IPH-926 human lobular breast cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE28089 | GEO | 2011/12/21
SECONDARY ACCESSION(S): PRJNA139743
REPOSITORIES: GEO
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Project description:IPH-926 is an anticancer drug-resistant tumor cell line derived from a chemo-refractory human infiltrating lobular breast cancer (ILBC). IPH-926 ILBC cells were subjected to gene expression profiling using an Affymetrix HG U133 Plus 2.0 array. To characterize the global gene expression of IPH-926, cells were subjected to transcriptional profiling using the Affymetrix HG U133 Plus 2.0 technology. The correct identity of the IPH-926 cells subjected to gene expression profiling was authenticated by short tandem repeat (STR) profiling.
2011-12-21 | E-GEOD-28089 | biostudies-arrayexpress
Project description:This experiment aims to study transcriptional alterations induced by reconstitution of wild type E-cadherin expression in human lobular breast cancer cells harbouring deleterious, somatic CDH-1 mutations Two cell lines (IPH-926 and MDA-MB-134) expressing synthetic Ecad (EcadEGFP) or not (EGFP) were compared against each other. Analysis were conducted in triplicates (IPH-926) and quadruplicates (MDA-MB-134), respectively.
2014-03-04 | E-GEOD-55529 | biostudies-arrayexpress
Project description:Setaria viridis strain:#926 | cultivar:#926 Genome sequencing
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Project description:Background: The prognostic value of histologic grade (HG) in invasive lobular carcinoma (ILC) remains uncertain, and most ILC tumors are graded as HG2. Genomic grade (GG) is a 97-gene signature that improves the prognostic value of HG. This study evaluates whether GG may overcome the limitations of HG in ILC. Methods: Gene expression data were generated from frozen tumor samples, and GG calculated according to the expression of 97 genes. The prognostic value of GG was assessed in a stratified Cox regression model for invasive disease-free survival (IDFS) and overall survival (OS).
2016-10-15 | GSE88770 | GEO
Project description:The ts-p53 E285K protein is a rare p53 mutant with temperature-sensitive (ts) loss of function characteristics. In cancer cells, which express ts-p53 E285K intrinsically, endogenous wild type p53 activity is reconstituted by appropriate cultivation temperature (permissive condition). At non-appropriate cultivation temperature (restrictive condition) this p53 mutant is inactive. The present study took advantage of this mechanism and employed IPH-926 lobular breast cancer cells and BT-474 ductal breast cancer cells, which both harbor endogenous ts-p53 E285K, for the transcriptional profiling of p53-responsive genes. This new approach eliminated the need for genetic modification or cytotoxic stimulation to achive a p53 response in the cells being investigated . Three subseqent passages of IPH-926 lobular breast cancer cells (harboring ts-p53 E285K) were seeded into two parallel culture dishes each and were allowed to adopt to restrictive and permissive condition for 24 h before analysis on Affymetrix U133 Plus 2.0 microarrays. Subsequently, this experiment was repeated with BT-474 ductal breast cancer cells (also harboring ts-p53 E285K). To gate out non-specific temperature effects, the same experiment was also performed with MCF-7 breast cancer cells (harboring wt p53). Probe sets differentially expressed at restrictive versus permissive condition in MCF-7 were considered as non-specifically regulated. These probe sets were excluded from the final statistical analysis of IPH-926 and BT-474 expression data. response to restored p53 activity
2012-12-31 | E-GEOD-35006 | biostudies-arrayexpress
Project description: Not available
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Project description:Mice bearing primary human chondrosarcoma xenografts were treated with IPI 926, and mRNA levels of known Hh pathway genes and endpoint tumor volumes were measured. Gene expression profiling of IPI-926 treated tumors was conducted to identify potential novel Hh target genes.
2014-03-18 | GSE44581 | GEO
Project description:Mice bearing primary human chondrosarcoma xenografts were treated with IPI 926, and mRNA levels of known Hh pathway genes and endpoint tumor volumes were measured. Gene expression profiling of IPI-926 treated tumors was conducted to identify potential novel Hh target genes. 4 Control treated and 4 IPI-926 treated NSG Mice. Primary tumor was obtained from a single chondrosarcoma patient.
2014-03-18 | E-GEOD-44581 | biostudies-arrayexpress
Project description:Streptomyces sp. CG 926 Genome sequencing and assembly
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Project description:Invasive lobular carcinoma (ILC) of the breast accounts for 5-15% of breast cancers and is characterized by loss of E-cadherin and believed to arise via a linear histological progression. Genomic studies have identified a clonal relationship between ILC and concurrent lobular carcinoma in situ (LCIS) lesions, suggesting that LCIS may be a precursor lesion. It has been shown that an LCIS diagnosis confers a 15-20% risk of progression to ILC, over a lifetime. Currently no molecular test or markers can identify LCIS lesions likely to progress to ILC. Since microRNA (miRNA) expression changes have been detected in a number of other cancer types, we explored whether their dysregulation might be detected during progression from LCIS to ILC. Using the Illumina miRNA profiling platform, designed for simultaneous analysis of 470 mature miRNAs, we analyzed the profiles of archived normal breast epithelium, LCIS lesions found alone, LCIS lesions concurrent with ILC, and the concurrent ILCs, as a model of linear histological progression toward ILC. We identified two sets of differentially expressed miRNAs, the first set highly expressed in normal epithelium, including hsa-miR-224, -139, -10b, -450, 140 and -365 and the second set upregulated during lobular neoplasia, including hsa-miR-375, -203, -425-5p, -183, -565 and -182. Using quantitative RT-PCR, we validated a trend of increased expression for hsa-mir-375, hsa-mir-182, and hsa-mir-183 correlating with ILC progression. As we detected increased expression of hsa-miR-375 in LCIS lesions synchronous with ILC, we sought to determine whether hsa-mir-375 might induce phenotypes reminiscent of lobular neoplasia by expressing it in the MCF10A 3D culture model of mammary acinar morphogenesis. Increased expression of hsa-miR-375 resulted in loss of cellular organization and acquisition of a hyperplastic phenotype. These data suggest that dysregulated miRNA expression contributes to lobular neoplastic progression. 6 specimens were analyzed in duplicate. One frozen normal lobular epithelium and the matched FFPE (1 month old) normal lobular epithelium. One lobular carcinoma in situ (LCIS) found alone, one LCIS synchronous with an invasive lobular carcinoma (ILC), the synchronous ILC (from a different archived block), and one ILC found alone without presence of any other breast cancer.
2011-04-11 | E-GEOD-28514 | biostudies-arrayexpress