ArticleSignal transduction and targeted therapy
The paradoxical functions of EGFR during breast cancer progression.
Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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
93 citing papers in PubMed, 161 citations in OpenAlex.
- Perspectives of EGFR co-targeting with nanocarriers for anti-TNBC purposes.Genes & diseases · 2026Review
- PHAROS: turning single-cell perturbation models into target-directed drug-combination screens.bioRxiv : the preprint server for biology · 2026Article
- Endophytic Aspergillus glaucus as a novel epothilone B producer: Antiproliferative activity and in silico analysis.Applied microbiology and biotechnology · 2026Article
- Identification and functional validation of EPS15L1 as a key driver of triple-negative breast cancer.NPJ breast cancer · 2026Article
- Endocrine therapy reprogramming of breast cancer facilitates metastatic escape via upregulation of P-Rex1/Rac1 signalling.Nature communications · 2026Article
- TGF-α/EGFR-mediated lymphatic metastasis reveals a repositionable therapeutic target in breast cancer.NPJ breast cancer · 2026Article
- Sortilin exhibits tumor suppressor-like activity by limiting EGFR transduction function.Oncogene · 2026Article
- OTUD4 deubiquitination stabilizes EGFR and activates the PI3K/AKT pathway to promote the invasiveness of triple-negative breast cancer.Cell death & disease · 2026Article
- MicroRNA cluster 7/17/155 as a potential driver for high-grade breast tumors transformation through EGFR-associated EMT.Frontiers in cell and developmental biology · 2026Article
- Targeting Key Molecular Mechanisms in Triple-Negative Breast Cancer Therapies with Natural Compounds.Current pharmaceutical design · 2026Review
- HER2 expression in breast cancer: evidence gaps and challenges.NPJ precision oncology · 2025Review
- miR-770-5p: A novel molecular target regulating KLF4/EGFR signaling through PRMT5 interaction.Medical oncology (Northwood, London, England) · 2025Article
- Spheroid-Based 3D Models to Decode Cell Function and Matrix Effectors in Breast Cancer.Cancers · 2025Article
- Targeting EGFR/IGF-IR Functional Crosstalk in 2D and 3D Triple-Negative Breast Cancer Models to Evaluate Tumor Progression.International journal of molecular sciences · 2025Article
- L858R/L718Q and L858R/L792H Mutations of EGFR Inducing Resistance Against Osimertinib by Forming Additional Hydrogen Bonds.Proteins · 2025Article
- Divide and Conquer-Targeted Therapy for Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Review
- Surface Functionalization of Nanocarriers with Anti-EGFR Ligands for Cancer Active Targeting.Nanomaterials (Basel, Switzerland) · 2025Review
- Exploring anti-cancer activities of epidermal growth factor-immobilized polymeric nanoparticles.Science and technology of advanced materials · 2025Article
- Advancements in Global Phosphoproteomics Profiling: Overcoming Challenges in Sensitivity and Quantification.Proteomics · 2025Review
- BC-predict: mining of signal biomarkers and production of models for early-stage breast cancer subtyping and prognosis.Frontiers in bioinformatics · 2025Article
33 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The epidermal growth factor receptor (EGFR) is one of the most well-studied signaling pathways in cancer progression. As a result, numerous therapeutics including small-molecule inhibitors and monoclonal antibodies have been developed to target this critical oncogenic driver. Several of these EGFR inhibitors (EGFRi) have been evaluated in metastatic breast cancer, as high-level EGFR expression in primary tumors correlates with the highly aggressive basal-like phenotype and predicts for poor patient prognosis. Surprisingly, these trials have been unanimously unsuccessful at improving patient outcomes. Numerous factors, such as lack of proper patient selection may have contributed to the failure of these trials. However, recent findings suggest that there are fundamental changes in EGFR signaling that take place during primary tumor invasion, dissemination and ultimate metastasis of breast cancer cells. Herein, we review the outcomes of EGFR-targeted clinical trials in breast cancer and explore our current understanding of EGFR signaling within primary mammary tumors and how these events are altered in the metastatic setting. Overall, we put forth the hypothesis that fundamental changes in EGFR signaling between primary and metastatic tumors, a process we term the 'EGFR paradox,' contribute to the clinically observed inherent resistance to EGFRi. Furthermore, this hypothesis introduces the possibility of utilizing EGFR agonism as a potential therapeutic approach for the treatment of metastatic breast cancer.
Identifiers
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.