Title : Targeting Tyrosine Kinase Inhibitor-Resistant Non-Small Cell Lung Cancer by Inducing Epidermal Growth Factor Receptor Degradation via Methionine 790 Oxidation.

Pub. Date : 2016 Feb 10

PMID : 26528827






5 Functional Relationships(s)
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1 RESULTS: The basal ROS levels in EGFR(T790M)-containing TKI-resistant NSCLC cell lines were substantially high. Reactive Oxygen Species epidermal growth factor receptor Homo sapiens
2 CONCLUSION: Targeting EGFR by elevating ROS and redox imbalance is a potential new strategy to develop a new EGFR inhibitor for TKI-resistant patients with a wide therapeutic window between EGFR(T790M) and EGFR(WT). Reactive Oxygen Species epidermal growth factor receptor Homo sapiens
3 CONCLUSION: Targeting EGFR by elevating ROS and redox imbalance is a potential new strategy to develop a new EGFR inhibitor for TKI-resistant patients with a wide therapeutic window between EGFR(T790M) and EGFR(WT). Reactive Oxygen Species epidermal growth factor receptor Homo sapiens
4 CONCLUSION: Targeting EGFR by elevating ROS and redox imbalance is a potential new strategy to develop a new EGFR inhibitor for TKI-resistant patients with a wide therapeutic window between EGFR(T790M) and EGFR(WT). Reactive Oxygen Species epidermal growth factor receptor Homo sapiens
5 CONCLUSION: Targeting EGFR by elevating ROS and redox imbalance is a potential new strategy to develop a new EGFR inhibitor for TKI-resistant patients with a wide therapeutic window between EGFR(T790M) and EGFR(WT). Reactive Oxygen Species epidermal growth factor receptor Homo sapiens