AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells
A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR -mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback...
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| Veröffentlicht in: | Nature communications Jg. 10; H. 1; S. 259 - 14 |
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| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
London
Nature Publishing Group UK
16.01.2019
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
| Online-Zugang: | Volltext |
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| Abstract | A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with
EGFR
-mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells.
Resistance to the new generation EGFR-TKI, Osimertinib, can emerge in patients with EGFR-mutated lung cancer. Here, the authors show that AXL, which is activated by osimertinib, can promote the emergence of tolerant lung cancer cell thus conferring resistance to osimertinib and propose the combination of Osimertinib with AXL inhibitor as a potential therapeutic approach in such resistant cancers. |
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| AbstractList | A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells.Resistance to the new generation EGFR-TKI, Osimertinib, can emerge in patients with EGFR-mutated lung cancer. Here, the authors show that AXL, which is activated by osimertinib, can promote the emergence of tolerant lung cancer cell thus conferring resistance to osimertinib and propose the combination of Osimertinib with AXL inhibitor as a potential therapeutic approach in such resistant cancers. A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR -mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells. Resistance to the new generation EGFR-TKI, Osimertinib, can emerge in patients with EGFR-mutated lung cancer. Here, the authors show that AXL, which is activated by osimertinib, can promote the emergence of tolerant lung cancer cell thus conferring resistance to osimertinib and propose the combination of Osimertinib with AXL inhibitor as a potential therapeutic approach in such resistant cancers. A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells.A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells. Resistance to the new generation EGFR-TKI, Osimertinib, can emerge in patients with EGFR-mutated lung cancer. Here, the authors show that AXL, which is activated by osimertinib, can promote the emergence of tolerant lung cancer cell thus conferring resistance to osimertinib and propose the combination of Osimertinib with AXL inhibitor as a potential therapeutic approach in such resistant cancers. A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells. A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR -mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells. |
| ArticleNumber | 259 |
| Author | Taniguchi, Hirokazu Uchino, Junji Adachi, Yuta Yoshimura, Akihiro Wang, Rong Watanabe, Satoshi Matsumoto, Isao Uehara, Hisanori Nishiyama, Akihiro Tanimura, Keiko Araujo, Luiz H. Kikuchi, Toshiaki Tanaka, Hiroshi Miura, Satoru Shiotsu, Shinsuke Mukae, Hiroshi Yamada, Tadaaki Takeuchi, Shinji Boroni, Mariana Yamaguchi, Hiroyuki Yano, Seiji Tanimoto, Azusa Kitazaki, Takeshi Takayama, Koichi |
| Author_xml | – sequence: 1 givenname: Hirokazu orcidid: 0000-0003-2414-8344 surname: Taniguchi fullname: Taniguchi, Hirokazu organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University, Department of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences – sequence: 2 givenname: Tadaaki orcidid: 0000-0002-6945-281X surname: Yamada fullname: Yamada, Tadaaki email: tayamada@koto.kpu-m.ac.jp organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University, Department of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine – sequence: 3 givenname: Rong surname: Wang fullname: Wang, Rong organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University – sequence: 4 givenname: Keiko surname: Tanimura fullname: Tanimura, Keiko organization: Department of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine – sequence: 5 givenname: Yuta surname: Adachi fullname: Adachi, Yuta organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University – sequence: 6 givenname: Akihiro surname: Nishiyama fullname: Nishiyama, Akihiro organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University – sequence: 7 givenname: Azusa surname: Tanimoto fullname: Tanimoto, Azusa organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University – sequence: 8 givenname: Shinji surname: Takeuchi fullname: Takeuchi, Shinji organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University – sequence: 9 givenname: Luiz H. surname: Araujo fullname: Araujo, Luiz H. organization: Division of Clinical Research, Brazilian National Cancer Institute – sequence: 10 givenname: Mariana surname: Boroni fullname: Boroni, Mariana organization: Division of Experimental and Translational Research, Bioinformatics and Computational Biology Lab, Brazilian National Cancer Institute – sequence: 11 givenname: Akihiro surname: Yoshimura fullname: Yoshimura, Akihiro organization: Department of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine – sequence: 12 givenname: Shinsuke surname: Shiotsu fullname: Shiotsu, Shinsuke organization: Department of Respiratory Medicine, Japanese Red Cross Kyoto Daiichi Hospital – sequence: 13 givenname: Isao surname: Matsumoto fullname: Matsumoto, Isao organization: Department of Thoracic, Cardiovascular and General Surgery, Kanazawa University – sequence: 14 givenname: Satoshi surname: Watanabe fullname: Watanabe, Satoshi organization: Department of Respiratory Medicine and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences – sequence: 15 givenname: Toshiaki surname: Kikuchi fullname: Kikuchi, Toshiaki organization: Department of Respiratory Medicine and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences – sequence: 16 givenname: Satoru surname: Miura fullname: Miura, Satoru organization: Department of Internal Medicine, Niigata Cancer Center Hospital – sequence: 17 givenname: Hiroshi surname: Tanaka fullname: Tanaka, Hiroshi organization: Department of Internal Medicine, Niigata Cancer Center Hospital – sequence: 18 givenname: Takeshi surname: Kitazaki fullname: Kitazaki, Takeshi organization: Department of Respiratory Medicine, Japanese Red Cross Nagasaki Genbaku Hospital – sequence: 19 givenname: Hiroyuki surname: Yamaguchi fullname: Yamaguchi, Hiroyuki organization: Department of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences – sequence: 20 givenname: Hiroshi surname: Mukae fullname: Mukae, Hiroshi organization: Department of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences – sequence: 21 givenname: Junji surname: Uchino fullname: Uchino, Junji organization: Department of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine – sequence: 22 givenname: Hisanori surname: Uehara fullname: Uehara, Hisanori organization: Department of Pathology and Laboratory Medicine, Institute of Biomedical Sciences, Tokushima University Graduate School – sequence: 23 givenname: Koichi surname: Takayama fullname: Takayama, Koichi organization: Department of Pulmonary Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine – sequence: 24 givenname: Seiji orcidid: 0000-0002-6151-2988 surname: Yano fullname: Yano, Seiji email: syano@staff.kanazawa-u.ac.jp organization: Division of Medical Oncology, Cancer Research Institute, Kanazawa University, Nano Life Science Institute, Kanazawa University, Kakuma |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30651547$$D View this record in MEDLINE/PubMed |
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| Snippet | A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with
EGFR
-mutated lung cancer. However, some patients show... A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutated lung cancer. However, some patients show intrinsic... Resistance to the new generation EGFR-TKI, Osimertinib, can emerge in patients with EGFR-mutated lung cancer. Here, the authors show that AXL, which is... |
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| SubjectTerms | 13/1 13/109 13/51 13/89 45/77 631/67/1612 631/67/1612/1350 64/60 82/80 Acrylamides Adenocarcinoma of Lung - drug therapy Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - pathology Adult Aniline Compounds Animals Antineoplastic Combined Chemotherapy Protocols - pharmacology Antineoplastic Combined Chemotherapy Protocols - therapeutic use Axl protein Cancer Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell survival Cell Survival - drug effects Cell Survival - genetics Disease-Free Survival Drug Resistance, Neoplasm - genetics Emergence Enzyme inhibitors Epidermal growth factor receptors ErbB Receptors - antagonists & inhibitors ErbB Receptors - genetics ErbB Receptors - metabolism Feedback loops Female Gene Knockdown Techniques Heterocyclic Compounds, 2-Ring - pharmacology Heterocyclic Compounds, 2-Ring - therapeutic use Humanities and Social Sciences Humans Inhibitors Lung - pathology Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - pathology Male Mice Mice, Inbred NOD multidisciplinary Mutation Negative feedback Neoplasm Recurrence, Local - genetics Neoplasm Recurrence, Local - pathology Neoplasm Recurrence, Local - prevention & control Patients Piperazines - pharmacology Piperazines - therapeutic use Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Protein-tyrosine kinase Proto-Oncogene Proteins - antagonists & inhibitors Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Pyrazoles - pharmacology Pyrazoles - therapeutic use Receptor Protein-Tyrosine Kinases - antagonists & inhibitors Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - metabolism Receptor, ErbB-3 - genetics Receptor, ErbB-3 - metabolism RNA, Small Interfering - metabolism Science Science (multidisciplinary) Targeted cancer therapy Treatment Outcome Tumors Tyrosine Viability Xenograft Model Antitumor Assays |
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| Title | AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells |
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