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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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Reciprocal and Complementary Role of MET Amplification and EGFR T790M Mutation in Acquired Resistance to Kinase Inhibitors in Lung Cancer

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

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

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

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.
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CD44 Facilitates Epithelial-to-Mesenchymal Transition Phenotypic Change at Acquisition of Resistance to EGFR Kinase Inhibitors in Lung Cancer.

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.