Uncoupling between epidermal growth factor receptor and downstream signals defines resistance to the antiproliferative effect of Gefitinib in bladder cancer cells.
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Summary
The data show that the uncoupling of EGFR with mitogenic pathways can cause resistance to EGFR inhibition in bladder cancer, and it is suggested that the resistance of bladder cancer cells to EG FR blockade can be predicted early in the course of treatment by measuring the activation of GSK-3beta and of nuclear cyclin D1.
- Type
- article
- Published
- 2005-11-15
- Cited by
- 88
- References
- 58
- Access
- Open access
- OpenAlex
- https://openalex.org/W16288045
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:619207
Keywords
Physics, Humanities, Philosophy
References
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Cited by
- Inhibition of the epidermal growth factor receptor in bladder cancer cells treated with the DNA‐damaging drug etoposide markedly increases apoptosis
- Signal Strength Dictates Phosphoinositide 3-Kinase Contribution to Ras/Extracellular Signal-Regulated Kinase 1 and 2 Activation via Differential Gab1/Shp2 Recruitment: Consequences for Resistance to Epidermal Growth Factor Receptor Inhibition
- Is Vascular Endothelial Growth Factor Modulation a Predictor of the Therapeutic Efficacy of Gefitinib for Bladder Cancer?
- Targeting the Epidermal Growth Factor Receptor in Epithelial Ovarian Cancer: Current Knowledge and Future Challenges
- MECHANISMS UNDERLYING DISTINCT EGFR VERSUS FGFR-3 AND -1 DEPENDENCY IN HUMAN BLADDER CANCER CELLS
- Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.
- Strategies to sensitize bladder cancer cells to small molecule inhibitors targeting the PI3K pathway
- A robustness-based approach to systems-oriented drug design
- Mechanotransduction and epidermal growth factor receptor signaling in bladder epithelium
- Effect of EGFR antagonists gefitinib (Iressa) and C225 (Cetuximab) on MnSOD-plasmid liposome transgene radiosensitization of a murine squamous cell carcinoma cell line.
- The GSK-3β/Cyclin D1 Pathway is Involved in the Resistance of Oral Cancer Cells to the EGFR Tyrosine Kinase Inhibitor ZD1839
- Chemoresistant tumor cell lines display altered epidermal growth factor receptor and HER3 signaling and enhanced sensitivity to gefitinib
- Aberrant expression of cortactin in head and neck squamous cell carcinoma cells is associated with enhanced cell proliferation and resistance to the epidermal growth factor receptor inhibitor gefitinib.
- Targeted therapies in non-muscle-invasive bladder cancer according to the signaling pathways.
- Receptor heterodimerization: a new mechanism for platelet-derived growth factor induced resistance to anti-epidermal growth factor receptor therapy for bladder cancer.
- Iressa strengthens the cytotoxic effect of docetaxel in NSCLC models that harbor specific molecular characteristics
- FGFR3, HRAS, KRAS, NRAS and PIK3CA Mutations in Bladder Cancer and Their Potential as Biomarkers for Surveillance and Therapy
- Inhibition of mammalian target of rapamycin as a therapeutic strategy in the management of bladder cancer
- Epidermal growth factor receptor status and the response of bladder carcinoma cells to erlotinib.
- Restoration of PTEN expression alters the sensitivity of prostate cancer cells to EGFR inhibitors
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