Unidentified
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB20013 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Differentially expressed genes in Gastric Cancer (CBX61)
| PRJDB20038 | ENA
Project description:Differentially expressed genes in S.pyogenes SSI-1 (CBX115)
| PRJDB20088 | ENA
Project description:Chromosomal structural mutations play an important role in determining the transcriptional landscape of human breast cancers. We determined that pro-oncogenic and anti-oncogenic genes are clustered throughout the genome and that these clusters coincide with regions of segmental amplification and deletion. We constructed detailed structural mutation maps of representative breast cancers and found that tandem duplications appear to nucleate regions for amplification. Subsequent rearrangements link distant pro-oncogenic elements for co-amplification, and are associated with loss of tumor suppressors. We show that genes engaged in co-amplifications or conjoint deletions on 17q and 8q have pro-growth effects that are additive in nature. Our results suggest structural mutations efficiently orchestrate the gain and loss of cancer gene cassettes that engage many oncogenic pathways simultaneously.
2013-06-29 | GSE48377 | GEO
Project description:Estrogen receptor positive breast cancer is the most prevalent form of breast cancer. Although a number of available drugs are highly effective at blocking estrogen mediated receptor activity, thousands of patients die every year from ER positive breast cancers because the disease progresses to a stage at which these drugs are no longer effective. Thus, it is crucial to establish a comprehensive understanding of the biology of the estrogen receptor (ER) in ER:positive breast cancers that progress despite hormone therapy, a gap in knowledge that remains a serious impediment to successful treatment of patients with ER positive breast cancer. A key question that must be answered is how the estrogen receptor retains the capacity to activate transcription in the absence or near absence of estrogen. We have found a partial answer to this question upon investigating the effect of amplification and overexpression of Wolf Hirschhorn Syndrome Candidate 1:Like 1 (WHSC1L1), a gene that is amplified in 15% of breast cancers that codes for a histone:lysine methyltransferase. WHSC1L1 lies in the 8p11:p12 amplicon, a region of gene amplification that is strongly associated with breast cancer. In this study, we performed shRNA knockdown of the catalytically inactive short isoform of WHSC1L1 in SUM44PE breast cancer cells and found that expression of the short isoform of WHSC1L1 is necessary for expression of the estrogen receptor in this highly ER:positive cell line. In addition, we found that the estrogen receptor binds chromatin extensively in the absence of exogenous estrogen, including several actively transcribed canonical ER target genes, indicating that estrogen receptor signaling is active in SUM44 cells in estrogen free conditions. These findings represent a novel model for ER biology in luminal B breast cancers harboring amplification of WHSC1L1 and provide insight into the mechanisms by which ER: positive breast cancers become unresponsive to SERMs or aromatase inhibitors.
2016-05-07 | E-MTAB-3739 | biostudies-arrayexpress
Project description:Differentially expressed genes in colon cancer derived fibroblasts (CBX125)
| PRJDB20091 | ENA
Project description:Differentially expressed genes in renal cell carcinoma cell lines (CBX96)
| PRJDB20072 | ENA
Project description:Differentially expressed genes in gastric carcinima cells by microRNA-375 (CBX92)
| PRJDB20069 | ENA
Project description:Gene expression profiles of breast cancers before and after treatment with doxorubicin or docetaxel (CBX91)
| PRJDB20067 | ENA
Project description:Chromosomal structural mutations play an important role in determining the transcriptional landscape of human breast cancers. We determined that pro-oncogenic and anti-oncogenic genes are clustered throughout the genome and that these clusters coincide with regions of segmental amplification and deletion. We constructed detailed structural mutation maps of representative breast cancers and found that tandem duplications appear to nucleate regions for amplification. Subsequent rearrangements link distant pro-oncogenic elements for co-amplification, and are associated with loss of tumor suppressors. We show that genes engaged in co-amplifications or conjoint deletions on 17q and 8q have pro-growth effects that are additive in nature. Our results suggest structural mutations efficiently orchestrate the gain and loss of cancer gene cassettes that engage many oncogenic pathways simultaneously. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from fresh-frozen breast tumors with >80% tumor cell content and their paired peripheral blood samples. Copy number analysis of the SNP arrays was done using the copy number pipeline implemented into Partek software version 6.5
2013-06-29 | E-GEOD-48377 | biostudies-arrayexpress