Transcription profiling of human cancer cell line profiles
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Alex Adai
PROVIDER: E-GEOD-10843 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:mRNA breast cancer cell lines were profiled to study the function of hsa-mir-221 and hsa-mir-222. MCF7 cell lines were profiled after treatment with mir-221/222 mimics, and compared to profiles with transfection controls. Similarly, MDA-MB-231 cell lines were profiled after treatment with mir-221/222 inhibitors, and compared to profiles with transfection controls. Since ESR1 is a predicted target of mir-221/222 we also profiled MCF7 cell lines after disrupting ESR1 with an siRNA. Other breast cancer cell lines are provided because all cell lines were normalized together. Experiment Overall Design: mRNA breast cancer cell line profiles with some samples in duplicate or triplicate. See summary for more information.
2009-01-13 | E-GEOD-10890 | biostudies-arrayexpress
Project description:Apo2L/TRAIL stimulates cancer-cell death through the proapoptotic receptors DR4 and DR5, but the determinants of tumor susceptibility to this ligand are not fully defined. mRNA expression of the peptidyl O-glycosyl transferase GALNT14 correlated with Apo2L/TRAIL sensitivity in pancreatic carcinoma, non-small cell lung carcinoma and melanoma cell lines (P < 0.00009; n=83), and up to 30% of samples from various human malignancies displayed GALNT14 overexpression. RNA interference of GALNT14 reduced cellular Apo2L/TRAIL sensitivity, whereas overexpression increased responsiveness. Biochemical analysis of DR5 identified several ectodomain O-GalNAc-Gal-Sialic acid structures. Sequence comparison predicted conserved extracellular DR4 and DR5 O-glycosylation sites; progressive mutation of the DR5 sites attenuated apoptosis signaling. O-glycosylation promoted ligand-stimulated clustering of DR4 and DR5, which mediated recruitment and activation of the apoptosis-initiating protease caspase-8. These results uncover a novel link between death receptor O-glycosylation and apoptosis signaling, providing potential predictive biomarkers for Apo2L/TRAIL-based cancer therapy. Experiment Overall Design: Gene expression for untreated cell lines analyzed. Some cell lines have one replicate profile, some two (Samples with 2 CEL files). Normalized data for replicates was averaged. Analysis involved a regularized t-test to identify genes with expression differences between Apo2L sensitive and resistant lines.
2008-06-16 | E-GEOD-8332 | biostudies-arrayexpress
Project description:tumor microenviroment facilitates metastatic spread by eliciting reversible changes in the phenotypes of cancer cells Experiment Overall Design: expression array of stromal samples prepared from 15 normal/DCIS and 7 IDC tumor specimans
2009-03-14 | E-GEOD-8977 | biostudies-arrayexpress
Project description:Array Comparative Genomic Hybridization (aCGH) of 70 pancreatic ductal adenocarcinoma (PDAC) samples was performed on Agilent 244K CGH arrays in order to find common genomic aberrations for cancer gene discovery. Additionally, matched expression profiling on Agilent 44K arrays was performed. Common copy number aberrations were identified in order to identify a list of putative cancer genes. Expression profiling data was used to further enrich this list of putative cancer genes for more likely candidates. Last, the most promising candidates were functionally interrogated using RNA interference-mediated knockdown to mimic loss. Well-known PDAC cancer genes were observed as amplified (KRAS and MYC) and deleted (CDKN2A, TGFBR2, SMAD4, and MAP2K4). 70 tumor samples (48 xenografts, 22 cell lines). 2-color arrays hybridized against a common reference pool of genomic DNA from 8 normal individuals. This dataset represents the aCGH component of the study.
2011-12-15 | E-GEOD-25273 | biostudies-arrayexpress
Project description:Expression profiling of 70 Pancreatic Ductal Adenocarcinoma (PDAC) samples was performed on Agilent 44K expression arrays for cancer gene discovery. Additionally, matched aCGH on Agilent 244K arrays was performed. These two datasets were integrated in order to identify driver mutations leading to pancreatic cancer. Promising candidates were interrogated further using functional studies. 68 tumor samples (48 xenografts, 20 cell lines). 2 color arrays hybridized against a common reference pool of RNA from 11 cancer cell lines
2011-12-15 | E-GEOD-26088 | biostudies-arrayexpress
Project description:bulk breast tumor RNA from patient; Abstract: Sporadic basal-like cancers (BLC) are a distinct class of human breast cancers that are phenotypically similar to BRCA1-associated cancers. Like BRCA1-deficient tumors, most BLC lack markers of a normal inactive X chromosome (Xi). Duplication of the active X chromosome and loss of Xi characterized almost half of BLC cases tested. Others contained biparental but nonheterochromatinized X chromosomes or gains of X chromosomal DNA. These abnormalities did not lead to a global increase in X chromosome transcription but were associated with overexpression of a small subset of X chromosomal genes. Other, equally aneuploid, but non-BLC rarely displayed these X chromosome abnormalities. These results suggest that X chromosome abnormalities contribute to the pathogenesis of BLC, both inherited and sporadic. total 62 sample incudes 43 tumor, 7 normal breast and 12 normal organelle Experiment Overall Design: compare expression of tumor to normal breast tissue
2008-06-16 | E-GEOD-7904 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE25273: Array Comparative Genomic Hybridization of Pancreatic Xenografts and Cell Lines GSE26088: Expression Profiling of Pancreatic Xenografts and Cell Lines Refer to individual Series
2011-12-15 | E-GEOD-26089 | biostudies-arrayexpress
Project description:We hypothesized that DNA methylation distributes into specific patterns in cancer cells, which reflect critical biological differences. We therefore examined the methylation profiles of 344 patients with acute myeloid leukemia (AML). Clustering of these patients by methylation data segregated patients into 16 groups. Five of these groups defined new AML subtypes that shared no other known feature. In addition, DNA methylation profiles segregated patients with CEBPA aberrations from other subtypes of leukemia, defined four epigenetically distinct forms of AML with NPM1 mutations, and showed that established AML1-ETO, CBFb-MYH11 and PML-RARA leukemia entities are associated with specific methylation profiles. We report a 15-gene methylation classifier predictive of overall survival in an independent patient cohort (p<0.001, adjusted for known covariates). Keywords: DNA methylation profiling DNA methylation profiling of a cohort of 344 AML patients from Erasmus Medical Center and enrolled in clinical trials from the Dutch-German cooperative group HOVON. Additionally, a control group consisting of 8 CD34+ bone marrow samples from healthy donors was also studied.
2010-01-12 | E-GEOD-18700 | biostudies-arrayexpress
Project description:Human prolactinomas (n=4, 3 males and 1 female) were obtained during trans-sphenoidal surgery as part of an ongoing accession of human pituitary tumors. The study was approved Institutional Review Board (IRB) of Emory University, and informed consent obtained for all subjects. Tumors were microdissected and removed using the surgical microscope, rinsed in sterile saline, snap-frozen in liquid nitrogen, and stored (-80 ℃) until analysis. Each tumor fragment was confirmed independently by a neuropathologist by histology and immunohistochemistry prior to molecular analysis. Three normal pituitary glands from cadavers were obtained from the National Resource Center (NDRI, www.ndriresource.org). Each human tissue sample was analyzed using Affymetrix Human Genome U95Av2 arrays. 4 prolactinoma and 3 normal pituitaries
2012-03-08 | E-GEOD-36314 | biostudies-arrayexpress
Project description:The molecular heterogeneity of acute leukemias and other tumors constitutes a major obstacle towards understanding disease pathogenesis and developing new targeted-therapies. Aberrant gene regulation is a hallmark of cancer and plays a central role in determining tumor phenotype. We predicted that integration of different genome-wide epigenetic regulatory marks along with gene expression levels would provide greater power in capturing biological differences between leukemia subtypes. Gene expression, cytosine methylation and histone H3 lysine 9 (H3K9) acetylation were measured using high-density oligonucleotide microarrays in primary human acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) specimens. We found that DNA methylation and H3K9 acetylation distinguished these leukemias of distinct cell lineage, as expected, but that an integrative analysis combining the information from each platform revealed hundreds of additional differentially expressed genes that were missed by gene expression arrays alone. This integrated analysis also enhanced the detection and statistical significance of biological pathways dysregulated in AML and ALL. Integrative epigenomic studies are thus feasible using clinical samples and provide superior detection of aberrant transcriptional programming than single-platform microarray studies. Keywords: DNA methylation by HELP 5 acute leukemia samples (2 ALL and 3 AML) in triplicate. Replicate #3 from sample ALL2 was discarded due to bad hybridization quality. No dye swap was performed.
2008-04-01 | E-GEOD-10894 | biostudies-arrayexpress