ReviewJournal of cellular and molecular medicine2012
Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.
Review in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 97 citations in OpenAlex.
- Detection, Characterization, and Inhibition of FGFR-TACC Fusions in IDH Wild-type Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Trial
- Targeting fusion proteins in solid tumors: from oncogenic mechanisms to clinical interventions.Acta pharmacologica Sinica · 2026Review
- Optogenetic Translocation to Subcellular Compartments through Regulation of Protein Avidity.ACS synthetic biology · 2026Article
- Low-order assemblies drive oncogenic RTK fusion signaling without condensation.bioRxiv : the preprint server for biology · 2025Article
- Landscape of gene fusions in hormone receptor-positive breast cancer reveals ADK fusions as drivers of progression and potential therapeutic targets.Cell discovery · 2025Article
- Head and Neck Classic Hodgkin, T and NK Lymphomas with Eosinophilia.Head and neck pathology · 2025Review
- Novel insight into mechanisms of ROS1 catalytic activation via loss of the extracellular domain.Scientific reports · 2024Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Fusion Challenges in Solid Tumors: Shaping the Landscape of Cancer Care in Precision Medicine.JCO precision oncology · 2024Review
- FusionNW, a potential clinical impact assessment of kinases in pan-cancer fusion gene network.Briefings in bioinformatics · 2024Article
- Review
- Comparative Atomistic Insights on Apo and ATP-I1171N/S/T in Nonsmall-Cell Lung Cancer.ACS omega · 2023Article
- Discovery of oncogenic ROS1 missense mutations with sensitivity to tyrosine kinase inhibitors.EMBO molecular medicine · 2023Article
- Kinase regulation by liquid-liquid phase separation.Trends in cell biology · 2023Review
- Therapeutic Advances of Rare ALK Fusions in Non-Small Cell Lung Cancer.Current oncology (Toronto, Ont.) · 2022Review
- Glioblastoma,Frontiers in neurology · 2022Review
- Review
- Fibroblast growth factor receptor fusions in cancer: opportunities and challenges.Journal of experimental & clinical cancer research : CR · 2021Review
- Genomic characterization and outcome evaluation of kinome fusions in lung cancer revealed novel druggable fusions.NPJ precision oncology · 2021Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine kinase fusion genes represent an important class of oncogenes associated with leukaemia and solid tumours. They are produced by translocations and other chromosomal rearrangements of a subset of tyrosine kinase genes, including ABL, PDGFRA, PDGFRB, FGFR1, SYK, RET, JAK2 and ALK. Based on recent findings, this review discusses the common mechanisms of activation of these fusion genes. Enforced oligomerization and inactivation of inhibitory domains are the two key processes that switch on the kinase domain. Activated tyrosine kinase fusions then signal via an array of transduction cascades, which are largely shared. In addition, the fusion partner provides a scaffold for the recruitment of proteins that contribute to signalling, protein stability, cellular localization and oligomerization. The expression level of the fusion protein is another critical parameter. Its transcription is controlled by the partner gene promoter, while translation may be regulated by miRNA. Several mechanisms also prevent the degradation of the oncoprotein by proteasomes and lysosomes, leading to its accumulation in cells. The selective inhibition of the tyrosine kinase activity by adenosine-5'-triphosphate competitors, such as imatinib, is a major therapeutic success. Imatinib induces remission in leukaemia patients that are positive for BCR-ABL or PDGFR fusions. Recently, crizotinib produced promising results in a subtype of lung cancers with ALK fusion. However, resistance was reported in both cases, partially due to mutations. To tackle this problem, additional levels of therapeutic interventions are suggested by the complex mechanisms of fusion tyrosine kinase activation. New approaches include allosteric inhibition and interfering with oligomerization or chaperones.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.