Stress hormones promote EGFR inhibitor resistance in NSCLC: Implications for combinations with β-blockers.

doi:10.1126/scitranslmed.aao4307

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Article

Stress hormones promote EGFR inhibitor resistance in NSCLC: Implications for combinations with β-blockers.

Science translational medicine - 8 Nov 2017

Nilsson Monique B, Sun Huiying, Diao Lixia, Tong Pan, Liu Diane, Li Lerong, Fan Youhong, Poteete Alissa, Lim Seung-Oe, Howells Kathryn, Haddad Vincent, Gomez Daniel, Tran Hai, Pena Guillermo Armaiz, Sequist Lecia V, Yang James C, Wang Jing, Kim Edward S, Herbst Roy, Lee J Jack, Hong Waun Ki, Wistuba Ignacio, Hung Mien-Chie, Sood Anil K, Heymach John V

Abstract excerpt

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) resistance mediated by T790M-independent mechanisms remains a major challenge in the treatment of non-small cell lung cancer (NSCLC). We identified a targetable mechanism of EGFR inhibitor resistance whereby stress hormones activate β2-adrenergic receptors (β2-ARs) on NSCLC cells, which cooperatively signal with mutant EGFR, resulting in the...

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PMID: 29118262
DOI: 10.1126/scitranslmed.aao4307
PMCID: PMC5870120

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EGFR

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