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GEO help: Mouse over screen elements for information. |
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Status |
Public on Aug 28, 2008 |
Title |
Analysis of genes associated with MYC in maintaining tumorigenesis |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
The MYC oncogene has been implicated in the regulation of up to thousands of genes involved in many cellular programs including proliferation, growth, differentiation, self-renewal, and apoptosis. MYC is thought to induce cancer through an exaggerated effect on these physiologic programs. Which of these genes are responsible for the ability of MYC to initiate and/or maintain tumorigenesis is not clear. Previously, we have shown that upon brief MYC inactivation, some tumors undergo sustained regression. Here we demonstrate that upon MYC inactivation there are global permanent changes in gene expression detected by microarray analysis. By applying StepMiner analysis, we identified genes whose expression most strongly correlated with the ability of MYC to induce a neoplastic state. Notably, genes were identified that exhibited permanent changes in mRNA expression upon MYC inactivation. Importantly, permanent changes in gene expression could be shown by chromatin immunoprecipitation (ChIP) to be associated with permanent changes in the ability of MYC to bind to the promoter regions. Our list of candidate genes associated with tumor maintenance was further refined by comparing our analysis with other published results to generate a gene signature associated with MYC-induced tumorigenesis in mice. To validate the role of gene signatures associated with MYC in human tumorigenesis, we examined the expression of human homologs in 273 published human lymphoma microarray datasets in Affymetrix U133A format. One large functional group of these genes included the ribosomal structural proteins. In addition, we identified a group of genes involved in a diverse array of cellular functions including: BZW2, H2AFY, SFRS3, NAP1L1, NOLA2, UBE2D2, CCNG1, LIFR, FABP3, and EDG1. Hence, through our analysis of gene expression in murine tumor models and human lymphomas, we have identified a novel gene signature correlated with the ability of MYC to maintain tumorigenesis. Time: time of doxycycline treatment or time after removal
Keywords: time_series_design
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Overall design |
Groups of assays that are related as part of a time series. Compound Based Treatment: Bone tumor cells 1325 were treated/not treated with 20ng/ml of doxycycline Computed
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Contributor(s) |
Wu N |
Citation(s) |
18535662 |
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Submission date |
Aug 25, 2008 |
Last update date |
Jan 18, 2013 |
Organization |
Stanford Microarray Database (SMD) |
E-mail(s) |
array@genome.stanford.edu
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Phone |
650-498-6012
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URL |
http://genome-www5.stanford.edu/
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Department |
Stanford University, School of Medicine
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Street address |
300 Pasteur Drive
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City |
Stanford |
State/province |
CA |
ZIP/Postal code |
94305 |
Country |
USA |
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Platforms (1) |
GPL7205 |
SMD Mus musculus 42K Print_942 |
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Samples (16)
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GSM315383 |
2-15-05_time_course_part_one_+dox_3.5hr |
GSM315384 |
2-15-05_time_course_part_one_+dox_7.5hr |
GSM315385 |
2-15-05_time_course_part_one_+dox_11.5hr |
GSM315386 |
2-15-05_time_course_part_one_+dox_18hr |
GSM315387 |
2-15-05_time_course_part_one_+dox_24hr |
GSM315388 |
3-22-05_time_course_part2_MYC_reactivate_18hr |
GSM315389 |
2-15-05_time_course_part_one_+dox_36hr |
GSM315390 |
3-22-05_time_course_part2_MYC_reactivate_24hr |
GSM315391 |
2-15-05_time_course_part_one_+dox_48hr |
GSM315392 |
3-22-05_time_course_part2_MYC_reactivate_36hr |
GSM315393 |
3-22-05_time_course_part2_MYC_reactivate_48hr |
GSM315394 |
3-22-05_time_course_part1_+dox48hr |
GSM315395 |
3-22-05_time_course_part2_MYC_reactivate_4hr |
GSM315396 |
3-22-05_time_course_part2_MYC_reactivate_8hr |
GSM315397 |
3-22-05_time_course_part2_MYC_reactivate_12hr |
GSM315398 |
2-15-05_time_course_part_one_+dox_0hr |
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Relations |
BioProject |
PRJNA112905 |
Supplementary file |
Size |
Download |
File type/resource |
GSE12544_RAW.tar |
2.6 Mb |
(http)(custom) |
TAR |
Processed data included within Sample table |
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