Novel mechanism of resistance to targeted therapies in lung cancer.

Walter Z Wang David P CarboneRajeswara Rao Arasada

Published in: Molecular & cellular oncology (2018)

We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.

Keyphrases

epidermal growth factor receptor
tyrosine kinase
advanced non small cell lung cancer
cell proliferation
epithelial mesenchymal transition
small cell lung cancer
induced apoptosis
cell cycle arrest
type diabetes
oxidative stress
drug induced
adverse drug
replacement therapy
combination therapy
bone marrow