The novel phosphoinositide 3‐kinase–mammalian target of rapamycin inhibitor, BEZ235, circumvents erlotinib resistance of epidermal growth factor receptor mutant lung cancer cells triggered by hepatocyte growth factor
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Summary
BEZ235, a dual inhibitor of PI3K and mTOR, could overcome the EGFR–TKI resistance induced by HGF in an EGFR mutant lung cancer model, and monotherapy results suggest that BEZ235 may be useful in managing HGF‐induced EGFR‐TKI resistant lung cancer.
- Type
- article
- Published
- 2013-07-15
- Cited by
- 27
- References
- 42
- Access
- Open access
- OpenAlex
- https://openalex.org/W1672420523
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:3496470
Keywords
Erlotinib, Hepatocyte growth factor, Epidermal growth factor receptor, Cancer research, Gefitinib
References
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- Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer
- Activation of the AXL Kinase Causes Resistance to EGFR-Targeted Therapy in Lung Cancer
- Pre-existence and clonal selection of MET amplification in EGFR mutant NSCLC
- MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
- Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
- EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.
- Differential induction of apoptosis in HER2 and EGFR addicted cancers following PI3K inhibition
- The PI3K pathway as drug target in human cancer.
- The Pharmacology of mTOR Inhibition
- The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism
- Oncogenic PI3K deregulates transcription and translation
- The tor pathway: a target for cancer therapy
- Epithelial to Mesenchymal Transition in an Epidermal Growth Factor Receptor-Mutant Lung Cancer Cell Line with Acquired Resistance to Erlotinib
- ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines.
- Phosphoinositide-3-Kinase Catalytic Alpha and KRAS Mutations are Important Predictors of Resistance to Therapy with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Patients with Advanced Non-small Cell Lung Cancer
Cited by
- Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.
- mTOR pathway in colorectal cancer: an update
- Tumor heterogeneity: evolution through space and time in EGFR mutant non small cell lung cancer patients.
- Combined therapy with EGFR TKI and gambogic acid for overcoming resistance in EGFR-T790M mutant lung cancer
- Epidermal growth factor receptor tyrosine-kinase inhibitor treatment resistance in non-small cell lung cancer: biological basis and therapeutic strategies
- Chemical constituents from the aerial parts of Melandrium firmum
- Ability of the Met Kinase Inhibitor Crizotinib and New Generation EGFR Inhibitors to Overcome Resistance to EGFR Inhibitors
- The dual PI3K/mTOR inhibitor PKI-587 enhances sensitivity to cetuximab in EGFR-resistant human head and neck cancer models
- Combine MEK inhibition with PI3K/mTOR inhibition exert inhibitory tumor growth effect on KRAS and PIK3CA mutation CRC xenografts due to reduced expression of VEGF and matrix metallopeptidase-9
- A new chromene from the fruiting bodies of Chroogomphus rutilus
- Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines
- Acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in EGFR-mutant non-small cell lung cancer: a new era begins.
- Cytotoxic anthraquinone dimers from Melandrium firmum
- New treatment strategy for patients with EGFR-mutant lung cancer
- Novel agents and strategies for overcoming EGFR TKIs resistance
- Targeting the PI3K/AKT/mTOR pathway: potential for lung cancer treatment
- Clinical development of phosphatidylinositol 3-kinase inhibitors for non-Hodgkin lymphoma
- Antitumor activity of selective MEK1/2 inhibitor AZD6244 in combination with PI3K/mTOR inhibitor BEZ235 in gefitinib-resistant NSCLC xenograft models
- Targeting the Mammalian Target of Rapamycin in Lung Cancer
- Plexin A1 signaling confers malignant phenotypes in lung cancer cells.
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