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The clinical/laboratory characteristics typically reflect features of chronic myeloid neoplasms and variable eosinophilia.9 Patients may also present as de novo AML without an antecedent MPN. There is a high incidence of T-lymphoblastic lymphomas, particularly in association with a t(8;13) and a ZMYM2-FGFR1 fusion gene,9,53,54 which may occur at diagnosis or during the course of disease, reflecting a myeloid/lymphoid stem cell origin. The clinical course is aggressive as a result of rapid progression to blast phase/secondary acute leukemia, usually of myeloid phenotype, less commonly B-ALL, within 1 or 2 years of diagnosis. The variability in the clinical presentation may be a result of specific moieties of the partner genes and signaling via different intracellular pathways.59 The t(8;22) is often associated with a clinical and hematologic picture very similar to that seen in BCR-ABL1-positive CML with basophilia,58,60 whereas thrombocytopenia and monocytosis resembling CMML are more frequently present in t(6;8)56 and t(8;9).55,61 The t(6;8) may also present with a PV-like disease,62 and eosinophilia may be absent in t(6;8) and t(8;22).(Reiter and Gotleib)

The clinical/laboratory characteristics typically reflect features of chronic myeloid neoplasms and variable eosinophilia.9 Patients may also present as de novo AML without an antecedent MPN. There is a high incidence of T-lymphoblastic lymphomas, particularly in association with a t(8;13) and a ZMYM2-FGFR1 fusion gene,9,53,54 which may occur at diagnosis or during the course of disease, reflecting a myeloid/lymphoid stem cell origin. The clinical course is aggressive as a result of rapid progression to blast phase/secondary acute leukemia, usually of myeloid phenotype, less commonly B-ALL, within 1 or 2 years of diagnosis. The variability in the clinical presentation may be a result of specific moieties of the partner genes and signaling via different intracellular pathways.59 The t(8;22) is often associated with a clinical and hematologic picture very similar to that seen in BCR-ABL1-positive CML with basophilia,58,60 whereas thrombocytopenia and monocytosis resembling CMML are more frequently present in t(6;8)56 and t(8;9).55,61 The t(6;8) may also present with a PV-like disease,62 and eosinophilia may be absent in t(6;8) and t(8;22).(Reiter and Gotleib)

==Gene Overview==

==Gene Overview==

Put your text here.

FGFR1 is a tyrosine kinase receptor and is a member (1 of 4) of the fibroblast growth factor receptor (FGFR) family.  FGFR1 differs from other members in the family in part by affinity to fibroblast growth factors(FGF) of which there are 22 members), having highest affinity for FGF1 (acidic) and FGF2 (basic).  Upon binding ligand, the ligand:receptor complex dimerizes and signals activation of downstream pathways, including RAS/RAF/MAPK, PI3K/ATK/mTor, Phospholipase C and Jak/STAT pathways, among others.

==Common Alteration Types==

==Common Alteration Types==

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| EXAMPLE: X ||EXAMPLE: X  || EXAMPLE: X  || EXAMPLE: X || EXAMPLE: X || EXAMPLE: X

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==Internal Pages==

==Internal Pages==

Reiter, A., & Gotlib, J. (2017). Myeloid neoplasms with eosinophilia. Blood, 129(6), 704-714. Accessed October 10, 2018. https://doi.org/10.1182/blood-2016-10-695973.

Reiter, A., & Gotlib, J. (2017). Myeloid neoplasms with eosinophilia. Blood, 129(6), 704-714. Accessed October 10, 2018. https://doi.org/10.1182/blood-2016-10-695973.

== Notes ==

== Notes ==