Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC

Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC

Treatment of EGFR mutant non-small cell lung cancer (NSCLC) often develops resistance to EGFR TKIs. In this study, the authors discover a non-canonical activation of β-catenin signaling through Notch3 as a mechanism of adaptation to and resistance to EGFR TKI treatment in NSCLC.

Bibliographic Details
Main Authors: Rajeswara Rao Arasada, Konstantin Shilo, Tadaaki Yamada, Jianying Zhang, Seiji Yano, Rashelle Ghanem, Walter Wang, Shinji Takeuchi, Koji Fukuda, Nobuyuki Katakami, Keisuke Tomii, Fumitaka Ogushi, Yasuhiko Nishioka, Tiffany Talabere, Shrilekha Misra, Wenrui Duan, Paolo Fadda, Mohammad A. Rahman, Patrick Nana-Sinkam, Jason Evans, Joseph Amann, Elena E. Tchekneva, Mikhail M. Dikov, David P. Carbone
Format: Article
Language:English
Published: Nature Portfolio 2018-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-05626-2

Internet

https://doi.org/10.1038/s41467-018-05626-2

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