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Status |
Public on Dec 10, 2018 |
Title |
Identification of Jun loss that promotes resistance to HDAC inhibitor Entinostat through Myc signaling in Luminal breast cancer [CGH] |
Organism |
Mus musculus |
Experiment type |
Genome variation profiling by array
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Summary |
The histone deacetylase inhibitor Entinostat is in phase III trials for patients with metastatic estrogen receptor-positive breast cancer. Predictors of sensitivity and resistance, however, remain unknown.
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Overall design |
A total of 8 cell lines and 9 mouse models of breast cancer were treated with Entinostat. Luminal cell lines were treated with or without Entinostat at their IC50 doses, and MMTV/Neu luminal mouse tumors were treated with Entinostat until progression. We investigated these models using gene expression profiling by microarray and copy number by arrayCGH. We also utilized the network-based Dawnrank algorithm, that integrates DNA and RNA data, to identify driver genes of resistance. The impact of a number of candidate drivers was investigated in The Cancer Genome Atlas and the METABRIC
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Contributor(s) |
Tanioka M, Hollern DP, Perou CM, Mott KR, Fan C, Soloway MG |
Citation(s) |
30497520 |
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Submission date |
Aug 19, 2018 |
Last update date |
Dec 10, 2018 |
Contact name |
Charles M. Perou |
E-mail(s) |
[email protected]
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Organization name |
University of North Carolina at Chapel Hill
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Department |
Professor of Genetics, and Pathology & Laboratory Medicine; Lineberger Comprehensive Cancer Center
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Street address |
12-044 Lineberger Comprehensive Cancer Center CB# 7295
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City |
Chapel Hill |
State/province |
NC |
ZIP/Postal code |
27599-7264 |
Country |
USA |
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Platforms (1) |
GPL4092 |
Agilent-014695 Mouse Genome CGH Microarray 244A (G4415A) (Feature Number version) |
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Samples (22)
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This SubSeries is part of SuperSeries: |
GSE118744 |
Identification of Jun loss that promotes resistance to HDAC inhibitor Entinostat through Myc signaling in Luminal breast cancer |
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Relations |
BioProject |
PRJNA486666 |