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Status |
Public on Dec 22, 2017 |
Title |
c-MYC drives a subset of high-risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification (ChIP-Seq) |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Childhood neuroblastoma is known for MYCN gene amplification, and here we show that in a separate subset of cases MYC-itself is activated due to enhancer hijacking from chromosomal translocations or duplications, thus defining a unique subset of high-risk disease.
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Overall design |
ChIP-Seq for H3K27ac and CTCF in high MYC expressing neuroblastoma cell types
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Contributor(s) |
Zimmerman MW, Liu Y, He S, Durbin AD, Abraham BJ, Weichert-Leahey N, Zhu S, Khan A, Zhang X, Young RA, Zhang J, Look AT |
Citation(s) |
29284669 |
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Submission date |
Jul 12, 2017 |
Last update date |
Jul 25, 2021 |
Contact name |
Richard A Young |
E-mail(s) |
young_computation@wi.mit.edu
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Phone |
617-258-5219
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Organization name |
Whitehead Institute for Biomedical Research
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Lab |
Young Lab
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Street address |
9 Cambridge Center
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City |
Cambridge |
State/province |
MA |
ZIP/Postal code |
02142 |
Country |
USA |
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Platforms (1) |
GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
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Samples (12)
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This SubSeries is part of SuperSeries: |
GSE101297 |
c-MYC drives a subset of high-risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification |
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Relations |
BioProject |
PRJNA398586 |
SRA |
SRP125903 |