics\|volume=264-265\|pages=50–59\|doi=10.1016/j.cancergen.2022.03.001\|issn=2210-7762\|pmc=9252326\|pmid=35366592}}</ref>.
			'''''Reverse transcriptase polymerase chain reaction (RT-PCR)'''''

			* Can only identify specific fusion pairs (e.g. ''ETV6::NTRK3''), such that alternate pairings will be missed. '' ''
			* With the availability of RNA-based sequencing, this technique is now rarely used clinically.


			'''''RNA-based sequencing'''''

			* Becoming widely used for comprehensive fusion detection. It is often performed as a comprehensive panel, so ''NTRK'' fusions can be assessed at the same time as many other sarcoma-associated fusions.
			* A platform that supports fusion detection in a partner agnostic manner such as anchored multiplex PCR or hybridization capture methods is preferred<ref>{{Cite journal\|last=Amatu\|first=A.\|last2=Sartore-Bianchi\|first2=A.\|last3=Bencardino\|first3=K.\|last4=Pizzutilo\|first4=E. G.\|last5=Tosi\|first5=F.\|last6=Siena\|first6=S.\|date=2019-11-01\|title=Tropomyosin receptor kinase (TRK) biology and the role of NTRK gene fusions in cancer\|url=https://pubmed.ncbi.nlm.nih.gov/31738427\|journal=Annals of Oncology: Official Journal of the European Society for Medical Oncology\|volume=30\|issue=Suppl_8\|pages=viii5–viii15\|doi=10.1093/annonc/mdz383\|issn=1569-8041\|pmc=6859819\|pmid=31738427}}</ref>.
			* A systematic approach should be used to assess oncogenicity of ''NTRK'' fusions including stranding and directionality, inclusion of the kinase domain, and review of the literature<ref>{{Cite journal\|last=Saliba\|first=Jason\|last2=Church\|first2=Alanna J.\|last3=Rao\|first3=Shruti\|last4=Danos\|first4=Arpad\|last5=Furtado\|first5=Larissa V.\|last6=Laetsch\|first6=Theodore\|last7=Zhang\|first7=Liying\|last8=Nardi\|first8=Valentina\|last9=Lin\|first9=Wan-Hsin\|date=2022-06\|title=Standardized evidence-based approach for assessment of oncogenic and clinical significance of NTRK fusions\|url=https://pubmed.ncbi.nlm.nih.gov/35366592\|journal=Cancer Genetics\|volume=264-265\|pages=50–59\|doi=10.1016/j.cancergen.2022.03.001\|issn=2210-7762\|pmc=9252326\|pmid=35366592}}</ref>.

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

Kathleen.Schieffer at 18:46, 26 February 2026

2026-02-26T18:46:22Z

Show changes

James.Solomon: Included references

2026-02-26T13:06:01Z

Included references

Show changes

Richard.Glen at 01:27, 26 February 2026

2026-02-26T01:27:41Z

← Older revision		Revision as of 20:27, 25 February 2026
Line 225:		Line 225:
	==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>		(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>
			<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.

James.Solomon: /* Characteristic Chromosomal or Other Global Mutational Patterns */

2025-11-07T16:00:44Z

Characteristic Chromosomal or Other Global Mutational Patterns

← Older revision		Revision as of 11:00, 7 November 2025
Line 88:		Line 88:
	\|}		\|}
	==Characteristic Chromosomal or Other Global Mutational Patterns==		==Characteristic Chromosomal or Other Global Mutational Patterns==
			N/A -

	Put your text here and fill in the table <span style="color:#0070C0">(I''nstructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>		Put your text here and fill in the table <span style="color:#0070C0">(I''nstructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>
	{\| class="wikitable sortable"		{\| class="wikitable sortable"
Line 123:		Line 125:
	\|}		\|}
	==Gene Mutations (SNV/INDEL)==		==Gene Mutations (SNV/INDEL)==
			N/A -

	Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.'') </span>		Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.'') </span>
	{\| class="wikitable sortable"		{\| class="wikitable sortable"

James.Solomon at 21:52, 22 September 2025

2025-09-22T21:52:27Z

@@ Line 44: / Line 44: @@
 ==Gene Rearrangements==
-Fusions involving ''NTRK1'' are the most common oncogenic driver in ''NTRK-''rearranged spindle cell neoplasm, but ''NTRK2'' or ''NTRK3'' fusions are also occasionally seen (PMID: 30276917, 30520818). In-frame fusions that include the kinase domain of any of ''NTRK1'', ''NTRK2'', or ''NTRK3'' could represent the oncogenic driver, and there are over 80 partners that have been reported for ''NTRK'' fusions (PMID: 31075511).  As this is an emerging entity, prevalence of specific pairings is unknown.  RNA sequencing-based fusion detection methods provide the most information about the identity of both gene partners (see Genetic Testing Diagnostic Methods section below). <span style="color:#0070C0">(''Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>
+Fusions involving ''NTRK1'' are the most common oncogenic driver in ''NTRK-''rearranged spindle cell neoplasm, but ''NTRK2'' or ''NTRK3'' fusions are also occasionally seen (PMID: 30276917, 30520818). In-frame fusions that include the kinase domain of any of ''NTRK1'', ''NTRK2'', or ''NTRK3'' could represent the oncogenic driver, and there are over 80 partners that have been reported for ''NTRK'' fusions (PMID: 31075511).  As this is an emerging entity, prevalence of specific pairings is unknown.  RNA sequencing-based fusion detection methods provide the most information about the identity of both gene partners (see Genetic Testing Diagnostic Methods section below).
 {| class="wikitable sortable"
 |-
@@ Line 53: / Line 53: @@
 !Clinical Relevance Details/Other Notes
 |-
-|''NTRK1''||''TPM3::NTRK1''||<span class="blue-text">EXAMPLE:</span> The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1.||<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2)
+|''NTRK1''||''TPM3::NTRK1''
-|<span class="blue-text">EXAMPLE:</span> Common (CML)
+''TPR::NTRK1''
-Other fusion partners include ''KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1''
+Many other fusion partners also possible
-|<span class="blue-text">EXAMPLE:</span> Fusions result in constitutive activation of the ''ALK'' tyrosine kinase. The most common ''ALK'' fusion is ''EML4::ALK'', with breakpoints in intron 19 of ''ALK''. At the transcript level, a variable (5’) partner gene is fused to 3’ ''ALK'' at exon 20. Rarely, ''ALK'' fusions contain exon 19 due to breakpoints in intron 18.
+|In-frame fusions that include the tyrosine kinase domain result in constitutive activation of the neurotrophic tyrosine receptor kinase and downstream pathways including the MAP-kinase and PI3-kinase pathways.||t(1;1)(q21.3;q23.1)
-|<span class="blue-text">EXAMPLE:</span> N/A
+t(1;1)(q31.1;q23.1)
-Both balanced and unbalanced forms are observed by FISH (add references).
+t(1;1)(q22;q23.1)
 |}
 ==Individual Region Genomic Gain/Loss/LOH==
@@ Line 96: / Line 79: @@
 !Clinical Relevance Details/Other Notes
 |-
-|<span class="blue-text">EXAMPLE:</span>
+|9
 |Loss
-|<span class="blue-text">EXAMPLE:</span> Loss
+|chr9p21
-|<span class="blue-text">EXAMPLE:</span>
+|''CDKN2A''
+|
+|
 |}

James.Solomon: /* Primary Author(s)* */

2025-09-22T21:19:17Z

Primary Author(s)*

Show changes

Bailey.Glen at 18:09, 3 July 2025

2025-07-03T18:09:04Z

← Older revision		Revision as of 13:09, 3 July 2025
Line 29:		Line 29:
	\|}		\|}

	~~==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 22:28, 25 May 2025

2025-05-25T22:28:33Z

← Older revision		Revision as of 17:28, 25 May 2025
Line 118:		Line 118:
	{\| 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>
Line 173:		Line 173:
	!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>
Line 206:		Line 206:
	{\| 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 21:04, 25 May 2025

2025-05-25T21:04:53Z

← Older revision		Revision as of 16:04, 25 May 2025
Line 44:		Line 44:
	<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
	\|		\|Lipofibromatosis-like neural tumour; NTRK-positive tumour resembling peripheral nerve sheath tumour
	\|-		\|-
	\|Not Recommended		\|Not Recommended
	\|		\|N/A
	\|}		\|}