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E-GEOD-40724 - Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer (ChIP-Seq)

Status
Released on 11 September 2012, last updated on 11 March 2013
Organism
Homo sapiens
Samples (2)
Protocols (4)
Description
Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. We applied ChIP-seq to identify PR-interaction sites in T47D breast cancer cells and primary uterine leiomyoma cells treated with RU486.
Experiment type
ChIP-seq 
Contacts
Damian S Roqueiro <geo@ncbi.nlm.nih.gov>, Bulun Serdar, Frasor Jonna
Citation
Genome-wide progesterone receptor binding: cell type-specific and shared mechanisms in T47D breast cancer cells and primary leiomyoma cells. Yin P, Roqueiro D, Huang L, Owen JK, Xie A, Navarro A, Monsivais D, Coon JS 5th, Kim JJ, Dai Y, Bulun SE. , PMID:22272226
MINSEQE
Exp. designProtocolsVariablesProcessedSeq. reads
Files
Investigation descriptionE-GEOD-40724.idf.txt
Sample and data relationshipE-GEOD-40724.sdrf.txt
Processed data (1)E-GEOD-40724.processed.1.zip
Additional data (1)E-GEOD-40724.additional.1.zip
Links