MET or NRAS amplification is an acquired resistance mechanism to the third-generation EGFR inhibitor naquotinib
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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2045-2322
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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MET or NRAS amplification is an acquired resistance mechanism to the third-generation EGFR inhibitor naquotinib ; volume:8 ; number:1 ; day:31 ; month:1 ; year:2018 ; pages:1-11 ; date:12.2018
Scientific reports ; 8, Heft 1 (31.1.2018), 1-11, 12.2018
- Creator
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Ninomiya, Kiichiro
- Contributor
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Ohashi, Kadoaki
Makimoto, Go
Tomida, Shuta
Higo, Hisao
Kayatani, Hiroe
Ninomiya, Takashi
Kubo, Toshio
Ichihara, Eiki
Hotta, Katsuyuki
Tabata, Masahiro
Maeda, Yoshinobu
Kiura, Katsuyuki
SpringerLink (Online service)
- DOI
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10.1038/s41598-018-20326-z
- URN
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urn:nbn:de:101:1-2018090623432466027337
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
15.08.2025, 7:23 AM CEST
Data provider
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Ninomiya, Kiichiro
- Ohashi, Kadoaki
- Makimoto, Go
- Tomida, Shuta
- Higo, Hisao
- Kayatani, Hiroe
- Ninomiya, Takashi
- Kubo, Toshio
- Ichihara, Eiki
- Hotta, Katsuyuki
- Tabata, Masahiro
- Maeda, Yoshinobu
- Kiura, Katsuyuki
- SpringerLink (Online service)
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Clinical utility of liquid biopsy for EGFR driver, T790M mutation and EGFR amplification in plasma in patients with acquired resistance to afatinib
Crizotinib with or without an EGFR-TKI in treating EGFR-mutant NSCLC patients with acquired MET amplification after failure of EGFR-TKI therapy: a multicenter retrospective study
CXCR1+ neutrophil infiltration orchestrates response to third-generation EGFR-TKI in EGFR mutant non-small-cell lung cancer
Inhibition and degradation of NRAS with a pan-NRAS monobody
Trastuzumab emtansine delays and overcomes resistance to the third-generation EGFR-TKI osimertinib in NSCLC EGFR mutated cell lines
Third-generation inhibitors targeting EGFR T790M mutation in advanced non-small cell lung cancer
An oligoclonal antibody durably overcomes resistance of lung cancer to third‐generation EGFR inhibitors
Multicenter real-world analysis of combined MET and EGFR inhibition in patients with non-small cell lung cancer and acquired MET amplification or polysomy after EGFR inhibition
The third-generation EGFR inhibitor AZD9291 overcomes primary resistance by continuously blocking ERK signaling in glioblastoma
Third-generation prospect theory
Plasma metabolomics profiling of EGFR-mutant NSCLC patients treated with third-generation EGFR-TKI
Emerging strategies to overcome resistance to third-generation EGFR inhibitors
Clinical utility of liquid biopsy for EGFR driver, T790M mutation and EGFR amplification in plasma in patients with acquired resistance to afatinib
Crizotinib with or without an EGFR-TKI in treating EGFR-mutant NSCLC patients with acquired MET amplification after failure of EGFR-TKI therapy: a multicenter retrospective study
CXCR1+ neutrophil infiltration orchestrates response to third-generation EGFR-TKI in EGFR mutant non-small-cell lung cancer
Inhibition and degradation of NRAS with a pan-NRAS monobody
Trastuzumab emtansine delays and overcomes resistance to the third-generation EGFR-TKI osimertinib in NSCLC EGFR mutated cell lines
Third-generation inhibitors targeting EGFR T790M mutation in advanced non-small cell lung cancer
An oligoclonal antibody durably overcomes resistance of lung cancer to third‐generation EGFR inhibitors
Multicenter real-world analysis of combined MET and EGFR inhibition in patients with non-small cell lung cancer and acquired MET amplification or polysomy after EGFR inhibition
The third-generation EGFR inhibitor AZD9291 overcomes primary resistance by continuously blocking ERK signaling in glioblastoma