Myeloid/lymphoid neoplasm with FGFR1 rearrangement

From Compendium of Cancer Genome Aberrations
Jump to navigation Jump to search


Haematolymphoid Tumours (WHO Classification, 5th ed.)

editContent 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.

(General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). Use HUGO-approved gene names and symbols (italicized when appropriate), 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 in a table, click nearby within the table and select the > symbol that appears. 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 Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support.)

Primary Author(s)*

Yanna Ding, MD PhD

WHO Classification of Disease

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

WHO Essential and Desirable Genetic Diagnostic Criteria

(Instructions: The table will have the diagnostic criteria from the WHO book autocompleted; remove any non-genetics related criteria. If applicable, add text about other classification systems that define this entity and specify how the genetics-related criteria differ.)

WHO Essential Criteria (Genetics)*
WHO Desirable Criteria (Genetics)*
Other Classification

*Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the WHO Classification of Tumours.

Related Terminology

(Instructions: The table will have the related terminology from the WHO autocompleted.)

Acceptable
Not Recommended

Gene Rearrangements

Put your text here and fill in the table (Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Driver Gene Fusion(s) and Common Partner Genes Molecular Pathogenesis Typical Chromosomal Alteration(s) Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE: ABL1 EXAMPLE: BCR::ABL1 EXAMPLE: The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1. EXAMPLE: t(9;22)(q34;q11.2) EXAMPLE: Common (CML) EXAMPLE: D, P, T EXAMPLE: Yes (WHO, NCCN) EXAMPLE:

The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference). BCR::ABL1 is generally favorable in CML (add reference).

EXAMPLE: CIC EXAMPLE: CIC::DUX4 EXAMPLE: Typically, the last exon of CIC is fused to DUX4. The fusion breakpoint in CIC is usually intra-exonic and removes an inhibitory sequence, upregulating PEA3 genes downstream of CIC including ETV1, ETV4, and ETV5. EXAMPLE: t(4;19)(q25;q13) EXAMPLE: Common (CIC-rearranged sarcoma) EXAMPLE: D EXAMPLE:

DUX4 has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references).

EXAMPLE: ALK EXAMPLE: ELM4::ALK


Other fusion partners include KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1

EXAMPLE: Fusions result in constitutive activation of the ALK tyrosine kinase. The most common ALK fusion is EML4::ALK, with breakpoints in intron 19 of ALK. At the transcript level, a variable (5’) partner gene is fused to 3’ ALK at exon 20. Rarely, ALK fusions contain exon 19 due to breakpoints in intron 18. EXAMPLE: N/A EXAMPLE: Rare (Lung adenocarcinoma) EXAMPLE: T EXAMPLE:

Both balanced and unbalanced forms are observed by FISH (add references).

EXAMPLE: ABL1 EXAMPLE: N/A EXAMPLE: Intragenic deletion of exons 2–7 in EGFR removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways. EXAMPLE: N/A EXAMPLE: Recurrent (IDH-wildtype Glioblastoma) EXAMPLE: D, P, T
editv4: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 [1].

Chromosomal Rearrangement Genes in Fusion (5’ or 3’ Segments) Prevalence
t(8;13)(p11.2;q12.1) ZMYM2-FGFR1 Most common, around 40% [2][3][4][5][6][7]
t(8;9)(p11.2;q33.2) CNTRL-FGFR1 Around 17% [7][8]
t(6;8)(q27;p11.2) FGFR1OP-FGFR1 Around 9% [7] [9]
t(8;22)(p11.2;q11.2) BCR-FGFR1 At least eight cases[10][11][12][13][14]
t(7;8)(q33;p11.2) TRIM24-FGFR1 At least two cases [15][16]
t(8;17)(p11.2;q23) MYO18A-FGFR1 At least one case[17]
t(8;19)(p11.2;q13.3) HERVK-FGFR1 At least one case [18][19]
ins(12;8)(p11.2;p11.2p22) FGFR1OP2-FGFR1 At least two cases [16][20]
t(1;8)(q31.1;p11.2) TRP-FGFR1 At least one case [21]
t(2;8)(q13;p11.2) RANBP2-FGFR1 At least one case [22]
t(2;8)(q37.3;p11.2) LRRFIP1-FGFR1 At least one case [23]
t(7;8)(q22.1;p11.2) CUX1-FGFR1 At least one case [24]
t(8;12)(p11.2;q15) CPSF6-FGFR1 At least two cases [16][25]
t(5;8)(q35;p11) SQSTM1-FGFR1 One case [26]
End of V4 Section


editv4: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 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 [27], and interferon has induced cytogenetic response in several cases [28] [29]. Nevertheless, haematopoietic stem cell transplantation should be considered even for patients in chronic phase.

End of V4 Section

Individual Region Genomic Gain/Loss/LOH

Put your text here and fill in the table (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.)

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 Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:

7

EXAMPLE: Loss EXAMPLE:

chr7

EXAMPLE:

Unknown

EXAMPLE: D, P EXAMPLE: No EXAMPLE:

Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference).  Monosomy 7/7q deletion is associated with a poor prognosis in AML (add references).

EXAMPLE:

8

EXAMPLE: Gain EXAMPLE:

chr8

EXAMPLE:

Unknown

EXAMPLE: D, P EXAMPLE:

Common recurrent secondary finding for t(8;21) (add references).

EXAMPLE:

17

EXAMPLE: Amp EXAMPLE:

17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb]

EXAMPLE:

ERBB2

EXAMPLE: D, P, T EXAMPLE:

Amplification of ERBB2 is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined.

Characteristic Chromosomal or Other Global Mutational Patterns

Put your text here and fill in the table (Instructions: 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.)

Chromosomal Pattern Molecular Pathogenesis Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:

Co-deletion of 1p and 18q

EXAMPLE: See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). EXAMPLE: Common (Oligodendroglioma) EXAMPLE: D, P
EXAMPLE:

Microsatellite instability - hypermutated

EXAMPLE: Common (Endometrial carcinoma) EXAMPLE: P, T
editv4: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 [30].

End of V4 Section

Gene Mutations (SNV/INDEL)

Put your text here and fill in the table (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.)

Gene Genetic Alteration Tumor Suppressor Gene, Oncogene, Other Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T   Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:EGFR


EXAMPLE: Exon 18-21 activating mutations EXAMPLE: Oncogene EXAMPLE: Common (lung cancer) EXAMPLE: T EXAMPLE: Yes (NCCN) EXAMPLE: Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references).
EXAMPLE: TP53; Variable LOF mutations


EXAMPLE: Variable LOF mutations EXAMPLE: Tumor Supressor Gene EXAMPLE: Common (breast cancer) EXAMPLE: P EXAMPLE: >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer.
EXAMPLE: BRAF; Activating mutations EXAMPLE: Activating mutations EXAMPLE: Oncogene EXAMPLE: Common (melanoma) EXAMPLE: T

Note: A more extensive list of mutations can be found in cBioportal, COSMIC, 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 (Instructions: Please include references throughout the table. Do not delete the table.)

Gene; Genetic Alteration Pathway Pathophysiologic Outcome
EXAMPLE: BRAF and MAP2K1; Activating mutations EXAMPLE: MAPK signaling EXAMPLE: Increased cell growth and proliferation
EXAMPLE: CDKN2A; Inactivating mutations EXAMPLE: Cell cycle regulation EXAMPLE: Unregulated cell division
EXAMPLE: KMT2C and ARID1A; Inactivating mutations EXAMPLE: Histone modification, chromatin remodeling EXAMPLE: Abnormal gene expression program
editv4: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 [31][32][33][34].

End of V4 Section

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 [35][7]. 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) [5] [19][36].

Familial Forms

Put your text here (Instructions: Include associated hereditary conditions/syndromes that cause this entity or are caused by this entity.)

Additional Information

Put your text here

Links

FGFR1

References

  1. ↑ Mozziconacci, Marie-Joëlle; et al. (2008). "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". Leukemia Research. 32 (8): 1304–1308. doi:10.1016/j.leukres.2007.11.012.
  2. ↑ Popovici, C.; et al. (1998). "Fibroblast growth factor receptor 1 is fused to FIM in stem-cell myeloproliferative disorder with t(8;13)(p12;q12)". Proceedings of the National Academy of Sciences. 95 (10): 5712–5717. doi:10.1073/pnas.95.10.5712. ISSN 0027-8424. PMC 20444. PMID 9576949.CS1 maint: PMC format (link)
  3. ↑ Cross, Nicholas C. P.; et al. (1998). "Consistent Fusion of ZNF198 to the Fibroblast Growth Factor Receptor-1 in the t(8;13)(p11;q12) Myeloproliferative Syndrome". Blood. 92 (5): 1735–1742. doi:10.1182/blood.V92.5.1735. ISSN 0006-4971.
  4. ↑ Smedley, D (1998). "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". Human Molecular Genetics. 7 (4): 637–642. doi:10.1093/hmg/7.4.637.
  5. ↑ Jump up to: 5.0 5.1 Xiao, Sheng; et al. (1998). "FGFR1 is fused with a novel zinc-finger gene, ZNF198, in the t(8;13) leukaemia/lymphoma syndrome". Nature Genetics. 18 (1): 84–87. doi:10.1038/ng0198-84. ISSN 1061-4036.
  6. ↑ Bain, Barbara J.; et al. (2007-08). "Chronic Eosinophilic Leukemias and the Myeloproliferative Variant of the Hypereosinophilic Syndrome". Immunology and Allergy Clinics of North America. 27 (3): 377–388. doi:10.1016/j.iac.2007.06.001. ISSN 0889-8561. Check date values in: |date= (help)
  7. ↑ Jump up to: 7.0 7.1 7.2 7.3 Jackson, Courtney C.; et al. (2010). "8p11 myeloproliferative syndrome: a review". Human Pathology. 41 (4): 461–476. doi:10.1016/j.humpath.2009.11.003. ISSN 0046-8177.
  8. ↑ Pébusque, Marie-Josèphe; et al. (2000). "FGFR1 is fused to the centrosome-associated proteinCEP110 in the 8p12 stem cell myeloproliferative disorder with t(8;9)(p12;q33)". Blood. 95 (5): 1788–1796. doi:10.1182/blood.V95.5.1788.005k15_1788_1796. ISSN 0006-4971.
  9. ↑ Pébusque, Marie-Josèphe; et al. (1999). "The t(6;8)(q27;p11) Translocation in a Stem Cell Myeloproliferative Disorder Fuses a Novel Gene, FOP, to Fibroblast Growth Factor Receptor 1". Blood. 93 (4): 1381–1389. doi:10.1182/blood.V93.4.1381. ISSN 0006-4971.
  10. ↑ Steer, E. J.; et al. (2001). E. J. Steer, A. Demiroglu, C. Heath, E. Pourgourides, K. Taylor, M. Bentley. "The t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteins". Blood. 98: pp.468A. ISSN 0006-4971.CS1 maint: Extra text (link)
  11. ↑ Ågerstam, Helena; et al. (2007). "Fusion gene-mediated truncation ofRUNX1 as a potential mechanism underlying disease progression in the 8p11 myeloproliferative syndrome". Genes, Chromosomes and Cancer. 46 (7): 635–643. doi:10.1002/gcc.20442.
  12. ↑ Liu, Jing; et al. (2018). "8p11 Myeloproliferative syndrome with t(8;22)(p11;q11): A case report". Experimental and Therapeutic Medicine. doi:10.3892/etm.2018.6328. ISSN 1792-0981. PMC 6090294. PMID 30116393.CS1 maint: PMC format (link)
  13. ↑ Fioretos, Thoas; et al. (2001). "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". Genes, Chromosomes and Cancer. 32 (4): 302–310. doi:10.1002/gcc.1195.
  14. ↑ Pini, Massimo; et al. (2002). "A fourth case of BCR-FGFR1 positive CML-like disease with t(8;22) translocation showing an extensive deletion on the derivative chromosome 8p". The Hematology Journal. 3 (6): 315–316. doi:10.1038/sj.thj.6200201.
  15. ↑ Belloni, Elena; et al. (2005). "8p11 myeloproliferative syndrome with a novel t(7;8) translocation leading to fusion of the FGFR1 and TIF1 genes". Genes, Chromosomes and Cancer. 42 (3): 320–325. doi:10.1002/gcc.20144. ISSN 1098-2264.
  16. ↑ Jump up to: 16.0 16.1 16.2 Sohal, Jastinder; et al. (2001). "Identification of four new translocations involvingFGFR1 in myeloid disorders". Genes, Chromosomes and Cancer. 32 (2): 155–163. doi:10.1002/gcc.1177. ISSN 1045-2257.
  17. ↑ Walz, C; et al. (2005). "The t(8;17)(p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1". Leukemia. 19 (6): 1005–1009. doi:10.1038/sj.leu.2403712. ISSN 0887-6924.
  18. ↑ Mugneret, Francine; et al. (2000). "The 8p12 myeloproliferative disorder. t(8;19)(p12;q13.3): a novel translocation involving the FGFR1 gene . SHORT REPORT". British Journal of Haematology. 111 (2): 647–649. doi:10.1046/j.1365-2141.2000.02355.x. ISSN 0007-1048.
  19. ↑ Jump up to: 19.0 19.1 Pébusque, Marie-Josèphe; et al. (2003). "Endogenous retroviral sequence is fused to FGFR1 kinase in the 8p12 stem-cell myeloproliferative disorder with t(8;19)(p12;q13.3)". Blood. 101 (1): 286–288. doi:10.1182/blood-2002-02-0577. ISSN 0006-4971.
  20. ↑ Grand, Effie K.; et al. (2004). "Identification of a novel gene,FGFR1OP2, fused toFGFR1 in 8p11 myeloproliferative syndrome". Genes, Chromosomes and Cancer. 40 (1): 78–83. doi:10.1002/gcc.20023. ISSN 1045-2257.
  21. ↑ Li, Feng; et al. (2012). "Identification of a novel partner gene, TPR, fused to FGFR1 in 8p11 myeloproliferative syndrome". Genes, Chromosomes and Cancer. 51 (9): 890–897. doi:10.1002/gcc.21973. ISSN 1098-2264.
  22. ↑ Mauvieux, L.; et al. (2013). "A translocation t(2;8)(q12;p11) fuses FGFR1 to a novel partner gene, RANBP2/NUP358 , in a myeloproliferative/myelodysplastic neoplasm". Leukemia. 27 (5): 1186–1188. doi:10.1038/leu.2012.286. ISSN 1476-5551.
  23. ↑ Soler, G; et al. (2009). "LRRFIP1, a new FGFR1 partner gene associated with 8p11 myeloproliferative syndrome". Leukemia. 23 (7): 1359–1361. doi:10.1038/leu.2009.79. ISSN 0887-6924.
  24. ↑ Wasag, B.; et al. (2011). "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)". Haematologica. 96 (6): 922–926. doi:10.3324/haematol.2010.036558. ISSN 0390-6078. PMC 3105656. PMID 21330321.CS1 maint: PMC format (link)
  25. ↑ Bae, Sook Young; et al. (2009). "Cytogenetic abnormality involving 8p11.2 in T-lymphoblastic lymphoma: report of a new case". Cancer Genetics and Cytogenetics. 191 (1): 57–58. doi:10.1016/j.cancergencyto.2009.02.003.
  26. ↑ Bessho, M.; et al. (2014). "A novel fusion of SQSTM1 and FGFR1 in a patient with acute myelomonocytic leukemia with t(5;8)(q35;p11) translocation". Blood Cancer Journal. 4 (12): e265–e265. doi:10.1038/bcj.2014.86. ISSN 2044-5385. PMC 4315892. PMID 25501022.CS1 maint: PMC format (link)
  27. ↑ Chen, J.; et al. (2004). "PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder". Proceedings of the National Academy of Sciences. 101 (40): 14479–14484. doi:10.1073/pnas.0404438101. ISSN 0027-8424. PMC 521956. PMID 15448205.CS1 maint: PMC format (link)
  28. ↑ Macdonald, Donald; et al. (2002). "The 8p11 Myeloproliferative Syndrome: A Distinct Clinical Entity Caused by Constitutive Activation of FGFR1". Acta Haematologica. 107 (2): 101–107. doi:10.1159/000046639. ISSN 0001-5792.
  29. ↑ Holmes, A L; et al. (1998). "Genetic analysis of Drosophila larval optic nerve development". Genetics. 148 (3): 1189–1201. ISSN 0016-6731. PMC 1460051. PMID 9539434.
  30. ↑ 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.
  31. ↑ Ollendorff, Vincent; et al. (1999). "Characterization of FIM-FGFR1, the Fusion Product of the Myeloproliferative Disorder-associated t(8;13) Translocation". Journal of Biological Chemistry. 274 (38): 26922–26930. doi:10.1074/jbc.274.38.26922. ISSN 0021-9258.
  32. ↑ Jiang, Guoqiang; et al. (2000). "Receptor-Like Protein Tyrosine Phosphatase α Homodimerizes on the Cell Surface". Molecular and Cellular Biology. 20 (16): 5917–5929. doi:10.1128/MCB.20.16.5917-5929.2000. ISSN 1098-5549. PMC 86069. PMID 10913175.CS1 maint: PMC format (link)
  33. ↑ Mason, Ivor J. (1994). "The ins and outs of fibroblast growth factors". Cell. 78 (4): 547–552. doi:10.1016/0092-8674(94)90520-7.
  34. ↑ Smedley, Damian; et al. (1999). "ZNF198-FGFR1 Transforms Ba/F3 Cells to Growth Factor Independence and Results in High Level Tyrosine Phosphorylation of STATS 1 and 5". Neoplasia. 1 (4): 349–355. doi:10.1038/sj.neo.7900035. PMC 1508104. PMID 10935490.CS1 maint: PMC format (link)
  35. ↑ A. Meloni-Ehrig (2013), The Cytogenetics of Hematologic Neoplasms in The Principles of Clinical Cytogenetics. 4th edition, Gersen, Steven L., Keagle, Martha B. ISBN 978-1-4899-9720-3, p320
  36. ↑ Cowell, John K.; et al. (1997). "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". Blood. 90 (8): 3136–3141. doi:10.1182/blood.V90.8.3136. ISSN 0006-4971.

Notes

*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.


*Citation of this Page: “Myeloid/lymphoid neoplasm with FGFR1 rearrangement”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 02/11/2025, https://ccga.io/index.php/HAEM5:Myeloid/lymphoid_neoplasm_with_FGFR1_rearrangement.

Retrieved from "https://ccga.io/index.php?title=HAEM5:Myeloid/lymphoid_neoplasm_with_FGFR1_rearrangement&oldid=16244"