Kinase and BET Inhibitors Together Clamp Inhibition of PI3K Signaling and Overcome Resistance to Therapy
Cancer Cell, ISSN: 1535-6108, Vol: 27, Issue: 6, Page: 837-851
2015
- 202Citations
- 207Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations202
- Citation Indexes201
- 201
- CrossRef164
- Patent Family Citations1
- Patent Families1
- Captures207
- Readers207
- 207
- Mentions1
- References1
- Wikipedia1
Article Description
Unsustained enzyme inhibition is a barrier to targeted therapy for cancer. Here, resistance to a class I PI3K inhibitor in a model of metastatic breast cancer driven by PI3K and MYC was associated with feedback activation of tyrosine kinase receptors (RTKs), AKT, mTOR, and MYC. Inhibitors of bromodomain and extra terminal domain (BET) proteins also failed to affect tumor growth. Interestingly, BET inhibitors lowered PI3K signaling and dissociated BRD4 from chromatin at regulatory regions of insulin receptor and EGFR family RTKs to reduce their expression. Combined PI3K and BET inhibition induced cell death, tumor regression, and clamped inhibition of PI3K signaling in a broad range of tumor cell lines to provide a strategy to overcome resistance to kinase inhibitor therapy.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1535610815001828; http://dx.doi.org/10.1016/j.ccell.2015.05.006; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84930582576&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/26058079; https://linkinghub.elsevier.com/retrieve/pii/S1535610815001828; https://secure.jbs.elsevierhealth.com/action/consumeSsoCookie?redirectUri=http%3A%2F%2Fwww.cell.com%2Faction%2FconsumeSharedSessionAction%3FJSESSIONID%3Daaaxn_1RCa6sI5X0ZwSyv%26MAID%3D5pgCNCKuMTj3gMEDSgfFmg%253D%253D%26SERVER%3DWZ6myaEXBLGvmNGtLlDx7g%253D%253D%26ORIGIN%3D890357590%26RD%3DRD&acw=&utt=; http://linkinghub.elsevier.com/retrieve/pii/S1535610815001828
Elsevier BV
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