ArticleCell reports2017
KIF5B-RET Oncoprotein Signals through a Multi-kinase Signaling Hub.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- The efficacy and safety of selective RET inhibitors in RET fusion-positive non-small cell lung cancer: a meta-analysis.Investigational new drugs · 2023Pooled it
- Safety, pharmacokinetics and efficacy of HA121-28 in patients with advanced solid tumors and RET fusion-positive non-small-cell lung cancer: a multicenter, open-label, single-arm phase 1/2 trial.Signal transduction and targeted therapy · 2025Trial
- Rigosertib Reverses Hypertrophic Cardiomyopathy in Noonan Syndrome.Circulation · 2026Article
- Real-world evidence of RET fusion prevalence and testing in patients with metastatic non-small cell lung cancer.Translational oncology · 2026Article
- Dual targeting of RET and SRC synergizes in RET fusion-positive cancer cells.Molecular oncology · 2026Article
- Optogenetic Translocation to Subcellular Compartments through Regulation of Protein Avidity.ACS synthetic biology · 2026Article
- KIF5B-driven unfolded protein response reprograms breast cancer immunosuppressive microenvironment for single-cell guided therapeutic targeting.Discover oncology · 2026Article
- Exploring the versatility ofFly · 2025Review
- AccurateInternational journal of molecular sciences · 2025Article
- Hinge binder modification into imidazopyridine for targeting actionable mutations of RET kinase.RSC medicinal chemistry · 2025Article
- Review
- Proteogenomic Identification and Analysis of KIF5B as a Prognostic Signature for Hepatocellular Carcinoma.Current gene therapy · 2025Article
- Identification of immunogenic KIF5B-RET fusion neopeptides driving immune stimulation in tumor specific CD8+ T cells.Frontiers in immunology · 2025Article
- Side Chain Investigation of Imidazopyridazine as a Hinge Binder for Targeting Actionable Mutations of RET Kinase.ACS medicinal chemistry letters · 2024Article
- Differences in Genomic Alterations and Accumulations of Heavy Metals Between Advanced Non-small Cell Lung Cancer Patients with and without Bone Metastasis.Journal of Cancer · 2024Article
- Progress and challenges in RET-targeted cancer therapy.Frontiers of medicine · 2023Review
- Fruit fly for anticancer drug discovery and repurposing.Annals of medicine and surgery (2012) · 2023Article
- Precious Gene: The Application of RET-Altered Inhibitors.Molecules (Basel, Switzerland) · 2022Review
- Pralsetinib treatment for multipleThe Journal of international medical research · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Gene fusions are increasingly recognized as important cancer drivers. The KIF5B-RET gene has been identified as a primary driver in a subset of lung adenocarcinomas. Targeting human KIF5B-RET to epithelia in Drosophila directed multiple aspects of transformation, including hyperproliferation, epithelial-to-mesenchymal transition, invasion, and extension of striking invadopodia-like processes. The KIF5B-RET-transformed human bronchial cell line showed similar aspects of transformation, including invadopodia-like processes. Through a combination of genetic and biochemical studies, we demonstrate that the kinesin and kinase domains of KIF5B-RET act together to establish an emergent microtubule and RAB-vesicle-dependent RET-SRC-EGFR-FGFR signaling hub. We demonstrate that drugs designed to inhibit RET alone work poorly in KIF5B-RET-transformed cells. However, combining the RET inhibitor sorafenib with drugs that target EGFR, microtubules, or FGFR led to strong efficacy in both Drosophila and human cell line KIF5B-RET models. This work demonstrates the utility of exploring the full biology of fusions to identify rational therapeutic strategies.
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Identifiers
What OpenQuestion holds
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.