Enhancer-targeted genome editing selectively blocks innate resistance to oncokinase inhibition

Thousands of putative enhancers are characterized in the human genome, yet few have been shown to have a functional role in cancer progression. Inhibiting oncokinases, such as EGFR, ALK, ERBB2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by up...

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Veröffentlicht in:	Genome research 2014-05, Vol.24 (5), p.751-760
Hauptverfasser:	Webster, Dan E, Barajas, Brook, Bussat, Rose T, Yan, Karen J, Neela, Poornima H, Flockhart, Ross J, Kovalski, Joanna, Zehnder, Ashley, Khavari, Paul A
Format:	Artikel
Sprache:	eng
Schlagworte:	Cell Line, Tumor Chromatin - genetics Chromatin - metabolism Drug Resistance, Neoplasm - genetics Enhancer Elements, Genetic Gene Expression Regulation, Neoplastic Genome, Human Humans Indoles - pharmacology Melanoma - genetics Microphthalmia-Associated Transcription Factor - genetics Microphthalmia-Associated Transcription Factor - metabolism Promoter Regions, Genetic Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins B-raf - antagonists & inhibitors Proto-Oncogene Proteins B-raf - genetics Proto-Oncogene Proteins B-raf - metabolism Proto-Oncogene Proteins c-met - genetics Proto-Oncogene Proteins c-met - metabolism Sulfonamides - pharmacology Transcriptome Vemurafenib
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