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Series GSE49232 Query DataSets for GSE49232
Status Public on Jan 23, 2015
Title Gene expression analysis of in vivo-grown tumors treated with compounds that either de-bulk the tumor or target cancer stem cells
Organism Homo sapiens
Experiment type Expression profiling by array
Summary A large body of evidence has demonstrated that many human tumors are maintained by a small cell population called cancer stem cells (CSCs) or tumor progenitors, which are responsible for tumor formation, therapy resistance and metastasis. We found that ionizing radiation treatment enriches for the CSC phenotype and properties by preferential survival and expansion of tumor progenitor cells. Our studies revealed that aldehyde dehydrogenase (ALDH) activity is indicative of prostate tumor progenitor cells with increased chemo- and radioresistance, enhanced migratory potential, improved DNA- double strand break repair and activation of the signaling pathways, which promote self-renewal and epithelial-mesenchymal transition. We found that X-ray irradiation can convert the bulk tumor cells to more clonogenic and radioresistant population positive for expression of CSC markers. For the first time we showed that irradiation increases histone H3K4 and H3K36 methylation in prostate cancer cells, thereby reactivating transcription of epigenetically silenced target genes. We showed that radioresistant tumor progenitor population undergoes a phenotypical switching during the course of irradiation, suggesting that controlling the phenotypical and functional properties of CSCs during radiation therapy is ultimative for the optimization of treatment strategies. Our studies have shown that CSC markers may be beneficial in prediction of tumor radiocurability, and combination of irradiation with therapies directed against CSCs can be a useful strategy to improve cancer treatment.
To identify potential biomarkers associated with CSC population in these xenograft tumors, we performed whole genome gene expression profiling of the xenograft tumors treated with NVP-BEZ235, which eliminates prostate cancer progenitor populations or with Taxotere, which targets the bulk tumor cells as compared with vehicle-treated control mice.
Overall design Treatment with either vehicle, Taxotere, NVP-BEZ235, or a combination of these two. There are no replicates
Contributor(s) Cojoc M, Peitzsch C, Kurth I, Trautmann F, Kunz-Schughart L, Telegeev GD, Stakhovsky EA, Walker JR, Simin K, Lyle S, Krause M, Baumann M, Dubrovska A
Citation(s) 25670168
Submission date Jul 25, 2013
Last update date Mar 25, 2019
Contact name John R Walker
Phone 858-812-1636
Organization name Genomics Institute of the Novartis Research Foundation
Lab Genetics Core
Street address 10675 John Jay Hopkins
City San Diego
State/province CA
ZIP/Postal code 92121
Country USA
Platforms (1)
GPL570 [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array
Samples (4)
GSM1195690 DU145 xenograft in NOD/SCID mice_vehicle_4 weeks
GSM1195691 DU145 xenograft in NOD/SCID mice_taxotere_4 weeks
GSM1195692 DU145 xenograft in NOD/SCID mice_NVP-BEZ235_4 weeks
BioProject PRJNA213323

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE49232_RAW.tar 33.1 Mb (http)(custom) TAR (of CEL)
Raw data provided as supplementary file
Processed data included within Sample table

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