Correction: The HDAC inhibitor, MPT0E028, enhances erlotinib induced cell death in EGFR-TKI-resistant NSCLC cells
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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1 Online-Ressource.
- Language
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Englisch
- Bibliographic citation
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Correction: The HDAC inhibitor, MPT0E028, enhances erlotinib induced cell death in EGFR-TKI-resistant NSCLC cells ; volume:15 ; number:7 ; day:9 ; month:7 ; year:2024 ; pages:1-4 ; date:7.2024
Cell death & disease ; 15, Heft 7 (9.7.2024), 1-4, 7.2024
- Creator
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Chen, M. -C
Chen, C. -H
Wang, J. -C
Tsai, A. -C
Liou, J. -P
Pan, S. -L
Teng, C. -M
- Contributor
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SpringerLink (Online service)
- DOI
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10.1038/s41419-024-06794-4
- URN
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urn:nbn:de:101:1-2409262136522.255947407693
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:27 AM CEST
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Associated
- Chen, M. -C
- Chen, C. -H
- Wang, J. -C
- Tsai, A. -C
- Liou, J. -P
- Pan, S. -L
- Teng, C. -M
- SpringerLink (Online service)
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NSCLC – Neuer TKI zeigt Wirksamkeit bei EGFR-Resistenzmutation
Combined use of anti-ErbB monoclonal antibodies and erlotinib enhances antibody-dependent cellular cytotoxicity of wild-type erlotinib-sensitive NSCLC cell lines
The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cells
Enhanced osteopontin splicing regulated by RUNX2 is HDAC-dependent and induces invasive phenotypes in NSCLC cells
Ramucirumab (NSCLC, Kombination mit Erlotinib) : Nutzenbewertung gemäß § 35a SGB V
TKi | TKi
Therapeutic effect of whole brain radiotherapy on advanced NSCLC between EGFR TKI-naïve and TKI-resistant
Promising Combination Therapy with Bevacizumab and Erlotinib in an EGFR-Mutated NSCLC Patient with MET Amplification Who Showed Intrinsic Resistance to Initial EGFR-TKI Therapy
Constitutive cell proliferation regulating inhibitor of protein phosphatase 2A (CIP2A) mediates drug resistance to erlotinib in an EGFR activating mutated NSCLC cell line
Constitutive Cell Proliferation Regulating Inhibitor of Protein Phosphatase 2A (CIP2A) Mediates Drug Resistance to Erlotinib in an EGFR Activating Mutated NSCLC Cell Line
Pooled safety analyses of ALK-TKI inhibitor in ALK-positive NSCLC
Trastuzumab emtansine delays and overcomes resistance to the third-generation EGFR-TKI osimertinib in NSCLC EGFR mutated cell lines
NSCLC – Neuer TKI zeigt Wirksamkeit bei EGFR-Resistenzmutation
Combined use of anti-ErbB monoclonal antibodies and erlotinib enhances antibody-dependent cellular cytotoxicity of wild-type erlotinib-sensitive NSCLC cell lines
The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cells
Enhanced osteopontin splicing regulated by RUNX2 is HDAC-dependent and induces invasive phenotypes in NSCLC cells
Ramucirumab (NSCLC, Kombination mit Erlotinib) : Nutzenbewertung gemäß § 35a SGB V
TKi | TKi
Therapeutic effect of whole brain radiotherapy on advanced NSCLC between EGFR TKI-naïve and TKI-resistant
Promising Combination Therapy with Bevacizumab and Erlotinib in an EGFR-Mutated NSCLC Patient with MET Amplification Who Showed Intrinsic Resistance to Initial EGFR-TKI Therapy
Constitutive cell proliferation regulating inhibitor of protein phosphatase 2A (CIP2A) mediates drug resistance to erlotinib in an EGFR activating mutated NSCLC cell line
Constitutive Cell Proliferation Regulating Inhibitor of Protein Phosphatase 2A (CIP2A) Mediates Drug Resistance to Erlotinib in an EGFR Activating Mutated NSCLC Cell Line
Pooled safety analyses of ALK-TKI inhibitor in ALK-positive NSCLC