ArticleBlood2011
Constitutive Notch pathway activation in murine ZMYM2-FGFR1-induced T-cell lymphomas associated with atypical myeloproliferative disease.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Computational-experimental strategy identifies Co-upregulated biomarkers linking coronary heart disease and type 2 diabetes pathogenesis.Frontiers in genetics · 2025Article
- ATF4 renders human T-cell acute lymphoblastic leukemia cell resistance to FGFR1 inhibitors through amino acid metabolic reprogramming.Acta pharmacologica Sinica · 2023Article
- The FACT-targeted drug CBL0137 enhances the effects of rituximab to inhibit B-cell non-Hodgkin's lymphoma tumor growth by promoting apoptosis and autophagy.Cell communication and signaling : CCS · 2023Article
- Sex-related differential susceptibility to ponatinib cardiotoxicity and differential modulation of the Notch1 signalling pathway in a murine model.Journal of cellular and molecular medicine · 2022Article
- Identification of a novel HOOK3-FGFR1 fusion gene involved in activation of the NF-kappaB pathway.Cancer cell international · 2022Article
- A proximity biotinylation-based approach to identify protein-E3 ligase interactions induced by PROTACs and molecular glues.Nature communications · 2022Article
- Review
- Mechanisms of resistance to FGFR1 inhibitors in FGFR1-driven leukemias and lymphomas: implications for optimized treatment.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Downregulation of PUMA underlies resistance to FGFR1 inhibitors in the stem cell leukemia/lymphoma syndrome.Cell death & disease · 2020Article
- Expression of Viral microRNAs in Serum and White Blood Cells of Cows Exposed to Bovine Leukemia Virus.Frontiers in veterinary science · 2020Article
- Single‑cell intratumoral stemness analysis reveals the involvement of cell cycle and DNA damage repair in two different types of esophageal cancer.Oncology reports · 2019Article
- Loss of the BCR-FGFR1 GEF Domain Suppresses RHOA Activation and Enhances B-Lymphomagenesis in Mice.Cancer research · 2019Article
- Genomic analysis reveals recurrent deletion of JAK-STAT signaling inhibitors HNRNPK and SOCS1 in mycosis fungoides.Genes, chromosomes & cancer · 2018Article
- FGFR1 fusion kinase regulation of MYC expression drives development of stem cell leukemia/lymphoma syndrome.Leukemia · 2018Article
- miR-339 Promotes Development of Stem Cell Leukemia/Lymphoma Syndrome via Downregulation of theCancer research · 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
- RAG Recombinase as a Selective Pressure for Genome Evolution.Genome biology and evolution · 2016Article
- Transformation of human CD34+ hematopoietic progenitor cells with DEK-NUP214 induces AML in an immunocompromised mouse model.Oncogene · 2016Article
- SCLLTargeting FGFR1 to suppress leukemogenesis in syndromic and de novo AML in murine models.Oncotarget · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ZMYM2-FGFR1 (formerly known as ZNF198-FGFR1) fusion kinase induces stem cell leukemia-lymphoma syndrome (SCLL), a hematologic malignancy characterized by rapid transformation to acute myeloid leukemia and T-lymphoblastic lymphoma. In the present study, we demonstrate frequent, constitutive activation of Notch1 and its downstream target genes in T-cell lymphomas that arose in a murine model of ZMYM2-FGFR1 SCLL. Notch up-regulation was also demonstrated in human SCLL- and FGFR1OP2-FGFR1-expressing KG-1 cells. To study the role of Notch in T-cell lymphomagenesis, we developed a highly tumorigenic cell line from ZMYM2-FGFR1-expressing cells. Pharmacologic inhibition of Notch signaling in these cells using γ-secretase inhibitors significantly delayed leukemogenesis in vivo. shRNA targeting of Notch1, as well as c-promoter-binding factor 1 (CBF1) and mastermind-like 1 (MAML1), 2 essential cofactors involved in transcriptional activation of Notch target genes, also significantly delayed or inhibited tumorigenesis in vivo. Mutation analysis demonstrated that 5' promoter deletions and alternative promoter usage were responsible for constitutive activation of Notch1 in all T-cell lymphomas. These data demonstrate the importance of Notch signaling in the etiology of SCLL, and suggest that targeting this pathway could provide a novel strategy for molecular therapies to treat SCLL patients.
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