ArticleCell death & disease2025
Growth factor receptor plasticity drives therapeutic persistence of metastatic breast cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- From residual risk to precision intervention: the evolving role of minimal residual disease in breast cancer management.Cancer biology & medicine · 2025Review
- Fibroblast growth factor receptor signaling modulates cholesterol storage in a SOAT1-dependent manner to promote mammary tumor cell invasion.Breast cancer research : BCR · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Metastatic breast cancer (MBC) remains a therapeutic challenge due to the persistence of minimal residual disease (MRD) and tumor recurrence. Herein we utilize a model of MBC that is sensitive to inhibition of fibroblast growth factor receptor (FGFR), resulting in robust regression of pulmonary lesions upon treatment with the FGFR inhibitor pemigatinib. Assessment of the remaining MRD revealed upregulation of platelet-derived growth factor receptor (PDGFR). Functionally, we demonstrate increased response to PDGF ligand stimulation following pemigatinib treatment. Depletion of PDGFR did not alter tumor growth under control conditions but did delay tumor recurrence following a treatment window of pemigatinib. To overcome this therapeutic hurdle, we found that inhibition of DNA methyltransferase 1 (DNMT1) prevents pemigatinib-induced cellular plasticity. Combined targeting of FGFR and DNMT1 prevented induction of PDGFR, enhanced pulmonary tumor regression, slowed tumor recurrence, and prolonged survival. These findings enhance our understanding of cellular plasticity during states of treatment-induced MRD and suggest that inhibition of DNA methylation could augment current approaches being used to treat MBC.
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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.