HAEM5:Myeloid/lymphoid neoplasm with FGFR1 rearrangement - Revision history

Bailey.Glen at 17:24, 3 July 2025

2025-07-03T17:24:22Z

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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 21:43, 25 May 2025

2025-05-25T21:43:51Z

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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 20:20, 25 May 2025

2025-05-25T20:20:10Z

← Older revision		Revision as of 15:20, 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
	\|		\|8p11.2 myeloproliferative syndrome; 8p11.2 stem cell syndrome; stem cell leukaemia/lymphoma syndrome; haematopoietic stem cell neoplasm with FGFR1 abnormalities; myeloid and lymphoid neoplasms with FGFR1 abnormalities
	\|}		\|}

Bailey.Glen at 17:42, 24 March 2025

2025-03-24T17:42:42Z

← Older revision		Revision as of 12:42, 24 March 2025
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	{{DISPLAYTITLE:Myeloid/lymphoid neoplasm with FGFR1 rearrangement}}		{{DISPLAYTITLE:Myeloid/lymphoid neoplasm with FGFR1 rearrangement}}

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

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	Yanna Ding, MD PhD		Yanna Ding, MD PhD

	~~__TOC__~~

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

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2025-02-11T14:17:45Z

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Bailey.Glen at 18:55, 10 February 2025

2025-02-10T18:55:21Z

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Bailey.Glen at 18:27, 10 February 2025

2025-02-10T18:27:18Z

← Older revision		Revision as of 13:27, 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>

	Systemic symptoms are common, including fatigue, fever, weight loss and night sweats. Some patients can be asymptomatic. Patients often present with peripheral blood eosinophilia without basophilia <ref name=":2" />. Cases with lymphoma features present as lymph nodes involvement and mediastinal mass; cases with myeloproliferative features present as splenomegaly and hypermetabolism. Cases can also present as acute myeloid leukaemia or myeloid sarcoma <ref name=":1" /> <ref>{{Cite journal\|last=Abruzzo\|first=Lynne V.\|last2=Jaffe\|first2=Elaine S.\|last3=Cotelingam\|first3=James D.\|last4=Whang-Peng\|first4=Jacqueline\|last5=Duca\|first5=Vincent Del\|last6=Medeiros\|first6=L. Jeffrey\|date=1992\|title=T-Cell Lymphoblastic Lymphoma With Eosinophilia Associated With Subsequent Myeloid Malignancy:\|url=http://journals.lww.com/00000478-199203000-00003\|journal=The American Journal of Surgical Pathology\|language=en\|volume=16\|issue=3\|pages=236–245\|doi=10.1097/00000478-199203000-00003\|issn=0147-5185}}</ref> <ref>{{Cite journal\|last=Vega\|first=Francisco\|last2=Medeiros\|first2=L. Jeffrey\|last3=Bueso-Ramos\|first3=Carlos E.\|last4=Arboleda\|first4=Patricia\|last5=Miranda\|first5=Roberto N.\|date=2015\|title=Hematolymphoid Neoplasms Associated With Rearrangements of PDGFRA, PDGFRB, and FGFR1\|url=https://academic.oup.com/ajcp/article/144/3/377/1760716\|journal=American Journal of Clinical Pathology\|language=en\|volume=144\|issue=3\|pages=377–392\|doi=10.1309/AJCPMORR5Z2IKCEM\|issn=1943-7722}}</ref>. Extranodal sites of disease include tonsil, lung, and breast in small subsets of patients <ref name=":2" />.		Systemic symptoms are common, including fatigue, fever, weight loss and night sweats. Some patients can be asymptomatic. Patients often present with peripheral blood eosinophilia without basophilia <ref name=":2" />. Cases with lymphoma features present as lymph nodes involvement and mediastinal mass; cases with myeloproliferative features present as splenomegaly and hypermetabolism. Cases can also present as acute myeloid leukaemia or myeloid sarcoma <ref name=":1" /> <ref>{{Cite journal\|last=Abruzzo\|first=Lynne V.\|last2=Jaffe\|first2=Elaine S.\|last3=Cotelingam\|first3=James D.\|last4=Whang-Peng\|first4=Jacqueline\|last5=Duca\|first5=Vincent Del\|last6=Medeiros\|first6=L. Jeffrey\|date=1992\|title=T-Cell Lymphoblastic Lymphoma With Eosinophilia Associated With Subsequent Myeloid Malignancy:\|url=http://journals.lww.com/00000478-199203000-00003\|journal=The American Journal of Surgical Pathology\|language=en\|volume=16\|issue=3\|pages=236–245\|doi=10.1097/00000478-199203000-00003\|issn=0147-5185}}</ref> <ref>{{Cite journal\|last=Vega\|first=Francisco\|last2=Medeiros\|first2=L. Jeffrey\|last3=Bueso-Ramos\|first3=Carlos E.\|last4=Arboleda\|first4=Patricia\|last5=Miranda\|first5=Roberto N.\|date=2015\|title=Hematolymphoid Neoplasms Associated With Rearrangements of PDGFRA, PDGFRB, and FGFR1\|url=https://academic.oup.com/ajcp/article/144/3/377/1760716\|journal=American Journal of Clinical Pathology\|language=en\|volume=144\|issue=3\|pages=377–392\|doi=10.1309/AJCPMORR5Z2IKCEM\|issn=1943-7722}}</ref>. Extranodal sites of disease include tonsil, lung, and breast in small subsets of patients <ref name=":2" />.

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Sites of Involvement==		==Sites of Involvement==
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	<blockquote class='blockedit'>{{Box-round\|title=v4:Immunophenotype\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Immunophenotype\|The content below was from the old template. Please incorporate above.}}</blockquote>

	Immunophenotypic analysis is not helpful in chronic phase disease. However, in lymphoblastic leukemia/lymphoma and in acute myeloid transformation, immunophenotypic analysis is important to distinguish the lineage origins, such as B- or T- lineage, or myeloid lineage <ref name=":0" />. Please refer to the above section "Morphologic Features".		Immunophenotypic analysis is not helpful in chronic phase disease. However, in lymphoblastic leukemia/lymphoma and in acute myeloid transformation, immunophenotypic analysis is important to distinguish the lineage origins, such as B- or T- lineage, or myeloid lineage <ref name=":0" />. Please refer to the above section "Morphologic Features".

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Chromosomal Rearrangements (Gene Fusions)==		==Chromosomal Rearrangements (Gene Fusions)==
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	<blockquote class='blockedit'>{{Box-round\|title=v4:Chromosomal Rearrangements (Gene Fusions)\|The content below was from the old template. Please incorporate above.}}		<blockquote class='blockedit'>{{Box-round\|title=v4:Chromosomal Rearrangements (Gene Fusions)\|The content below was from the old template. Please incorporate above.}}</blockquote>

	Various translocations with an 8p11 breakpoint are found. Depending on the partners, a variety of fusion genes with part of ''FGFR1'' from 8p11 can be formed, encoding aberrant tyrosine kinases. Note: Some precise mapping has positioned ''FGFR1'' locus to 8p12, instead of 8p11 <ref>{{Cite journal\|last=Mozziconacci\|first=Marie-Joëlle\|last2=Carbuccia\|first2=Nadine\|last3=Prebet\|first3=Thomas\|last4=Charbonnier\|first4=Aude\|last5=Murati\|first5=Anne\|last6=Vey\|first6=Norbert\|last7=Chaffanet\|first7=Max\|last8=Birnbaum\|first8=Daniel\|date=2008\|title=Common features of myeloproliferative disorders with t(8;9)(p12;q33) and CEP110–FGFR1 fusion: Report of a new case and review of the literature\|url=https://linkinghub.elsevier.com/retrieve/pii/S0145212607004444\|journal=Leukemia Research\|language=en\|volume=32\|issue=8\|pages=1304–1308\|doi=10.1016/j.leukres.2007.11.012}}</ref>.		Various translocations with an 8p11 breakpoint are found. Depending on the partners, a variety of fusion genes with part of ''FGFR1'' from 8p11 can be formed, encoding aberrant tyrosine kinases. Note: Some precise mapping has positioned ''FGFR1'' locus to 8p12, instead of 8p11 <ref>{{Cite journal\|last=Mozziconacci\|first=Marie-Joëlle\|last2=Carbuccia\|first2=Nadine\|last3=Prebet\|first3=Thomas\|last4=Charbonnier\|first4=Aude\|last5=Murati\|first5=Anne\|last6=Vey\|first6=Norbert\|last7=Chaffanet\|first7=Max\|last8=Birnbaum\|first8=Daniel\|date=2008\|title=Common features of myeloproliferative disorders with t(8;9)(p12;q33) and CEP110–FGFR1 fusion: Report of a new case and review of the literature\|url=https://linkinghub.elsevier.com/retrieve/pii/S0145212607004444\|journal=Leukemia Research\|language=en\|volume=32\|issue=8\|pages=1304–1308\|doi=10.1016/j.leukres.2007.11.012}}</ref>.
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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>

	Unlike myeloid/lymphoid neoplasms with ''[[Myeloid/Lymphoid Neoplasms with PDGFRA Rearrangement#cite ref-:0 1-4\|PDGFRA]]'' or ''PDGFRB'' rearrangement, the prognosis for this ''FGFR1'' associated entity is poor even for patient in the chronic phase, due to the high incidence of transformation. There is no established tyrosine kinase inhibitor therapy for myeloproliferative neoplasms with ''FGFR1'' rearrangement. Midostaurin (PKC412) was reported to be effective in one case <ref>{{Cite journal\|last=Chen\|first=J.\|last2=DeAngelo\|first2=D. J.\|last3=Kutok\|first3=J. L.\|last4=Williams\|first4=I. R.\|last5=Lee\|first5=B. H.\|last6=Wadleigh\|first6=M.\|last7=Duclos\|first7=N.\|last8=Cohen\|first8=S.\|last9=Adelsperger\|first9=J.\|date=2004\|title=PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder\|url=http://www.pnas.org/cgi/doi/10.1073/pnas.0404438101\|journal=Proceedings of the National Academy of Sciences\|language=en\|volume=101\|issue=40\|pages=14479–14484\|doi=10.1073/pnas.0404438101\|issn=0027-8424\|pmc=PMC521956\|pmid=15448205}}</ref>, and interferon has induced cytogenetic response in several cases <ref name=":1" /> <ref>{{Cite journal\|last=Holmes\|first=A L\|last2=Raper\|first2=R N\|last3=Heilig\|first3=J S\|date=1998\|title=Genetic analysis of Drosophila larval optic nerve development.\|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1460051/\|journal=Genetics\|volume=148\|issue=3\|pages=1189–1201\|issn=0016-6731\|pmc=1460051\|pmid=9539434}}</ref>. Nevertheless, haematopoietic stem cell transplantation should be considered even for patients in chronic phase.		Unlike myeloid/lymphoid neoplasms with ''[[Myeloid/Lymphoid Neoplasms with PDGFRA Rearrangement#cite ref-:0 1-4\|PDGFRA]]'' or ''PDGFRB'' rearrangement, the prognosis for this ''FGFR1'' associated entity is poor even for patient in the chronic phase, due to the high incidence of transformation. There is no established tyrosine kinase inhibitor therapy for myeloproliferative neoplasms with ''FGFR1'' rearrangement. Midostaurin (PKC412) was reported to be effective in one case <ref>{{Cite journal\|last=Chen\|first=J.\|last2=DeAngelo\|first2=D. J.\|last3=Kutok\|first3=J. L.\|last4=Williams\|first4=I. R.\|last5=Lee\|first5=B. H.\|last6=Wadleigh\|first6=M.\|last7=Duclos\|first7=N.\|last8=Cohen\|first8=S.\|last9=Adelsperger\|first9=J.\|date=2004\|title=PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder\|url=http://www.pnas.org/cgi/doi/10.1073/pnas.0404438101\|journal=Proceedings of the National Academy of Sciences\|language=en\|volume=101\|issue=40\|pages=14479–14484\|doi=10.1073/pnas.0404438101\|issn=0027-8424\|pmc=PMC521956\|pmid=15448205}}</ref>, and interferon has induced cytogenetic response in several cases <ref name=":1" /> <ref>{{Cite journal\|last=Holmes\|first=A L\|last2=Raper\|first2=R N\|last3=Heilig\|first3=J S\|date=1998\|title=Genetic analysis of Drosophila larval optic nerve development.\|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1460051/\|journal=Genetics\|volume=148\|issue=3\|pages=1189–1201\|issn=0016-6731\|pmc=1460051\|pmid=9539434}}</ref>. Nevertheless, haematopoietic stem cell transplantation should be considered even for patients in chronic phase.

			<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: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>

	A variety of translocations involving 8p11 breakpoint. Secondary cytogenetic abnormalities also occur, most commonly trisomy 21 <ref name=":0" />.		A variety of translocations involving 8p11 breakpoint. Secondary cytogenetic abnormalities also occur, most commonly trisomy 21 <ref name=":0" />.

			<blockquote class="blockedit">
			<center><span style="color:Maroon">'''End of V4 Section'''</span>
			----
	</blockquote>		</blockquote>
	==Gene Mutations (SNV / INDEL)==		==Gene Mutations (SNV / INDEL)==
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	\|}		\|}

	<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>

	Normal FGFR1 is a transmembrane protein with an extracellular ligand-binding domain, a transmembrane domain and a cytoplasmic tyrosine kinase domain. In inactive state, FGFR1 presents as monomers in cell membrane. Binding with ligands--the fibroblast growth factors (FGFs), induces dimerization and a conformational change that partially activates the enzymatic activity leading to transphosphorylation of the key tyrosine residue, an increase in enzymatic activity, phosphorylation of additional tyrosines and subsequent phosphorylation of downstream target substrates. The signaling pathways include Ras/MAPK, P13K, PLCÁ and STAT proteins. Fusion proteins with FGFR1 mimic the initial tyrosine kinase activation and thus possess constitutive tyrosine kinase activity to activate multiple signal transduction pathways in myeloid/lymphoid neoplasms <ref>{{Cite journal\|last=Ollendorff\|first=Vincent\|last2=Guasch\|first2=Géraldine\|last3=Isnardon\|first3=Daniel\|last4=Galindo\|first4=Rémy\|last5=Birnbaum\|first5=Daniel\|last6=Pébusque\|first6=Marie-Josèphe\|date=1999\|title=Characterization of FIM-FGFR1, the Fusion Product of the Myeloproliferative Disorder-associated t(8;13) Translocation\|url=http://www.jbc.org/lookup/doi/10.1074/jbc.274.38.26922\|journal=Journal of Biological Chemistry\|language=en\|volume=274\|issue=38\|pages=26922–26930\|doi=10.1074/jbc.274.38.26922\|issn=0021-9258}}</ref><ref>{{Cite journal\|last=Jiang\|first=Guoqiang\|last2=den Hertog\|first2=Jeroen\|last3=Hunter\|first3=Tony\|date=2000\|title=Receptor-Like Protein Tyrosine Phosphatase α Homodimerizes on the Cell Surface\|url=https://mcb.asm.org/content/20/16/5917\|journal=Molecular and Cellular Biology\|language=en\|volume=20\|issue=16\|pages=5917–5929\|doi=10.1128/MCB.20.16.5917-5929.2000\|issn=1098-5549\|pmc=PMC86069\|pmid=10913175}}</ref><ref>{{Cite journal\|last=Mason\|first=Ivor J.\|date=1994\|title=The ins and outs of fibroblast growth factors\|url=https://linkinghub.elsevier.com/retrieve/pii/0092867494905207\|journal=Cell\|language=en\|volume=78\|issue=4\|pages=547–552\|doi=10.1016/0092-8674(94)90520-7}}</ref><ref>{{Cite journal\|last=Smedley\|first=Damian\|last2=Demiroglu\|first2=Asuman\|last3=Abdul-Rauf\|first3=Munah\|last4=Heatht\|first4=Carol\|last5=Cooper\|first5=Colin\|last6=Shipley\|first6=Janet\|last7=Cross\|first7=Nicholas C.P.\|date=1999\|title=ZNF198-FGFR1 Transforms Ba/F3 Cells to Growth Factor Independence and Results in High Level Tyrosine Phosphorylation of STATS 1 and 5\|url=https://linkinghub.elsevier.com/retrieve/pii/S1476558699800268\|journal=Neoplasia\|language=en\|volume=1\|issue=4\|pages=349–355\|doi=10.1038/sj.neo.7900035\|pmc=PMC1508104\|pmid=10935490}}</ref>.		Normal FGFR1 is a transmembrane protein with an extracellular ligand-binding domain, a transmembrane domain and a cytoplasmic tyrosine kinase domain. In inactive state, FGFR1 presents as monomers in cell membrane. Binding with ligands--the fibroblast growth factors (FGFs), induces dimerization and a conformational change that partially activates the enzymatic activity leading to transphosphorylation of the key tyrosine residue, an increase in enzymatic activity, phosphorylation of additional tyrosines and subsequent phosphorylation of downstream target substrates. The signaling pathways include Ras/MAPK, P13K, PLCÁ and STAT proteins. Fusion proteins with FGFR1 mimic the initial tyrosine kinase activation and thus possess constitutive tyrosine kinase activity to activate multiple signal transduction pathways in myeloid/lymphoid neoplasms <ref>{{Cite journal\|last=Ollendorff\|first=Vincent\|last2=Guasch\|first2=Géraldine\|last3=Isnardon\|first3=Daniel\|last4=Galindo\|first4=Rémy\|last5=Birnbaum\|first5=Daniel\|last6=Pébusque\|first6=Marie-Josèphe\|date=1999\|title=Characterization of FIM-FGFR1, the Fusion Product of the Myeloproliferative Disorder-associated t(8;13) Translocation\|url=http://www.jbc.org/lookup/doi/10.1074/jbc.274.38.26922\|journal=Journal of Biological Chemistry\|language=en\|volume=274\|issue=38\|pages=26922–26930\|doi=10.1074/jbc.274.38.26922\|issn=0021-9258}}</ref><ref>{{Cite journal\|last=Jiang\|first=Guoqiang\|last2=den Hertog\|first2=Jeroen\|last3=Hunter\|first3=Tony\|date=2000\|title=Receptor-Like Protein Tyrosine Phosphatase α Homodimerizes on the Cell Surface\|url=https://mcb.asm.org/content/20/16/5917\|journal=Molecular and Cellular Biology\|language=en\|volume=20\|issue=16\|pages=5917–5929\|doi=10.1128/MCB.20.16.5917-5929.2000\|issn=1098-5549\|pmc=PMC86069\|pmid=10913175}}</ref><ref>{{Cite journal\|last=Mason\|first=Ivor J.\|date=1994\|title=The ins and outs of fibroblast growth factors\|url=https://linkinghub.elsevier.com/retrieve/pii/0092867494905207\|journal=Cell\|language=en\|volume=78\|issue=4\|pages=547–552\|doi=10.1016/0092-8674(94)90520-7}}</ref><ref>{{Cite journal\|last=Smedley\|first=Damian\|last2=Demiroglu\|first2=Asuman\|last3=Abdul-Rauf\|first3=Munah\|last4=Heatht\|first4=Carol\|last5=Cooper\|first5=Colin\|last6=Shipley\|first6=Janet\|last7=Cross\|first7=Nicholas C.P.\|date=1999\|title=ZNF198-FGFR1 Transforms Ba/F3 Cells to Growth Factor Independence and Results in High Level Tyrosine Phosphorylation of STATS 1 and 5\|url=https://linkinghub.elsevier.com/retrieve/pii/S1476558699800268\|journal=Neoplasia\|language=en\|volume=1\|issue=4\|pages=349–355\|doi=10.1038/sj.neo.7900035\|pmc=PMC1508104\|pmid=10935490}}</ref>.

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

Bailey.Glen at 22:21, 6 September 2024

2024-09-06T22:21:36Z

← Older revision		Revision as of 17:21, 6 September 2024
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	__TOC__		__TOC__

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

	Myeloid/lymphoid neoplasms		{\| class="wikitable"
			!Structure
	~~==Cancer Sub~~-~~Classification / Subtype==~~		!Disease
			\|-
	Myeloid/lymphoid neoplasms with eosinophilia and gene rearrangement		\|Book
			\|Haematolymphoid Tumours (5th ed.)
			\|-
			\|Category
			\|Myeloid proliferations and neoplasms
			\|-
			\|Family
			\|Myeloid/lymphoid neoplasms
			\|-
			\|Type
			\|Myeloid/lymphoid neoplasms with eosinophilia and defining gene rearrangement
			\|-
			\|Subtype(s)
			\|Myeloid/lymphoid neoplasm with FGFR1 rearrangement
			\|}

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

Bailey.Glen at 22:05, 6 September 2024

2024-09-06T22:05:55Z

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Bailey.Glen at 19:34, 13 December 2023

2023-12-13T19:34:11Z

← Older revision		Revision as of 14:34, 13 December 2023
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	<blockquote class='blockedit'>{{Box-round\|title=HAEM5 Conversion Notes\|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Myeloid/Lymphoid Neoplasms with FGFR1 Rearrangement]].		<blockquote class='blockedit'>{{Box-round\|title=HAEM5 Conversion Notes\|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Myeloid/Lymphoid Neoplasms with FGFR1 Rearrangement]].
	}}</blockquote>		}}</blockquote>

			<span style="color:#0070C0">(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ HGVS-based nomenclature for variants], as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples). Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see </span><u>[[Author_Instructions]]</u><span style="color:#0070C0"> and [[Frequently Asked Questions (FAQs)\|<u>FAQs</u>]] as well as contact your [[Leadership\|<u>Associate Editor</u>]] or [mailto:CCGA@cancergenomics.org <u>Technical Support</u>])</span>

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