ArticleThe Journal of clinical investigation2020
FGFR4 regulates tumor subtype differentiation in luminal breast cancer and metastatic disease.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01377363 (Evaluation of Degree of Conversion of HER2 Receptor Between Primary Breast Cancer and Metastasis), which is not on this map. Cited by 70 papers.
What it found
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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.
Evaluation of Degree of Conversion of HER2 Receptor Between Primary Breast Cancer and Metastasis
Who cites it
70 citing papers in PubMed, 109 citations in OpenAlex.
- Molecular evaluation of residual disease following neoadjuvant chemotherapy in triple-negative breast cancer CALGB 40603 (Alliance).The Journal of clinical investigation · 2026Trial
- Transcriptomic Predictors of Survival for Palbociclib + Endocrine Therapy Versus Capecitabine in Aromatase Inhibitor-Resistant Breast Cancer From the GEICAM/2013-02 PEARL Trial.JCO precision oncology · 2025Trial
- Survival, Pathologic Response, and Genomics in CALGB 40601 (Alliance), a Neoadjuvant Phase III Trial of Paclitaxel-Trastuzumab With or Without Lapatinib in HER2-Positive Breast Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Trial
- FGFR4-associated APOBEC3 mutagenesis characterizes HER2-enriched subtype of human breast cancer.British journal of cancer · 2026Article
- Genomic Characterization of RTK-RAS Pathway Alterations in Juvenile Myelomonocytic Leukemia Through Whole-Exome Sequencing.Medical sciences (Basel, Switzerland) · 2026Article
- Breast cancer ovarian metastases show increased activity of GPCR pathways.bioRxiv : the preprint server for biology · 2026Article
- Colorectal cancer-derived FGF19 is a metabolically active serum biomarker that exerts enteroendocrine effects on mouse liver.Molecular oncology · 2026Article
- Brain FGF2 and NCAM1 contribute to FGFR1-dependent progression of estrogen receptor-positive breast cancer brain metastases.Nature communications · 2026Article
- Comprehensive genomic profiling of triple-negative breast cancer metastases identifies role of PKD1 in immunotherapy resistance.The Journal of clinical investigation · 2026Article
- FGFR4 and HER2 co-expression is associated with the proinflammatory tumor microenvironment in HR + breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- FGF19 in Solid Tumors: Molecular Mechanisms, Metabolic Reprogramming, and Emerging Therapeutic Opportunities.Theranostics · 2026Review
- Exploring the crosstalk between the FGF/FGFR pathway and tumor microenvironment in clear cell renal cell carcinoma.PloS one · 2026Article
- Nicheformer: a foundation model for single-cell and spatial omics.Nature methods · 2025Article
- Integration of Gene Expression and Digital Histology to Predict Treatment-Specific Responses in Breast Cancer.medRxiv : the preprint server for health sciences · 2025Article
- Targeting FGFR4 abrogates HNF1A-driven metastasis in pancreatic ductal adenocarcinoma.Molecular cancer · 2025Article
- Mediating factors between autoimmune thyroiditis and breast cancer: a bidirectional Mendelian randomization study.Discover oncology · 2025Article
- FGFR4 in endocrine resistance: overexpression and estrogen regulation without direct causative role.Breast cancer research and treatment · 2025Article
- Extraction of a stromal metastatic gene signature in breast cancer via spatial profiling.Journal of experimental & clinical cancer research : CR · 2025Article
- Genomic characterization of the HER2-enriched intrinsic molecular subtype in primary ER-positive HER2-negative breast cancer.Nature communications · 2025Article
- Subtype-specific transcription factors affect polyamine metabolism and the tumor microenvironment in breast cancer.Cancer innovation · 2025Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 7 institutions in 2 countries.
Funding
Abstract
Mechanisms driving tumor progression from less aggressive subtypes to more aggressive states represent key targets for therapy. We identified a subset of luminal A primary breast tumors that give rise to HER2-enriched (HER2E) subtype metastases, but remain clinically HER2 negative (cHER2-). By testing the unique genetic and transcriptomic features of these cases, we developed the hypothesis that FGFR4 likely participates in this subtype switching. To evaluate this, we developed 2 FGFR4 genomic signatures using a patient-derived xenograft (PDX) model treated with an FGFR4 inhibitor, which inhibited PDX growth in vivo. Bulk tumor gene expression analysis and single-cell RNA sequencing demonstrated that the inhibition of FGFR4 signaling caused molecular switching. In the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohort, FGFR4-induced and FGFR4-repressed signatures each predicted overall survival. Additionally, the FGFR4-induced signature was an independent prognostic factor beyond subtype and stage. Supervised analysis of 77 primary tumors with paired metastases revealed that the FGFR4-induced signature was significantly higher in luminal/ER+ tumor metastases compared with their primaries. Finally, multivariate analysis demonstrated that the FGFR4-induced signature also predicted site-specific metastasis for lung, liver, and brain, but not for bone or lymph nodes. These data identify a link between FGFR4-regulated genes and metastasis, suggesting treatment options for FGFR4-positive patients, whose high expression is not caused by mutation or amplification.
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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.