ArticleExperimental cell research2012
A targeted enzyme approach to sensitization of tyrosine kinase inhibitor-resistant breast cancer cells.
Article in Experimental cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The trial behind it
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Who cites it
13 citing papers in PubMed.
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Association betweenDiagnostics (Basel, Switzerland) · 2020Article
- Role of GPX4-Mediated Ferroptosis in the Sensitivity of Triple Negative Breast Cancer Cells to Gefitinib.Frontiers in oncology · 2020Article
- Identification of potential microRNAs and their targets in promoting gefitinib resistance by integrative network analysis.Journal of thoracic disease · 2019Article
- Integrating 5hmC and gene expression data to infer regulatory mechanisms.Bioinformatics (Oxford, England) · 2018Article
- The interplay of reactive oxygen species and the epidermal growth factor receptor in tumor progression and drug resistance.Journal of experimental & clinical cancer research : CR · 2018Review
- The enhanced tumor inhibitory effects of gefitinib and L-ascorbic acid combination therapy in non-small cell lung cancer cells.Oncology letters · 2017Article
- Treating triple negative breast cancer cells with erlotinib plus a select antioxidant overcomes drug resistance by targeting cancer cell heterogeneity.Scientific reports · 2017Article
- Amyloid-beta neuroprotection mediated by a targeted antioxidant.Scientific reports · 2014Article
- Integrin β3 links therapy resistance and cancer stem cell properties.Nature cell biology · 2014Article
- Genetic polymorphisms in oxidative stress-related genes are associated with clinical outcome in patients with advanced non-small cell lung cancer receiving tyrosine kinase inhibitors.American journal of cancer research · 2014Article
- NADPH oxidase biology and the regulation of tyrosine kinase receptor signaling and cancer drug cytotoxicity.International journal of molecular sciences · 2013Article
- Peroxisomes, cell senescence, and rates of aging.Biochimica et biophysica acta · 2012Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Gefitinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) of potential use in patients with breast cancer. Unfortunately, in clinical studies, gefitinib is often ineffective indicating that resistance to EGFR inhibitors may be a common occurrence in cancer of the breast. EGFR has been shown to be overexpressed in breast cancer, and in particular remains hyperphosphorylated in cell lines such as MDA-MB-468 that are resistant to EGFR inhibitors. Here, we investigate the cause of this sustained phosphorylation and the molecular basis for the ineffectiveness of gefitinib. We show that reactive oxygen species (ROS), known to damage cellular macromolecules and to modulate signaling cascades in a variety of human diseases including cancers, appear to play a critical role in mediating EGFR TKI-resistance. Furthermore, elimination of these ROS through use of a cell-penetrating catalase derivative sensitizes the cells to gefitinib. These results suggest a new approach for the treatment of TKI-resistant breast cancer patients specifically, the targeting of ROS and attendant downstream oxidative stress and their effects on signaling cascades.
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