HAEM5:B lymphoblastic leukaemia/lymphoma with IGH::IL3 fusion - Revision history

Miguel.GonzalezMancera: /* Gene Rearrangements */

2025-11-11T20:27:36Z

Gene Rearrangements

← Older revision		Revision as of 15:27, 11 November 2025
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	T: N/A		T: N/A

	P: Too few cases to accurately assess prognosis		P: Too few cases to accurately assess prognosis; however, A small case series suggested an intermediate prognosis, with a poor response to treatment and high levels of measurable residual disease at the end of induction<ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.
	\|No (NCCN)		\|No (NCCN)
	\|~~A small case series suggested an intermediate prognosis~~, with a ~~poor response to treatment~~ and ~~high levels of measurable residual disease at the end of induction~~<ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.		\|Clinical presentations vary widely. Some patients present with a typical B-ALL/LBL phenotype characterized by elevated blasts, while others exhibit only asymptomatic eosinophilia with minimal or no circulating blasts. In additional cases, the disease manifests as hypereosinophilic syndrome, featuring organomegaly, respiratory symptoms, cutaneous lesions, neurologic findings, thrombotic events, or eosinophilic cardiac involvement<ref>{{Cite journal\|last=Tono-oka\|first=T.\|last2=Sato\|first2=Y.\|last3=Matsumoto\|first3=T.\|last4=Ueno\|first4=N.\|last5=Ohkawa\|first5=M.\|last6=Shikano\|first6=T.\|last7=Takeda\|first7=T.\|date=1984\|title=Hypereosinophilic syndrome in acute lymphoblastic leukemia with a chromosome translocation [t(5q;14q)]\|url=https://pubmed.ncbi.nlm.nih.gov/6583469\|journal=Medical and Pediatric Oncology\|volume=12\|issue=1\|pages=33–37\|doi=10.1002/mpo.2950120109\|issn=0098-1532\|pmid=6583469}}</ref><ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref><ref>{{Cite journal\|last=Toboso\|first=Dolores Gómez\|last2=Campos\|first2=Carmen Benet\|date=2017-07-20\|title=Peripheral eosinophilia as the first manifestation of B-cell acute lymphoblastic leukemia with t(5;14)(q31;q32)\|url=https://pubmed.ncbi.nlm.nih.gov/28729339\|journal=Blood\|volume=130\|issue=3\|pages=380\|doi=10.1182/blood-2016-12-754812\|issn=1528-0020\|pmid=28729339}}</ref>.
	\|}		\|}

Miguel.GonzalezMancera: /* Individual Region Genomic Gain/Loss/LOH */

2025-11-11T20:20:42Z

Individual Region Genomic Gain/Loss/LOH

← Older revision		Revision as of 15:20, 11 November 2025
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	==Individual Region Genomic Gain/Loss/LOH==		==Individual Region Genomic Gain/Loss/LOH==

			No recurrent chromosomal gains or losses have been described<ref name=":0">{{Cite journal\|title=BlueBooksOnline\|url=https://tumourclassification.iarc.who.int/chaptercontent/63/340}}</ref>.
	Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. 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: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.'') </span>
	{\| class="wikitable sortable"		{\| class="wikitable sortable"
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	==Characteristic Chromosomal or Other Global Mutational Patterns==		==Characteristic Chromosomal or Other Global Mutational Patterns==

			No recurrent chromosomal or other global mutational patterns have been described<ref name=":0" />.
	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"

Miguel.GonzalezMancera: /* Genetic Diagnostic Testing Methods */

2025-11-11T20:00:03Z

Genetic Diagnostic Testing Methods

← Older revision		Revision as of 15:00, 11 November 2025
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	==Genetic Diagnostic Testing Methods==		==Genetic Diagnostic Testing Methods==

	The t(5;14)(q31.1;q32) translocation can be detected by karyotyping or FISH; however, in cases with a low blast count, or a cytogenetically cryptic rearrangement may require Next-generation sequencing assays to increase sensitivity<ref>{{Cite journal\|last=Guenzel\|first=Adam J.\|last2=Smadbeck\|first2=James B.\|last3=Golden\|first3=Crystal L.\|last4=Williamson\|first4=Cynthia M.\|last5=Benevides Demasi\|first5=Jonna C.\|last6=Vasmatzis\|first6=George\|last7=Pearce\|first7=Kathryn E.\|last8=Olteanu\|first8=Horatiu\|last9=Xu\|first9=Xinjie\|date=2021-08\|title=Clinical utility of next generation sequencing to detect IGH/IL3 rearrangements [t(5;14)(q31.1;q32.1)] in B-lymphoblastic leukemia/lymphoma\|url=https://pubmed.ncbi.nlm.nih.gov/33991782\|journal=Annals of Diagnostic Pathology\|volume=53\|pages=151761\|doi=10.1016/j.anndiagpath.2021.151761\|issn=1532-8198\|pmid=33991782}}</ref><ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.		The t(5;14)(q31.1;q32) translocation can be detected by karyotyping or FISH; however, cases with a low blast count or a cytogenetically cryptic rearrangement may require Next-generation sequencing assays to increase sensitivity<ref>{{Cite journal\|last=Guenzel\|first=Adam J.\|last2=Smadbeck\|first2=James B.\|last3=Golden\|first3=Crystal L.\|last4=Williamson\|first4=Cynthia M.\|last5=Benevides Demasi\|first5=Jonna C.\|last6=Vasmatzis\|first6=George\|last7=Pearce\|first7=Kathryn E.\|last8=Olteanu\|first8=Horatiu\|last9=Xu\|first9=Xinjie\|date=2021-08\|title=Clinical utility of next generation sequencing to detect IGH/IL3 rearrangements [t(5;14)(q31.1;q32.1)] in B-lymphoblastic leukemia/lymphoma\|url=https://pubmed.ncbi.nlm.nih.gov/33991782\|journal=Annals of Diagnostic Pathology\|volume=53\|pages=151761\|doi=10.1016/j.anndiagpath.2021.151761\|issn=1532-8198\|pmid=33991782}}</ref><ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.
	Put your text here <span style="color:#0070C0">(''Instructions: Include recommended testing type(s) to identify the clinically significant genetic alterations.'')</span>		Put your text here <span style="color:#0070C0">(''Instructions: Include recommended testing type(s) to identify the clinically significant genetic alterations.'')</span>
	==Familial Forms==		==Familial Forms==

Miguel.GonzalezMancera: /* Genetic Diagnostic Testing Methods */

2025-11-11T19:59:23Z

Genetic Diagnostic Testing Methods

← Older revision		Revision as of 14:59, 11 November 2025
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	==Genetic Diagnostic Testing Methods==		==Genetic Diagnostic Testing Methods==

			The t(5;14)(q31.1;q32) translocation can be detected by karyotyping or FISH; however, in cases with a low blast count, or a cytogenetically cryptic rearrangement may require Next-generation sequencing assays to increase sensitivity<ref>{{Cite journal\|last=Guenzel\|first=Adam J.\|last2=Smadbeck\|first2=James B.\|last3=Golden\|first3=Crystal L.\|last4=Williamson\|first4=Cynthia M.\|last5=Benevides Demasi\|first5=Jonna C.\|last6=Vasmatzis\|first6=George\|last7=Pearce\|first7=Kathryn E.\|last8=Olteanu\|first8=Horatiu\|last9=Xu\|first9=Xinjie\|date=2021-08\|title=Clinical utility of next generation sequencing to detect IGH/IL3 rearrangements [t(5;14)(q31.1;q32.1)] in B-lymphoblastic leukemia/lymphoma\|url=https://pubmed.ncbi.nlm.nih.gov/33991782\|journal=Annals of Diagnostic Pathology\|volume=53\|pages=151761\|doi=10.1016/j.anndiagpath.2021.151761\|issn=1532-8198\|pmid=33991782}}</ref><ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.
	Put your text here <span style="color:#0070C0">(''Instructions: Include recommended testing type(s) to identify the clinically significant genetic alterations.'')</span>		Put your text here <span style="color:#0070C0">(''Instructions: Include recommended testing type(s) to identify the clinically significant genetic alterations.'')</span>
	==Familial Forms==		==Familial Forms==

Miguel.GonzalezMancera: /* Gene Mutations (SNV/INDEL) */

2025-11-11T19:56:29Z

Gene Mutations (SNV/INDEL)

← Older revision		Revision as of 14:56, 11 November 2025
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	==Gene Mutations (SNV/INDEL)==		==Gene Mutations (SNV/INDEL)==

			No recurrent gene mutations have been described.
	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"

Miguel.GonzalezMancera: /* Gene Rearrangements */

2025-11-11T19:52:37Z

Gene Rearrangements

← Older revision		Revision as of 14:52, 11 November 2025
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	\|D: This translocation must be detected by karyotyping or FISH		\|D: This translocation must be detected by karyotyping or FISH
	T: N/A		T: N/A

	P: Too few cases to accurately assess prognosis		P: Too few cases to accurately assess prognosis
	\|No (NCCN)		\|No (NCCN)

Miguel.GonzalezMancera: /* Gene Rearrangements */

2025-11-11T16:05:40Z

Gene Rearrangements

← Older revision		Revision as of 11:05, 11 November 2025
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	\|A small case series suggested an intermediate prognosis, with a poor response to treatment and high levels of measurable residual disease at the end of induction<ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.		\|A small case series suggested an intermediate prognosis, with a poor response to treatment and high levels of measurable residual disease at the end of induction<ref>{{Cite journal\|last=Fournier\|first=Benjamin\|last2=Balducci\|first2=Estelle\|last3=Duployez\|first3=Nicolas\|last4=Clappier\|first4=Emmanuelle\|last5=Cuccuini\|first5=Wendy\|last6=Arfeuille\|first6=Chloé\|last7=Caye-Eude\|first7=Aurélie\|last8=Delabesse\|first8=Eric\|last9=Bottollier-Lemallaz Colomb\|first9=Elodie\|date=2019\|title=B-ALL With t(5;14)(q31;q32); IGH-IL3 Rearrangement and Eosinophilia: A Comprehensive Analysis of a Peculiar IGH-Rearranged B-ALL\|url=https://pubmed.ncbi.nlm.nih.gov/31921638\|journal=Frontiers in Oncology\|volume=9\|pages=1374\|doi=10.3389/fonc.2019.01374\|issn=2234-943X\|pmc=6914849\|pmid=31921638}}</ref>.
	\|}		\|}

	==Individual Region Genomic Gain/Loss/LOH==		==Individual Region Genomic Gain/Loss/LOH==

Miguel.GonzalezMancera: /* Primary Author(s)* */

2025-11-11T15:59:33Z

Primary Author(s)*

@@ Line 11: / Line 11: @@
 ==Primary Author(s)*==
-Binu Porath, PhD. Vanderbilt University Medical Center, Nashville, TN
+Miguel Gonzalez Mancera, MD
 ==WHO Classification of Disease==
@@ Line 59: / Line 57: @@
 !Clinical Relevance Details/Other Notes
 |-
-|<span class="blue-text">EXAMPLE:</span> ''ABL1''||<span class="blue-text">EXAMPLE:</span> ''BCR::ABL1''||<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)
+|''IL3''||''IGH::IL3''||Balanced translocation that joins the IGH enhancer (14q32) to the  ''IL3'' gene promoter (5q31.1)<ref>{{Cite journal|last=Meeker|first=T. C.|last2=Hardy|first2=D.|last3=Willman|first3=C.|last4=Hogan|first4=T.|last5=Abrams|first5=J.|date=1990-07-15|title=Activation of the interleukin-3 gene by chromosome translocation in acute lymphocytic leukemia with eosinophilia|url=https://pubmed.ncbi.nlm.nih.gov/2114933|journal=Blood|volume=76|issue=2|pages=285–289|issn=0006-4971|pmid=2114933}}</ref>. This results in IL-3 overexpression that drives the leukemic clone in an autocrine manner and induces eosinophil maturation in the bone marrow and reactive eosinophilia in the peripheral blood<ref>{{Cite journal|last=Knuutila|first=S.|last2=Alitalo|first2=R.|last3=Ruutu|first3=T.|date=1993-12|title=Power of the MAC (morphology-antibody-chromosomes) method in distinguishing reactive and clonal cells: report of a patient with acute lymphatic leukemia, eosinophilia, and t(5;14)|url=https://pubmed.ncbi.nlm.nih.gov/7512364|journal=Genes, Chromosomes & Cancer|volume=8|issue=4|pages=219–223|doi=10.1002/gcc.2870080403|issn=1045-2257|pmid=7512364}}</ref><ref>{{Cite journal|last=Kobayashi|first=Kenichiro|last2=Mizuta|first2=Shumpei|last3=Yamane|first3=Noriko|last4=Ueno|first4=Hiroo|last5=Yoshida|first5=Kenichi|last6=Kato|first6=Itaru|last7=Umeda|first7=Katsutsugu|last8=Hiramatsu|first8=Hidefumi|last9=Suehiro|first9=Minoru|date=2019-01|title=Paraneoplastic hypereosinophilic syndrome associated with IL3-IgH positive acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/30207070|journal=Pediatric Blood & Cancer|volume=66|issue=1|pages=e27449|doi=10.1002/pbc.27449|issn=1545-5017|pmid=30207070}}</ref>.||t(5;14)(q31.1;q32)
+|
 |}
 ==Individual Region Genomic Gain/Loss/LOH==

Bailey.Glen at 17:10, 3 July 2025

2025-07-03T17:10:07Z

← Older revision		Revision as of 12:10, 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 21:29, 25 May 2025

2025-05-25T21:29:31Z

← Older revision		Revision as of 16:29, 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''