Article
Oncogenic switch and single-agent MET inhibitor sensitivity in a subset of EGFR-mutant lung cancer.
Science translational medicine - 1 Sept 2021
Eser Pınar Özden, Paranal Raymond M, Son Jieun, Ivanova Elena, Kuang Yanan, Haikala Heidi M, To Ciric, Okoro Jeffrey J, Dholakia Kshiti H, Choi Jihyun, Eum Yoonji, Ogino Atsuko, Missios Pavlos, Ercan Dalia, Xu Man, Poitras Michael J, Wang Stephen, Ngo Kenneth, Dills Michael, Yanagita Masahiko, Lopez Timothy, Lin Mika, Tsai Jeanelle, Floch Nicolas, Chambers Emily S, Heng Jennifer, Anjum Rana, Santucci Alison D, Michael Kesi, Schuller Alwin G, Cross Darren, Smith Paul D, Oxnard Geoffrey R, Barbie David A, Sholl Lynette M, Bahcall Magda, Palakurthi Sangeetha, Gokhale Prafulla C, Paweletz Cloud P, Daley George Q, Jänne Pasi A
Abstract excerpt
The clinical efficacy of epidermal growth factor receptor (EGFR)–targeted therapy in EGFR-mutant non–small cell lung cancer is limited by the development of drug resistance. One mechanism of EGFR inhibitor resistance occurs through amplification of the human growth factor receptor (MET) proto-oncogene, which bypasses EGFR to reactivate downstream signaling. Tumors exhibiting concurrent EGFR mutation and MET...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.