ArticleNPJ precision oncology2022
Functional characterization of NPM1-TYK2 fusion oncogene.
Article in NPJ precision oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- T cell lymphomas: cancers of aberrant immune synapse signalling.Nature reviews. Immunology · 2026Review
- Long-Read Transcriptome Sequencing and Functional Validation Reveals Novel and Oncogenic Gene Fusions in Fusion Panel-Negative Gliomas.bioRxiv : the preprint server for biology · 2026Article
- Architects and Partners: The Dual Roles of Non-coding RNAs in Gene Fusion Events.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Systemic ALK-negative anaplastic large cell lymphoma with NPM1::TYK2 rearrangement.Journal of hematopathology · 2024Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Targeting and Monitoring Acute Myeloid Leukaemia with Nucleophosmin-1 (International journal of molecular sciences · 2023Review
- Recent advances in cancer fusion transcript detection.Briefings in bioinformatics · 2023Review
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
Gene fusions are known to drive many human cancers. Therefore, the functional characterization of newly discovered fusions is critical to understanding the oncobiology of these tumors and to enable therapeutic development. NPM1-TYK2 is a novel fusion identified in CD30 + lymphoproliferative disorders, and here we present the functional evaluation of this fusion gene as an oncogene. The chimeric protein consists of the amino-terminus of nucleophosmin 1 (NPM1) and the carboxyl-terminus of tyrosine kinase 2 (TYK2), including the kinase domain. Using in vitro lymphoid cell transformation assays and in vivo tumorigenic xenograft models we present direct evidence that the fusion gene is an oncogene. NPM1 fusion partner provides the critical homodimerization needed for the fusion kinase constitutive activation and downstream signaling that are responsible for cell transformation. As a result, our studies identify NPM1-TYK2 as a novel fusion oncogene and suggest that inhibition of fusion homodimerization could be a precision therapeutic approach in cutaneous T-cell lymphoma patients expressing this chimera.
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Registered trials
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