ReviewBritish journal of cancer2024
FGFR4-driven plasticity in breast cancer progression and resistance to therapy.
Review in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- FGFR4-associated APOBEC3 mutagenesis characterizes HER2-enriched subtype of human breast cancer.British journal of cancer · 2026Article
- METTL3-Modified FOXM1 Promotes Proliferation, Invasion, Stemness, and Immune Escape of Gastric Cancer by Influencing the Transcription of FGFR4.Applied biochemistry and biotechnology · 2026Article
- FGFR4 and HER2 co-expression is associated with the proinflammatory tumor microenvironment in HR + breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- Identification of high-risk signatures and therapeutic targets through molecular characterization and immune profiling of TP53-mutant breast cancer.Journal, genetic engineering & biotechnology · 2025Article
- Mechanistic study of glutamine metabolic reprogramming driving non-small cell lung cancer progression via the FGF17-FGFR4 axis mediating epithelial-mesenchymal transition.Frontiers in molecular biosciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer (BCa) is a complex and heterogeneous disease, with different intrinsic molecular subtypes that have distinct clinical outcomes and responses to therapy. Although intrinsic subtyping provides guidance for treatment decisions, it is now widely recognised that, in some cases, the switch of the BCa intrinsic subtype (which embodies cellular plasticity), may be responsible for therapy failure and disease progression. Aberrant FGFR4 signalling has been implicated in various cancers, including BCa, where it had been shown to be associated with aggressive subtypes, such as HER2-enriched BCa, and poor prognosis. More importantly, FGFR4 is also emerging as a potential driver of BCa intrinsic subtype switching, and an essential promoter of brain metastases, particularly in the HER2-positive BCa. Although the available data are still limited, the findings may have far-reaching clinical implications. Here, we provide an updated summary of the existing both pre- and clinical studies of the role of FGFR4 in BCa, with a special focus on its contribution to subtype switching during metastatic spread and/or induced by therapy. We also discuss a potential clinical benefit of targeting FGFR4 in the development of new treatment strategies.
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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.