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Status |
Public on Feb 06, 2016 |
Title |
Expression profiling by high throughput sequencing of tumors derived from human prostate epithelial cells transformed with the oncogenes N-Myc and myrAKT1. |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
MYCN amplification and overexpression are common in neuroendocrine prostate cancer (NEPC). However, the impact of aberrant N-Myc expression in prostate tumorigenesis and the cellular origin of NEPC have not been established. We define N-Myc and activated AKT1 as oncogenic components sufficient to transform human prostate epithelial cells to prostate adenocarcinoma and NEPC including the small cell prostate carcinoma (SCPC) variant with phenotypic and molecular features of aggressive, late-stage human disease. We directly show that prostate adenocarcinoma and NEPC can both arise from a common epithelial clone. Further, N-Myc is required for tumor maintenance and destabilization of N-Myc through Aurora A kinase inhibition reduces tumor burden. Our findings establish N-Myc as a driver of NEPC and a target for therapeutic intervention. Expression profiling by high throughput sequencing of experimentally generated human tumors with mixed NEPC and prostate adenocarcinoma.
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Overall design |
Gene expression analysis of laser capture microdissected NEPC and adenocarcinoma from three independent engineered human tumors of mixed NEPC and prostate adenocarcinoma phenotype.
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Contributor(s) |
Lee JK |
Citation(s) |
27050099 |
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Submission date |
Feb 05, 2016 |
Last update date |
May 15, 2019 |
Contact name |
John K Lee |
E-mail(s) |
jklee5@fredhutch.org
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Phone |
206-667-6819
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Organization name |
Fred Hutchinson Cancer Research Center
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Department |
Human Biology Division
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Lab |
Lee Lab
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Street address |
1100 Fairview Ave N, E2-112
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City |
Seattle |
State/province |
WA |
ZIP/Postal code |
98109 |
Country |
USA |
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Platforms (1) |
GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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Samples (6)
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Relations |
BioProject |
PRJNA311066 |
SRA |
SRP069723 |