Overcoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589)

scientific article published on 30 January 2020

Overcoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589) is …
instance of (P31):
scholarly articleQ13442814

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P356DOI10.1002/CNCR.32744
P932PMC publication ID7241261
P698PubMed publication ID31999837

P50authorSuresh S RamalingamQ88301479
Shi-Yong SunQ89461552
Songqing FanQ89547572
P2093author name stringTaofeek K Owonikoko
Dan Zong
Hongjing Zang
Guoqing Qian
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BIM Deletion Polymorphism Confers Resistance to Osimertinib in EGFR T790M Lung Cancer: a Case Report and Literature ReviewQ89122108
Co-inhibition of BET and proteasome enhances ER stress and Bim-dependent apoptosis with augmented cancer therapeutic efficacyQ90613188
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Combined Inhibition of HDAC and EGFR Reduces Viability and Proliferation and Enhances STAT3 mRNA Expression in Glioblastoma CellsQ92467508
The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cellsQ35870933
The HDAC inhibitor, MPT0E028, enhances erlotinib-induced cell death in EGFR-TKI-resistant NSCLC cells.Q37212017
Overcoming mTOR inhibition-induced paradoxical activation of survival signaling pathways enhances mTOR inhibitors' anticancer efficacyQ37389181
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Osimertinib As First-Line Treatment of EGFR Mutation-Positive Advanced Non-Small-Cell Lung CancerQ38371667
SAHA, an HDAC inhibitor, overcomes erlotinib resistance in human pancreatic cancer cells by modulating E-cadherinQ38421269
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Fighting cancer drug resistance: Opportunities and challenges for mutation-specific EGFR inhibitors.Q38506135
Third generation EGFR TKIs in EGFR-mutated NSCLC: Where are we now and where are we goingQ38625391
Met gene amplification and protein hyperactivation is a mechanism of resistance to both first and third generation EGFR inhibitors in lung cancer treatmentQ38756221
The combination of irreversible EGFR TKIs and SAHA induces apoptosis and autophagy-mediated cell death to overcome acquired resistance in EGFR T790M-mutated lung cancerQ38941593
HDACs and HDAC Inhibitors in Cancer Development and TherapyQ38947405
EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition.Q39199561
HDAC inhibitor vorinostat enhances the antitumor effect of gefitinib in squamous cell carcinoma of head and neck by modulating ErbB receptor expression and reverting EMT.Q39527047
Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer cell lines.Q40327522
Extracellular signal-regulated kinases 1/2 are serum-stimulated "Bim(EL) kinases" that bind to the BH3-only protein Bim(EL) causing its phosphorylation and turnoverQ40606380
Phosphorylation of Bim-EL by Erk1/2 on serine 69 promotes its degradation via the proteasome pathway and regulates its proapoptotic function.Q40626751
Activation of the ERK1/2 signaling pathway promotes phosphorylation and proteasome-dependent degradation of the BH3-only protein, Bim.Q40662652
Overcoming Acquired Resistance to AZD9291, A Third-Generation EGFR Inhibitor, through Modulation of MEK/ERK-Dependent Bim and Mcl-1 DegradationQ47814631
Inhibition of histone deacetylases sensitizes EGF receptor-TK inhibitor-resistant non-small-cell lung cancer cells to erlotinib in vitro and in vivoQ48021721
P433issue9
P921main subjectnon-small-cell lung carcinomaQ3658562
P304page(s)2024-2033
P577publication date2020-01-30
P1433published inCancerQ326041
P1476titleOvercoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589)
P478volume126

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