View source for HAEM5:Myeloid/lymphoid neoplasm with FGFR1 rearrangement

{{DISPLAYTITLE:Myeloid/lymphoid neoplasm with FGFR1 rearrangement}}
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]

{{Under Construction}}

<blockquote class='blockedit'>{{Box-round|title=Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification|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]].
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<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); to add (or move) a row or column to a table, click within the table and select the > symbol that appears to be given options. 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)*==

Yanna Ding, MD PhD

__TOC__

==WHO Classification of Disease==

{| class="wikitable"
!Structure
!Disease
|-
|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==

Myeloid/lymphoid neoplasms with ''FGFR1'' rearrangement are a heterogenous group of aggressive neoplasms with translocations involving the fibroblast growth factor receptor 1(''FGFR1)'' tyrosine kinase gene on chromosome 8p11-12<ref name=":2">{{Cite journal|last=Jackson|first=Courtney C.|last2=Medeiros|first2=L. Jeffrey|last3=Miranda|first3=Roberto N.|date=2010|title=8p11 myeloproliferative syndrome: a review|url=http://www.sciencedirect.com/science/article/pii/S0046817709004067|journal=Human Pathology|volume=41|issue=4|pages=461–476|doi=10.1016/j.humpath.2009.11.003|issn=0046-8177}}</ref>.  The neoplastic cells derive from a pluripotent haematopoietic stem cell and may be immature or mature<ref name=":0">Bain BJ, et al., (2017). Myeloid/lymphoid neoplasms with FGFR1 rearrangement 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, p77-78.</ref>. Cases can present as a myeloproliferative neoplasm or as acute myeloid leukaemia, T- or B-lymphoblastic leukaemia/lymphoma or mixed-phenotype acute leukaemia. T-cell lymphoblastic lymphoma/leukemia is common, frequently with eosinophilia, and subsequently rapidly transforms into acute myeloid leukaemia.  

Coexistence of atypical chronic myeloid leukaemia, ''BCR-ABL1''-negative, with t(8;19)(p11.2;q13.1) and ''KIT'' D816V-positive systemic mastocytosis with an associated haematological neoplasm has been reported <ref name=":6">{{Cite journal|last=Duckworth|first=Christina B|last2=Zhang|first2=Linsheng|last3=Li|first3=Shiyong|date=2014|title=Systemic mastocytosis with associated myeloproliferative neoplasm with t(8;19)(p12;q13.1) and abnormality of FGFR1: report of a unique case|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925931/|journal=International Journal of Clinical and Experimental Pathology|volume=7|issue=2|pages=801–807|issn=1936-2625|pmc=3925931|pmid=24551307}}</ref>. 

==Synonyms / Terminology==

8p11 myeloproliferative syndrome (EMS)

8p11 stem cell syndrome

8p11 stem cell leukaemia/lymphoma syndrome

Haematopoietic stem cell neoplasm with FGFR1 abnormalities

Myeloid and lymphoid neoplasms with FGFR1 abnormalities <ref name=":0" />

==Epidemiology / Prevalence==

The median age at disease onset is 32 years, although it can occur within a wide age range of 3-84 years <ref name=":1">{{Cite journal|last=Macdonald|first=Donald|last2=Reiter|first2=Andreas|last3=Cross|first3=Nicholas C.P.|date=2002|title=The 8p11 Myeloproliferative Syndrome: A Distinct Clinical Entity Caused by Constitutive Activation of FGFR1|url=https://www.karger.com/Article/FullText/46639|journal=Acta Haematologica|language=en|volume=107|issue=2|pages=101–107|doi=10.1159/000046639|issn=0001-5792}}</ref>. There is a moderate predominance of male with male-to-female ratio of 1.5:1, unlike in myeloid/lymphoid neoplasms with ''[http://www.ccga.io/index.php/Myeloid/Lymphoid_Neoplasms_with_PDGFRA_Rearrangement#cite_ref-:0_1-4 PDGFRA]'' or ''PDGFRB'' rearrangement <ref name=":0" />.

==Clinical Features==

Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table. Do not delete table.'') </span>
{| class="wikitable"
|'''Signs and Symptoms'''
|<span class="blue-text">EXAMPLE:</span> Asymptomatic (incidental finding on complete blood counts)

<span class="blue-text">EXAMPLE:</span> B-symptoms (weight loss, fever, night sweats)

<span class="blue-text">EXAMPLE:</span> Fatigue

<span class="blue-text">EXAMPLE:</span> Lymphadenopathy (uncommon)
|-
|'''Laboratory Findings'''
|<span class="blue-text">EXAMPLE:</span> Cytopenias

<span class="blue-text">EXAMPLE:</span> Lymphocytosis (low level)
|}


<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}

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>
==Sites of Involvement==

Bone marrow, peripheral blood, lymph nodes, liver and spleen are primarily involved. Lymphoblasts or myeloid cells infiltration results in lymphadenopathy <ref name=":0" />.

==Morphologic Features==

Peripheral blood: Most cases have leukocytosis with increased neutrophils, bands, metamyelocytes, and myelocytes. Circulating blasts and eosinophilia are common. Monocytosis can be found. Hemoglobin levels have ranged from 6.3 to 21 g/dL and platelet counts have ranged from 8 to 546 × 10<sup>9</sup>/L<ref name=":2" />.

Bone marrow biopsy: often hypercellularity due to increased granulocytic precursors and eosinophilia. Hypocellular cases also exist. Many cases were interpreted as myeloid hyperplasia or myeloproliferative neoplasm, including chronic myelogenous leukemia, atypical chronic myeloid leukemia, or chronic myelomonocytic leukemia. Primary diagnoses also include myelodysplastic syndrome, myelodysplastic syndrome/myeloproliferative neoplasm due to dysplasia. 16% of the cases may have 20% or more blasts, in the range of acute leukemia with blasts of a myeloid lineage or bilineal lineage in two thirds of the cases, and of pure immature lymphoid lineage in one third of the cases <ref>{{Cite journal|last=Roy|first=Sukanya|last2=Szer|first2=Jeff|last3=Campbell|first3=Lynda J.|last4=Juneja|first4=Surender|date=2002|title=Sequential Transformation of t(8;13)-Related Disease|url=https://www.karger.com/Article/FullText/46637|journal=Acta Haematologica|language=en|volume=107|issue=2|pages=95–97|doi=10.1159/000046637|issn=0001-5792}}</ref>. Lymphoblastic lymphoma is more commonly seen in patients with t(8;13)<ref name=":6" />.

Lymph node biopsy: For patients who did undergo lymph node biopsy, 79% had T-lymphoblastic lymphoma and 21% myeloid sarcoma. Lymph nodes are infiltreated by small- or mediumsized lymphoblasts with fine or “dusty” chromatin and minimal cytoplasm. Eosinophils are frequently admixed with the lymphoblasts. Subtle myeloid component can be found in perivascular area. lymphoblastic component can be immunoreactive to TdT (terminal deoxynucleotidyl transferase), CD1a and pan-T-cell antigens while the subtle myeloid component can be positive for myeloperoxidase, CD15, CD68, CD117, lysozyme, or other myeloid-associated antigens<ref>{{Cite journal|last=Somers|first=Gino R.|last2=Slater|first2=Howard|last3=Rockman|first3=Steven|last4=Ekert|first4=Henry|last5=Southey|first5=Melissa C.|last6=Chow|first6=C.W.|last7=Armes|first7=Jane E.|last8=Venter|first8=Deon J.|date=1997|title=Coexistent T-Cell Lymphoblastic Lymphoma and an Atypical Myeloproliferative Disorder Associated with t(8;13)(p21;q14)|url=http://www.tandfonline.com/doi/full/10.1080/15513819709168354|journal=Pediatric Pathology & Laboratory Medicine|language=en|volume=17|issue=1|pages=141–158|doi=10.1080/15513819709168354|issn=1077-1042}}</ref> .

Basophilia can be found in cases with ''BCR-FGFR1'' fusion <ref>{{Cite journal|last=Roumiantsev|first=Sergei|last2=Krause|first2=Daniela S|last3=Neumann|first3=Carola A|last4=Dimitri|first4=Christopher A|last5=Asiedu|first5=Frances|last6=Cross|first6=Nicholas C.P|last7=Van Etten|first7=Richard A|date=2004|title=Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocations|url=https://linkinghub.elsevier.com/retrieve/pii/S1535610804000534|journal=Cancer Cell|language=en|volume=5|issue=3|pages=287–298|doi=10.1016/S1535-6108(04)00053-4}}</ref>, and in cases with t(1;8)(q31.1;p11.2)/''TRP-FGFR1'' fusion <ref>{{Cite journal|last=Li|first=Feng|last2=Zhai|first2=Yong-Ping|last3=Tang|first3=Yu-Mei|last4=Wang|first4=Li-Ping|last5=Wan|first5=Pin-Jun|date=2012|title=Identification of a novel partner gene, TPR, fused to FGFR1 in 8p11 myeloproliferative syndrome|url=http://doi.wiley.com/10.1002/gcc.21973|journal=Genes, Chromosomes and Cancer|language=en|volume=51|issue=9|pages=890–897|doi=10.1002/gcc.21973}}</ref>''.'' Polycythaemia vera has been reported in cases with t(6;8)(q27;p11.2)/''FGFR1OP-FGFR1'' fusion <ref>{{Cite journal|last=Vizmanos|first=José L|last2=Hernández|first2=Roberto|last3=Vidal|first3=María J|last4=Larráyoz|first4=María J|last5=Odero|first5=María D|last6=Marín|first6=Julián|last7=Ardanaz|first7=María T|last8=Calasanz|first8=María J|last9=Cross|first9=Nicholas C P|date=2004|title=Clinical variability of patients with the t(6;8)(q27;p12) and FGFR1OP-FGFR1 fusion: two further cases|url=http://www.nature.com/doifinder/10.1038/sj.thj.6200561|journal=The Hematology Journal|volume=5|issue=6|pages=534–537|doi=10.1038/sj.thj.6200561|issn=1466-4860}}</ref>.  

==Immunophenotype==

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{| class="wikitable sortable"
|-
!Finding!!Marker
|-
|Positive (universal)||<span class="blue-text">EXAMPLE:</span> CD1
|-
|Positive (subset)||<span class="blue-text">EXAMPLE:</span> CD2
|-
|Negative (universal)||<span class="blue-text">EXAMPLE:</span> CD3
|-
|Negative (subset)||<span class="blue-text">EXAMPLE:</span> CD4
|}


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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>
==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
|-
|<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2)||<span class="blue-text">EXAMPLE:</span> 3'ABL1 / 5'BCR||<span class="blue-text">EXAMPLE:</span> der(22)||<span class="blue-text">EXAMPLE:</span> 20% (COSMIC)
<span class="blue-text">EXAMPLE:</span> 30% (add reference)
|Yes
|No
|Yes
|<span class="blue-text">EXAMPLE:</span>

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).
|}		
			

<blockquote class='blockedit'>{{Box-round|title=v4:Chromosomal Rearrangements (Gene Fusions)|The content below was from the old template. Please incorporate above.}}

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>.

{| class="wikitable sortable"
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Prevalence
|-
|t(8;13)(p11.2;q12.1)
|''ZMYM2-FGFR1''
|Most common, around 40% <ref>{{Cite journal|last=Popovici|first=C.|last2=Adelaide|first2=J.|last3=Ollendorff|first3=V.|last4=Chaffanet|first4=M.|last5=Guasch|first5=G.|last6=Jacrot|first6=M.|last7=Leroux|first7=D.|last8=Birnbaum|first8=D.|last9=Pebusque|first9=M.-J.|date=1998|title=Fibroblast growth factor receptor 1 is fused to FIM in stem-cell myeloproliferative disorder with t(8;13)(p12;q12)|url=http://www.pnas.org/cgi/doi/10.1073/pnas.95.10.5712|journal=Proceedings of the National Academy of Sciences|language=en|volume=95|issue=10|pages=5712–5717|doi=10.1073/pnas.95.10.5712|issn=0027-8424|pmc=PMC20444|pmid=9576949}}</ref><ref>{{Cite journal|last=Cross|first=Nicholas C. P.|last2=Goldman|first2=John M.|last3=Jennings|first3=Barbara A.|last4=Hernandez|first4=Jesus M.|last5=Gonçalves|first5=Cristina|last6=Aguiar|first6=Ricardo C. T.|last7=Macdonald|first7=Donald H. C.|last8=Chase|first8=Andrew|last9=Kulkarni|first9=Shashikant|date=1998|title=Consistent Fusion of ZNF198 to the Fibroblast Growth Factor Receptor-1 in the t(8;13)(p11;q12) Myeloproliferative Syndrome|url=https://ashpublications.org/blood/article/92/5/1735/247374/Consistent-Fusion-of-ZNF198-to-the-Fibroblast|journal=Blood|language=en|volume=92|issue=5|pages=1735–1742|doi=10.1182/blood.V92.5.1735|issn=0006-4971}}</ref><ref>{{Cite journal|last=Smedley|first=D|date=1998|title=The t(8;13)(p11;q11-12) rearrangement associated with an atypical myeloproliferative disorder fuses the fibroblast growth factor receptor 1 gene to a novel gene RAMP|url=https://academic.oup.com/hmg/article-lookup/doi/10.1093/hmg/7.4.637|journal=Human Molecular Genetics|volume=7|issue=4|pages=637–642|doi=10.1093/hmg/7.4.637}}</ref><ref name=":3">{{Cite journal|last=Xiao|first=Sheng|last2=Nalabolu|first2=Srinivasa R.|last3=Aster|first3=Jon C.|last4=Ma|first4=Junli|last5=Abruzzo|first5=Lynne|last6=Jaffe|first6=Elaine S.|last7=Stone|first7=Richard|last8=Weissman|first8=Sherman M.|last9=Hudson|first9=Thomas J.|date=1998|title=FGFR1 is fused with a novel zinc-finger gene, ZNF198, in the t(8;13) leukaemia/lymphoma syndrome|url=http://www.nature.com/articles/ng0198-84|journal=Nature Genetics|language=en|volume=18|issue=1|pages=84–87|doi=10.1038/ng0198-84|issn=1061-4036}}</ref><ref>{{Cite journal|last=Bain|first=Barbara J.|last2=Fletcher|first2=Sarah H.|date=2007-08|title=Chronic Eosinophilic Leukemias and the Myeloproliferative Variant of the Hypereosinophilic Syndrome|url=http://dx.doi.org/10.1016/j.iac.2007.06.001|journal=Immunology and Allergy Clinics of North America|volume=27|issue=3|pages=377–388|doi=10.1016/j.iac.2007.06.001|issn=0889-8561}}</ref><ref name=":2" />
|-
|t(8;9)(p11.2;q33.2)
|''CNTRL-FGFR1''
|Around 17% <ref name=":2" /><ref>{{Cite journal|last=Pébusque|first=Marie-Josèphe|last2=Rattner|first2=Jérome B.|last3=Birnbaum|first3=Daniel|last4=Dastugue|first4=Nicole|last5=Popovici|first5=Cornel|last6=Mack|first6=Gary J.|last7=Guasch|first7=Géraldine|date=2000|title=FGFR1 is fused to the centrosome-associated proteinCEP110 in the 8p12 stem cell myeloproliferative disorder with t(8;9)(p12;q33)|url=https://ashpublications.org/blood/article/95/5/1788/138772/FGFR1-is-fused-to-the-centrosome-associated|journal=Blood|language=en|volume=95|issue=5|pages=1788–1796|doi=10.1182/blood.V95.5.1788.005k15_1788_1796|issn=0006-4971}}</ref>
|-
|t(6;8)(q27;p11.2)
|''FGFR1OP-FGFR1''
|Around 9% <ref name=":2" /> <ref>{{Cite journal|last=Pébusque|first=Marie-Josèphe|last2=Birnbaum|first2=Daniel|last3=Lafage-Pochitaloff|first3=Marina|last4=Jonveaux|first4=Philippe|last5=Grégoire|first5=Marie-José|last6=Zhang|first6=Bin|last7=Popovici|first7=Cornel|date=1999|title=The t(6;8)(q27;p11) Translocation in a Stem Cell Myeloproliferative Disorder Fuses a Novel Gene, FOP, to Fibroblast Growth Factor Receptor 1|url=https://ashpublications.org/blood/article/93/4/1381/258789/The-t-6-8-q27-p11-Translocation-in-a-Stem-Cell|journal=Blood|language=en|volume=93|issue=4|pages=1381–1389|doi=10.1182/blood.V93.4.1381|issn=0006-4971}}</ref>
|-
|t(8;22)(p11.2;q11.2)
|''BCR-FGFR1''
|At least eight cases<ref>{{Cite journal|last=Steer|first=E. J.|last2=Demiroglu|first2=A.|last3=Heath|first3=C.|last4=Pourgourides|first4=E.|last5=Taylor|first5=K.|last6=Bentley|first6=M.|last7=Allen|first7=S. L.|last8=Koduru|first8=P.|last9=Brody|first9=J. P.|date=2001|others=E. J. Steer, A. Demiroglu, C. Heath, E. Pourgourides, K. Taylor, M. Bentley|title=The t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteins|url=https://eprints.soton.ac.uk/60717/|journal=Blood|volume=98|pages=pp.468A|issn=0006-4971}}</ref><ref>{{Cite journal|last=Ågerstam|first=Helena|last2=Lilljebjörn|first2=Henrik|last3=Lassen|first3=Carin|last4=Swedin|first4=Agneta|last5=Richter|first5=Johan|last6=Vandenberghe|first6=Peter|last7=Johansson|first7=Bertil|last8=Fioretos|first8=Thoas|date=2007|title=Fusion gene-mediated truncation ofRUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome|url=http://doi.wiley.com/10.1002/gcc.20442|journal=Genes, Chromosomes and Cancer|language=en|volume=46|issue=7|pages=635–643|doi=10.1002/gcc.20442}}</ref><ref>{{Cite journal|last=Liu|first=Jing|last2=Meng|first2=Li|date=2018|title=8p11 Myeloproliferative syndrome with t(8;22)(p11;q11): A case report|url=http://www.spandidos-publications.com/10.3892/etm.2018.6328|journal=Experimental and Therapeutic Medicine|doi=10.3892/etm.2018.6328|issn=1792-0981|pmc=PMC6090294|pmid=30116393}}</ref><ref>{{Cite journal|last=Fioretos|first=Thoas|last2=Panagopoulos|first2=Ioannis|last3=Lassen|first3=Carin|last4=Swedin|first4=Agneta|last5=Billström|first5=Rolf|last6=Isaksson|first6=Margareth|last7=Strömbeck|first7=Bodil|last8=Olofsson|first8=Tor|last9=Mitelman|first9=Felix|date=2001|title=Fusion of the BCR and the fibroblast growth factor receptor-1 ( FGFR1 ) genes as a result of t(8;22)(p11;q11) in a myeloproliferative disorder: The first fusion gene involving BCR but not ABL: Fusion of the BCR and FGFR1 Genes|url=http://doi.wiley.com/10.1002/gcc.1195|journal=Genes, Chromosomes and Cancer|language=en|volume=32|issue=4|pages=302–310|doi=10.1002/gcc.1195}}</ref><ref>{{Cite journal|last=Pini|first=Massimo|last2=Gottardi|first2=Enrico|last3=Scaravaglio|first3=Patrizia|last4=Giugliano|first4=Emilia|last5=Libener|first5=Roberta|last6=Baraldi|first6=Anna|last7=Muzio|first7=Alberto|last8=Cornaglia|first8=Elisa|last9=Saglio|first9=Giuseppe|date=2002|title=A fourth case of BCR-FGFR1 positive CML-like disease with t(8;22) translocation showing an extensive deletion on the derivative chromosome 8p|url=http://www.nature.com/doifinder/10.1038/sj.thj.6200201|journal=The Hematology Journal|volume=3|issue=6|pages=315–316|doi=10.1038/sj.thj.6200201}}</ref>
|-
|t(7;8)(q33;p11.2)
|''TRIM24-FGFR1''
|At least two cases <ref>{{Cite journal|last=Belloni|first=Elena|last2=Trubia|first2=Maurizio|last3=Gasparini|first3=Patrizia|last4=Micucci|first4=Carla|last5=Tapinassi|first5=Cinzia|last6=Confalonieri|first6=Stefano|last7=Nuciforo|first7=Paolo|last8=Martino|first8=Bruno|last9=Lo‐Coco|first9=Francesco|date=2005|title=8p11 myeloproliferative syndrome with a novel t(7;8) translocation leading to fusion of the FGFR1 and TIF1 genes|url=https://onlinelibrary.wiley.com/doi/abs/10.1002/gcc.20144|journal=Genes, Chromosomes and Cancer|language=en|volume=42|issue=3|pages=320–325|doi=10.1002/gcc.20144|issn=1098-2264}}</ref><ref name=":4">{{Cite journal|last=Sohal|first=Jastinder|last2=Chase|first2=Andrew|last3=Mould|first3=Sarah|last4=Corcoran|first4=Martin|last5=Oscier|first5=David|last6=Iqbal|first6=Sameena|last7=Parker|first7=Sally|last8=Welborn|first8=Jeanna|last9=Harris|first9=Richard I.|date=2001|title=Identification of four new translocations involvingFGFR1 in myeloid disorders|url=http://doi.wiley.com/10.1002/gcc.1177|journal=Genes, Chromosomes and Cancer|language=en|volume=32|issue=2|pages=155–163|doi=10.1002/gcc.1177|issn=1045-2257}}</ref>
|-
|t(8;17)(p11.2;q23)
|''MYO18A-FGFR1''
|At least one case<ref>{{Cite journal|last=Walz|first=C|last2=Chase|first2=A|last3=Schoch|first3=C|last4=Weisser|first4=A|last5=Schlegel|first5=F|last6=Hochhaus|first6=A|last7=Fuchs|first7=R|last8=Schmitt-Gräff|first8=A|last9=Hehlmann|first9=R|date=2005|title=The t(8;17)(p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1|url=http://www.nature.com/articles/2403712|journal=Leukemia|language=en|volume=19|issue=6|pages=1005–1009|doi=10.1038/sj.leu.2403712|issn=0887-6924}}</ref>
|-
|t(8;19)(p11.2;q13.3)
|''HERVK-FGFR1''
|At least one case <ref>{{Cite journal|last=Mugneret|first=Francine|last2=Chaffanet|first2=Max|last3=Maynadie|first3=Marc|last4=Guasch|first4=Geraldine|last5=Favre|first5=Bernardine|last6=Casasnovas|first6=Olivier|last7=Birnbaum|first7=Daniel|last8=Pebusque|first8=Marie-Josephe|date=2000|title=The 8p12 myeloproliferative disorder. t(8;19)(p12;q13.3): a novel translocation involving the FGFR1 gene . SHORT REPORT|url=http://doi.wiley.com/10.1046/j.1365-2141.2000.02355.x|journal=British Journal of Haematology|language=en|volume=111|issue=2|pages=647–649|doi=10.1046/j.1365-2141.2000.02355.x|issn=0007-1048}}</ref><ref name=":5">{{Cite journal|last=Pébusque|first=Marie-Josèphe|last2=Birnbaum|first2=Daniel|last3=Pontarotti|first3=Pierre|last4=Chaffanet|first4=Max|last5=Mugneret|first5=Francine|last6=Popovici|first6=Cornel|last7=Guasch|first7=Géraldine|date=2003|title=Endogenous retroviral sequence is fused to FGFR1 kinase in the 8p12 stem-cell myeloproliferative disorder with t(8;19)(p12;q13.3)|url=https://ashpublications.org/blood/article/101/1/286/89004/Endogenous-retroviral-sequence-is-fused-to-FGFR1|journal=Blood|language=en|volume=101|issue=1|pages=286–288|doi=10.1182/blood-2002-02-0577|issn=0006-4971}}</ref>
|-
|ins(12;8)(p11.2;p11.2p22)
|''FGFR1OP2-FGFR1''
|At least two cases <ref name=":4" /><ref>{{Cite journal|last=Grand|first=Effie K.|last2=Grand|first2=Francis H.|last3=Chase|first3=Andrew J.|last4=Ross|first4=Fiona M.|last5=Corcoran|first5=Martin M|last6=Oscier|first6=David G.|last7=Cross|first7=Nicholas C. P.|date=2004|title=Identification of a novel gene,FGFR1OP2, fused toFGFR1 in 8p11 myeloproliferative syndrome|url=http://doi.wiley.com/10.1002/gcc.20023|journal=Genes, Chromosomes and Cancer|language=en|volume=40|issue=1|pages=78–83|doi=10.1002/gcc.20023|issn=1045-2257}}</ref>
|-
|t(1;8)(q31.1;p11.2)
|''TRP-FGFR1''
|At least one case <ref>{{Cite journal|last=Li|first=Feng|last2=Zhai|first2=Yong-Ping|last3=Tang|first3=Yu-Mei|last4=Wang|first4=Li-Ping|last5=Wan|first5=Pin-Jun|date=2012|title=Identification of a novel partner gene, TPR, fused to FGFR1 in 8p11 myeloproliferative syndrome|url=https://onlinelibrary.wiley.com/doi/abs/10.1002/gcc.21973|journal=Genes, Chromosomes and Cancer|language=en|volume=51|issue=9|pages=890–897|doi=10.1002/gcc.21973|issn=1098-2264}}</ref>
|-
|t(2;8)(q13;p11.2)
|''RANBP2-FGFR1''
|At least one case <ref>{{Cite journal|last=Mauvieux|first=L.|last2=Bilger|first2=K.|last3=Herbrecht|first3=R.|last4=Ittel|first4=A.|last5=A.-C. Galoisy|last6=Jeandidier|first6=E.|last7=Hélias|first7=C.|last8=Perrusson|first8=N.|last9=Dano|first9=L.|date=2013|title=A translocation t(2;8)(q12;p11) fuses FGFR1 to a novel partner gene, RANBP2/NUP358 , in a myeloproliferative/myelodysplastic neoplasm|url=https://www.nature.com/articles/leu2012286|journal=Leukemia|language=en|volume=27|issue=5|pages=1186–1188|doi=10.1038/leu.2012.286|issn=1476-5551}}</ref>
|-
|t(2;8)(q37.3;p11.2)
|''LRRFIP1-FGFR1''
|At least one case <ref>{{Cite journal|last=Soler|first=G|last2=Nusbaum|first2=S|last3=Varet|first3=B|last4=Macintyre|first4=E A|last5=Vekemans|first5=M|last6=Romana|first6=S P|last7=Radford-Weiss|first7=I|date=2009|title=LRRFIP1, a new FGFR1 partner gene associated with 8p11 myeloproliferative syndrome|url=http://www.nature.com/articles/leu200979|journal=Leukemia|language=en|volume=23|issue=7|pages=1359–1361|doi=10.1038/leu.2009.79|issn=0887-6924}}</ref>
|-
|t(7;8)(q22.1;p11.2)
|''CUX1-FGFR1''
|At least one case <ref>{{Cite journal|last=Wasag|first=B.|last2=Lierman|first2=E.|last3=Meeus|first3=P.|last4=Cools|first4=J.|last5=Vandenberghe|first5=P.|date=2011|title=The kinase inhibitor TKI258 is active against the novel CUX1-FGFR1 fusion detected in a patient with T-lymphoblastic leukemia/lymphoma and t(7;8)(q22;p11)|url=http://www.haematologica.org/cgi/doi/10.3324/haematol.2010.036558|journal=Haematologica|language=en|volume=96|issue=6|pages=922–926|doi=10.3324/haematol.2010.036558|issn=0390-6078|pmc=PMC3105656|pmid=21330321}}</ref>
|-
|t(8;12)(p11.2;q15)
|''CPSF6-FGFR1''
|At least two cases <ref name=":4" /><ref>{{Cite journal|last=Bae|first=Sook Young|last2=Kim|first2=Jang Su|last3=Han|first3=Eun Ae|last4=Lee|first4=Hae Jin|last5=Ryeu|first5=Bung Jun|last6=Lee|first6=Kap No|last7=Lee|first7=Chang Kyu|last8=Cho|first8=Yunjung|last9=Kim|first9=Young Kee|date=2009|title=Cytogenetic abnormality involving 8p11.2 in T-lymphoblastic lymphoma: report of a new case|url=https://linkinghub.elsevier.com/retrieve/pii/S0165460809000867|journal=Cancer Genetics and Cytogenetics|language=en|volume=191|issue=1|pages=57–58|doi=10.1016/j.cancergencyto.2009.02.003}}</ref>
|-
|t(5;8)(q35;p11)
|SQSTM1-FGFR1
|One case <ref>{{Cite journal|last=Bessho|first=M.|last2=Uchida|first2=Y.|last3=E. Kakegawa|last4=Wakimoto|first4=N.|last5=Ito|first5=Y.|last6=Nakamura|first6=Y.|date=2014|title=A novel fusion of SQSTM1 and FGFR1 in a patient with acute myelomonocytic leukemia with t(5;8)(q35;p11) translocation|url=https://www.nature.com/articles/bcj201486|journal=Blood Cancer Journal|language=en|volume=4|issue=12|pages=e265–e265|doi=10.1038/bcj.2014.86|issn=2044-5385|pmc=PMC4315892|pmid=25501022}}</ref>
|}

</blockquote>


<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|Please incorporate this section into the relevant tables found in:
* Chromosomal Rearrangements (Gene Fusions)
* Individual Region Genomic Gain/Loss/LOH
* Characteristic Chromosomal Patterns
* Gene Mutations (SNV/INDEL)}}

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

Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable. Do not delete table.'') </span>

{| 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
|-
|<span class="blue-text">EXAMPLE:</span>

7
|<span class="blue-text">EXAMPLE:</span> Loss
|<span class="blue-text">EXAMPLE:</span>

chr7:1- 159,335,973 [hg38]
|<span class="blue-text">EXAMPLE:</span>

chr7
|Yes
|Yes
|No
|<span class="blue-text">EXAMPLE:</span>

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).
|-
|<span class="blue-text">EXAMPLE:</span>

8
|<span class="blue-text">EXAMPLE:</span> Gain
|<span class="blue-text">EXAMPLE:</span>

chr8:1-145,138,636 [hg38]
|<span class="blue-text">EXAMPLE:</span>

chr8
|No
|No
|No
|<span class="blue-text">EXAMPLE:</span>

Common recurrent secondary finding for t(8;21) (add reference).
|}
==Characteristic Chromosomal Patterns==

Put your text here <span style="color:#0070C0">(''EXAMPLE PATTERNS: 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. Do not delete table.'')</span>

{| class="wikitable sortable"
|-
!Chromosomal Pattern
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|<span class="blue-text">EXAMPLE:</span>

Co-deletion of 1p and 18q
|Yes
|No
|No
|<span class="blue-text">EXAMPLE:</span>

See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).
|}

<blockquote class='blockedit'>{{Box-round|title=v4:Characteristic Chromosomal Aberrations / Patterns|The content below was from the old template. Please incorporate above.}}

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

</blockquote>
==Gene Mutations (SNV / INDEL)==

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 and common as well as either disease defining and/or clinically significant. Can include references 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. Do not delete table.'') </span>

{| 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
|-
|<span class="blue-text">EXAMPLE:</span> TP53; Variable LOF mutations

<span class="blue-text">EXAMPLE:</span>

EGFR; Exon 20 mutations

<span class="blue-text">EXAMPLE:</span> BRAF; Activating mutations
|<span class="blue-text">EXAMPLE:</span> TSG
|<span class="blue-text">EXAMPLE:</span> 20% (COSMIC)

<span class="blue-text">EXAMPLE:</span> 30% (add Reference)
|<span class="blue-text">EXAMPLE:</span> IDH1 R123H
|<span class="blue-text">EXAMPLE:</span> EGFR amplification
|
|
|
|<span class="blue-text">EXAMPLE:</span>  Excludes hairy cell leukemia (HCL) (add reference).
<br />
|}
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 <span style="color:#0070C0">(''Instructions: Can include references in the table. Do not delete table.'')</span>
{| class="wikitable sortable"
|-
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
|-
|<span class="blue-text">EXAMPLE:</span> BRAF and MAP2K1; Activating mutations
|<span class="blue-text">EXAMPLE:</span> MAPK signaling
|<span class="blue-text">EXAMPLE:</span> Increased cell growth and proliferation
|-
|<span class="blue-text">EXAMPLE:</span> CDKN2A; Inactivating mutations
|<span class="blue-text">EXAMPLE:</span> Cell cycle regulation
|<span class="blue-text">EXAMPLE:</span> Unregulated cell division
|-
|<span class="blue-text">EXAMPLE:</span>  KMT2C and ARID1A; Inactivating mutations
|<span class="blue-text">EXAMPLE:</span>  Histone modification, chromatin remodeling
|<span class="blue-text">EXAMPLE:</span>  Abnormal gene expression program
|}

<blockquote class='blockedit'>{{Box-round|title=v4:Genes and Main Pathways Involved|The content below was from the old template. Please incorporate above.}}

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>
==Genetic Diagnostic Testing Methods==

Diagnosis is based on integration of morphology, immunophenotype, cytogenetics analysis and molecular analysis. Identification of translocations involving ''FGFR1'' and the corresponding fusion genes is diagnostic in the setting of myeloid or lymphoid neoplasm with prominent eosinophilia. Conventional cytogenetic analysis is useful since almost all the translocations or insertions involving ''FGFR1'' have been cytogenetically visible <ref>A. Meloni-Ehrig (2013), The Cytogenetics of Hematologic Neoplasms in The Principles of Clinical Cytogenetics. 4<sup>th</sup> edition, '''Gersen''', Steven L., '''Keagle''', Martha B. <nowiki>ISBN 978-1-4899-9720-3</nowiki>, p320</ref><ref name=":2" />. Translocations of ''FGFR1'' and the associated fusion genes can be more specifically detected by two-color fluorescence in situ hybridization (FISH), and reverse transcriptase–polymerase chain reaction (RT-PCR) <ref name=":3" /> <ref name=":5" /><ref>{{Cite journal|last=Cowell|first=John K.|last2=Stone|first2=Richard M.|last3=Hurd|first3=David|last4=Chernova|first4=Olga|last5=Still|first5=Ivan H.|date=1997|title=Molecular Characterization of the t(8; 13)(p11;q12) Translocation Associated With an Atypical Myeloproliferative Disorder: Evidence for Three Discrete Loci Involved in Myeloid Leukemias on 8p11|url=https://ashpublications.org/blood/article/90/8/3136/139329/Molecular-Characterization-of-the-t-8-13-p11-q12|journal=Blood|language=en|volume=90|issue=8|pages=3136–3141|doi=10.1182/blood.V90.8.3136|issn=0006-4971}}</ref>.

==Familial Forms==

Put your text here <span style="color:#0070C0">(''Instructions: Include associated hereditary conditions/syndromes that cause this entity or are caused by this entity.'') </span>

==Additional Information==

Put your text here

==Links==

[[FGFR1]]

==References==




<references />
==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.
<references />

<nowiki>*</nowiki>''Citation of this Page'': “Myeloid/lymphoid neoplasm with FGFR1 rearrangement”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:Myeloid/lymphoid_neoplasm_with_FGFR1_rearrangement</nowiki>.
[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases M]]