ArticlePloS one2013
Activating somatic FGFR2 mutations in breast cancer.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Phenotypic spectrum ofPeerJ · 2022Pooled it
- Proteome-Wide Analysis of Functional Phosphosites in the FGFR Family of Proteins: Insights from Large-Scale Phosphoproteomic Analysis.Proteomes · 2026Article
- LowerBiology · 2024Article
- Expansion of the complex genotypic and phenotypic spectrum of FGFR2-associated neurocutaneous syndromes.Human genetics · 2024Article
- Efficacy of futibatinib, an irreversible fibroblast growth factor receptor inhibitor, in FGFR-altered breast cancer.Scientific reports · 2023Article
- Fibroblast growth factor receptor signalling dysregulation and targeting in breast cancer.Open biology · 2022Review
- Signaling Pathway and Small-Molecule Drug Discovery of FGFR: A Comprehensive Review.Frontiers in chemistry · 2022Review
- Article
- Fibroblast growth factor receptors as treatment targets in clinical oncology.Nature reviews. Clinical oncology · 2019Review
- Neomorphic PDGFRA extracellular domain driver mutations are resistant to PDGFRA targeted therapies.Nature communications · 2018Article
- Regulation of FGF10 Signaling in Development and Disease.Frontiers in genetics · 2018Review
- Fibroblast Growth Factor Receptor 2 Signaling in Breast Cancer.International journal of biological sciences · 2017Review
- FGFR inhibitors: Effects on cancer cells, tumor microenvironment and whole-body homeostasis (Review).International journal of molecular medicine · 2016Review
- Identification of Targetable Kinase Alterations in Patients with Colorectal Carcinoma That are Preferentially Associated with Wild-Type RAS/RAF.Molecular cancer research : MCR · 2016Article
- Genomic differences between pure ductal carcinoma in situ and synchronous ductal carcinoma in situ with invasive breast cancer.Oncotarget · 2015Article
- Development of covalent inhibitors that can overcome resistance to first-generation FGFR kinase inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Copy number variation in CCND1 gene is implicated in the pathogenesis of sporadic parathyroid carcinoma.World journal of surgery · 2014Article
- Fine-scale mapping of the FGFR2 breast cancer risk locus: putative functional variants differentially bind FOXA1 and E2F1.American journal of human genetics · 2013Article
- The FGF/FGFR axis as a therapeutic target in breast cancer.Expert review of endocrinology & metabolism · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is known that FGFR2 gene variations confer a risk for breast cancer. FGFR2 and FGF10, the main ligand of FGFR2, are both overexpressed in 5-10% of breast tumors. In our study, we sequenced the most important coding regions of FGFR2 in somatic tumor tissue of 140 sporadic breast cancer patients and performed MLPA analysis to detect copy number variations in FGFR2 and FGF10. We identified one somatic heterozygous missense mutation, p.K660N (c.1980G>C), within the tyrosine kinase domain of FGFR2 in tumor tissue of a sporadic breast cancer patient, which is likely mediated by the FGFR2-IIIb isoform. The presence of wild type and mutated alleles in equal quantities suggests that the mutation has driven clonal amplification of mutant cells. We have analyzed the tyrosine kinase activity of p.K660N and another recently described somatic breast cancer mutation in FGFR2, p.R203C, after expression in HEK293 cells and demonstrated that the intrinsic tyrosine kinase activity of both mutant proteins is strongly increased resulting in elevated phosphorylation and activity of downstream effectors. To our knowledge, this is the first report of functional analysis of somatic breast cancer mutations in FGFR2 providing evidence for the activating nature of FGFR2-mediated signalling in the pathogenesis of breast cancer.
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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.