Novel mechanism of resistance to targeted therapies in lung cancer
We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of dru...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2019-01-01
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| Series: | Molecular & Cellular Oncology |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/23723556.2018.1551015 |
| _version_ | 1827809384234745856 |
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| author | Walter Wang David P. Carbone Rajeswara Rao Arasada |
| author_facet | Walter Wang David P. Carbone Rajeswara Rao Arasada |
| author_sort | Walter Wang |
| collection | DOAJ |
| description | We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models. |
| first_indexed | 2024-03-11T22:40:26Z |
| format | Article |
| id | doaj.art-0c92c8b39b1c4b8996394162fbc7cf1b |
| institution | Directory Open Access Journal |
| issn | 2372-3556 |
| language | English |
| last_indexed | 2024-03-11T22:40:26Z |
| publishDate | 2019-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Molecular & Cellular Oncology |
| spelling | doaj.art-0c92c8b39b1c4b8996394162fbc7cf1b2023-09-22T09:11:00ZengTaylor & Francis GroupMolecular & Cellular Oncology2372-35562019-01-016110.1080/23723556.2018.15510151551015Novel mechanism of resistance to targeted therapies in lung cancerWalter Wang0David P. Carbone1Rajeswara Rao Arasada2The Ohio State University Medical CenterThe Ohio State University Medical CenterThe Ohio State University Medical CenterWe have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.http://dx.doi.org/10.1080/23723556.2018.1551015egfrnotch3egfr tkidrug persister cellscancer stem cells |
| spellingShingle | Walter Wang David P. Carbone Rajeswara Rao Arasada Novel mechanism of resistance to targeted therapies in lung cancer Molecular & Cellular Oncology egfr notch3 egfr tki drug persister cells cancer stem cells |
| title | Novel mechanism of resistance to targeted therapies in lung cancer |
| title_full | Novel mechanism of resistance to targeted therapies in lung cancer |
| title_fullStr | Novel mechanism of resistance to targeted therapies in lung cancer |
| title_full_unstemmed | Novel mechanism of resistance to targeted therapies in lung cancer |
| title_short | Novel mechanism of resistance to targeted therapies in lung cancer |
| title_sort | novel mechanism of resistance to targeted therapies in lung cancer |
| topic | egfr notch3 egfr tki drug persister cells cancer stem cells |
| url | http://dx.doi.org/10.1080/23723556.2018.1551015 |
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