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Isao Murakami
Publications - 12
Citations - 445
Isao Murakami is an academic researcher. The author has contributed to research in topics: Lung cancer & T790M. The author has an hindex of 9, co-authored 12 publications receiving 389 citations.
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Journal ArticleDOI
Reciprocal and Complementary Role of MET Amplification and EGFR T790M Mutation in Acquired Resistance to Kinase Inhibitors in Lung Cancer
Kenichi Suda,Isao Murakami,Tatsuya Katayama,Kenji Tomizawa,Hirotaka Osada,Yoshitaka Sekido,Yoshihiko Maehara,Yasushi Yatabe,Tetsuya Mitsudomi +8 more
TL;DR: Results indicate a reciprocal and complementary relationship between T790M and MET amplification and the necessity of concurrent inhibition of both for further improving patient outcomes.
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Small cell lung cancer transformation and T790M mutation: complimentary roles in acquired resistance to kinase inhibitors in lung cancer
Kenichi Suda,Kenichi Suda,Isao Murakami,Kazuko Sakai,Hiroshi Mizuuchi,Shigeki Shimizu,Katsuaki Sato,Kenji Tomizawa,Shuta Tomida,Yasushi Yatabe,Kazuto Nishio,Tetsuya Mitsudomi +11 more
TL;DR: In the present study, through an in-depth analysis of multiple EGFR-TKI refractory lesions obtained from an autopsy case, a complementary relationship between SCLC transformation and EGFR T790M secondary mutation (resistance mutation) is observed.
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Heterogeneity in resistance mechanisms causes shorter duration of epidermal growth factor receptor kinase inhibitor treatment in lung cancer
Kenichi Suda,Isao Murakami,Kazuko Sakai,Kenji Tomizawa,Hiroshi Mizuuchi,Katsuaki Sato,Kazuto Nishio,Tetsuya Mitsudomi +7 more
TL;DR: Heterogeneity of resistance mechanisms in two of four patients analyzed are observed, and quantitative heterogeneity in EGFR T790M mutation ratio among EGFR-TKI refractory lesions is identified, which may lead to better treatment strategies after acquisition of resistance to first generation EG FR-TKIs in lung cancer patients with EGFR mutations.
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Oncogene swap as a novel mechanism of acquired resistance to epidermal growth factor receptor‐tyrosine kinase inhibitor in lung cancer
Hiroshi Mizuuchi,Kenichi Suda,Isao Murakami,Kazuko Sakai,Katsuaki Sato,Yoshihisa Kobayashi,Masaki Shimoji,Masato Chiba,Yuichi Sesumi,Kenji Tomizawa,Toshiki Takemoto,Yoshitaka Sekido,Kazuto Nishio,Tetsuya Mitsudomi +13 more
TL;DR: An “oncogene swap” from EGFR to MET is a novel resistant mechanism to the EGFR‐TKI and this novel mechanism should be considered in order to avoid futile inhibition of the original oncogene.
Journal ArticleDOI
CD44 Facilitates Epithelial-to-Mesenchymal Transition Phenotypic Change at Acquisition of Resistance to EGFR Kinase Inhibitors in Lung Cancer.
Kenichi Suda,Isao Murakami,Hui Yu,Jihye Kim,Aik Choon Tan,Hiroshi Mizuuchi,Leslie Rozeboom,Kim Ellison,Christopher J. Rivard,Tetsuya Mitsudomi,Fred R. Hirsch +10 more
TL;DR: It is suggested that upregulation of CD44 facilitates EMT-phenotypic change in lung cancers with EGFR mutations when treated with EG FR-TKIs and that CD44 can be a useful biomarker to predict the emergence of EMT upon EGFR-TKI monotherapy.