ArticleOncotarget2016
Landscape of activating cancer mutations in FGFR kinases and their differential responses to inhibitors in clinical use.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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
57 citing papers in PubMed, 115 citations in OpenAlex.
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- Diagnosis of hypochondroplasia: international Delphi consensus recommendations.Nature reviews. Endocrinology · 2026Review
- Response to letter to the editor for "Infigratinib low dose therapy is an effective strategy to treat hypochondroplasia".Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Substrate-derived peptides for selective covalent inhibition of protein tyrosine kinases.bioRxiv : the preprint server for biology · 2026Article
- CDK4/6 Inhibitors for Breast Cancer Therapy-A Review of Clinical Trials, Structural and Computational Approaches.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Gene duplication is associated with gene diversification and potential neofunctionalization in lung cancer evolution.Genome research · 2026Article
- Case Report: Proportionate short stature in a three-generation family harboringFrontiers in endocrinology · 2026Article
- Saturation mutagenesis identifies activating and resistance-inducing FGFR kinase domain mutations.Nature genetics · 2026Article
- Green Synthesis of Gold Nanoparticles and Their Cytotoxic Effect in Breast Cancer: An Experimental and Theoretical Study.ACS applied bio materials · 2025Article
- Gene Dosage Sensitivity and Human Genetic Diseases.Journal of inherited metabolic disease · 2025Review
- Structure-Property Relationships Reported for the New Drugs Approved in 2024.Mini reviews in medicinal chemistry · 2025Review
- FGFR-Altered Urothelial Carcinoma: Resistance Mechanisms and Therapeutic Strategies.Targeted oncology · 2025Review
- A Promising Paradigm Shift in Cancer Treatment with FGFR Inhibitors.Anti-cancer agents in medicinal chemistry · 2025Review
- Overcoming resistance in advanced urothelial carcinoma: mechanisms of escape from antibody-drug conjugates and FGFR3 inhibition.Frontiers in oncology · 2025Review
- Multiple allostery in the regulation of PDGFR beta kinase activities.Acta biochimica et biophysica Sinica · 2024Article
- The FGF/FGFR/c-Myc axis as a promising therapeutic target in multiple myeloma.Journal of experimental & clinical cancer research : CR · 2024Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Review
- Structural basis and selectivity of sulfatinib binding to FGFR and CSF-1R.Communications chemistry · 2024Article
- Pyrazine-based small molecule kinase inhibitors: clinical applications and patent review (2019-2023).Future medicinal chemistry · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Frequent genetic alterations discovered in FGFRs and evidence implicating some as drivers in diverse tumors has been accompanied by rapid progress in targeting FGFRs for anticancer treatments. Wider assessment of the impact of genetic changes on the activation state and drug responses is needed to better link the genomic data and treatment options. We here apply a direct comparative and comprehensive analysis of FGFR3 kinase domain variants representing the diversity of point-mutations reported in this domain. We reinforce the importance of N540K and K650E and establish that not all highly activating mutations (for example R669G) occur at high-frequency and conversely, that some "hotspots" may not be linked to activation. Further structural characterization consolidates a mechanistic view of FGFR kinase activation and extends insights into drug binding. Importantly, using several inhibitors of particular clinical interest (AZD4547, BGJ-398, TKI258, JNJ42756493 and AP24534), we find that some activating mutations (including different replacements of the same residue) result in distinct changes in their efficacy. Considering that there is no approved inhibitor for anticancer treatments based on FGFR-targeting, this information will be immediately translatable to ongoing clinical trials.
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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.