ArticleCancer research2011
Src activation plays an important key role in lymphomagenesis induced by FGFR1 fusion kinases.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- Constitutive activation of the Src-family kinases Fgr and Hck enhances the tumor burden of acute myeloid leukemia cells in immunocompromised mice.Scientific reports · 2025Article
- Formyl-peptide receptor 2 signalling triggers aerobic metabolism of glucose through Nox2-dependent modulation of pyruvate dehydrogenase activity.Open biology · 2023Article
- Ruscogenin ameliorates dasatinib-induced intestinal barrier dysfunction via ErbB4/YAP and ROCK/MLC pathways.Journal of natural medicines · 2023Article
- A truncated derivative of FGFR1 kinase cooperates with FLT3 and KIT to transform hematopoietic stem cells in syndromic and de novo AML.Molecular cancer · 2022Article
- IRAK1-regulated IFN-γ signaling induces MDSC to facilitate immune evasion in FGFR1-driven hematological malignancies.Molecular cancer · 2021Article
- Review
- Mechanisms of resistance to FGFR1 inhibitors in FGFR1-driven leukemias and lymphomas: implications for optimized treatment.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Rac1/2 activation promotes FGFR1 driven leukemogenesis in stem cell leukemia/lymphoma syndrome.Haematologica · 2020Article
- A new FGFR inhibitor disrupts the TGF-β1-induced fibrotic process.Journal of cellular and molecular medicine · 2020Article
- Article
- Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer.Nature communications · 2019Article
- FGFR1 fusion kinase regulation of MYC expression drives development of stem cell leukemia/lymphoma syndrome.Leukemia · 2018Article
- Fibroblast growth factor receptor 1 antagonism attenuates lipopolysaccharide-induced activation of hepatic stellate cells via suppressing inflammation.Experimental and therapeutic medicine · 2018Article
- The miR-17/92 cluster is involved in the molecular etiology of the SCLL syndrome driven by the BCR-FGFR1 chimeric kinase.Oncogene · 2018Article
- Mutation in the FGFR1 tyrosine kinase domain or inactivation of PTEN is associated with acquired resistance to FGFR inhibitors in FGFR1-driven leukemia/lymphomas.International journal of cancer · 2017Article
- Response to Tyrosine Kinase Inhibitors in Myeloproliferative Neoplasia with 8p11 Translocation andThe oncologist · 2017Article
- Development of ZMYM2-FGFR1 driven AML in human CD34+ cells in immunocompromised mice.International journal of cancer · 2016Article
- Identification of novel peptoid agonists of fibroblast growth factor receptor using microarray-based screening.MedChemComm · 2016Article
- Integrated genomic characterization reveals novel, therapeutically relevant drug targets in FGFR and EGFR pathways in sporadic intrahepatic cholangiocarcinoma.PLoS genetics · 2014Article
- Sepantronium is a DNA damaging agent that synergizes with PLK1 inhibitor volasertib.American journal of cancer research · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chromosomal translocations and activation of the fibroblast growth factor (FGF) receptor 1 (FGFR1) are a feature of stem cell leukemia-lymphoma syndrome (SCLL), an aggressive malignancy characterized by rapid transformation to acute myeloid leukemia and lymphoblastic lymphoma. It has been suggested that FGFR1 proteins lose their ability to recruit Src kinase, an important mediator of FGFR1 signaling, as a result of the translocations that delete the extended FGFR substrate-2 (FRS2) interacting domain that Src binds. In this study, we report evidence that refutes this hypothesis and reinforces the notion that Src is a critical mediator of signaling from the FGFR1 chimeric fusion genes generated by translocation in SCLL. Src was constitutively active in BaF3 cells expressing exogenous FGFR1 chimeric kinases cultured in vitro as well as in T-cell or B-cell lymphomas they induced in vivo. Residual components of the FRS2-binding site retained in chimeric kinases that were generated by translocation were sufficient to interact with FRS2 and activate Src. The Src kinase inhibitor dasatinib killed transformed BaF3 cells and other established murine leukemia cell lines expressing chimeric FGFR1 kinases, significantly extending the survival of mice with SCLL syndrome. Our results indicated that Src kinase is pathogenically activated in lymphomagenesis induced by FGFR1 fusion genes, implying that Src kinase inhibitors may offer a useful option to treatment of FGFR1-associated myeloproliferative/lymphoma disorders.
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