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Nukaga, Shigenari; Yasuda, Hiroyuki; Tsuchihara, Katsuya; Hamamoto, Junko; Masuzawa, Keita; Kawada, Ichiro; Naoki, Katsuhiko; Matsumoto, Shingo; Mimaki, Sachiyo; Ikemura, Shinnosuke; Goto, Koichi; Betsuyaku, Tomoko; Soejima, Kenzo
Cancer research (Chicago, Ill.), 04/2017, Volume: 77, Issue: 8Journal Article
EGFR-mutated lung cancers account for a significant subgroup of non-small cell lung cancers overall. Third-generation EGFR tyrosine kinase inhibitors (TKI) are mutation-selective inhibitors with minimal effects on wild-type EGFR. Acquired resistance develops to these agents, however, the mechanisms are as yet uncharacterized. In this study, we report that the Src-AKT pathway contributes to acquired resistance to these TKI. In addition, amplification of EGFR wild-type alleles but not mutant alleles was sufficient to confer acquired resistance. These findings underscore the importance of signals from wild-type EGFR alleles in acquiring resistance to mutant-selective EGFR-TKI. Our data provide evidence of wild-type allele-mediated resistance, a novel concept of acquired resistance in response to mutation-selective inhibitor therapy in cancer treatment. .
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