Gene expression profiling of MCF-7 cells treated with 6-shogaol
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Chee-Onn Leong
PROVIDER: E-GEOD-36973 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2013-09-03 | E-GEOD-43185 | biostudies-arrayexpress
Project description:Neural stem cells (NSCs) are considered to be the cell-of-origin of brain tumor stem cells. To identify the genetic pathways responsible for the transformation of normal NSCs to brain-tumor-initiating cells, we used Sleeping Beauty (SB) transposons, to mutagenize NSCs. Mobilized SB transposons induced the immortalization of NSCs. Immortalized NSCs induced tumors upon subcutaneous transplantation in immunocompromized mice. To further classify the immortalized cells and mouse tumors, we performed Gene Set Enrichment Analysis (GSEA) using DNA microarray data. Ten immortalized NSC lines (four WT and six p53 mutant lines) and two normal NSCs were used for RNA extraction and hybridization on Affymetrix microarrays. CEL files were processed using the RMA algorithm to normalize the data. Unsupervised hierarchical clustering was applied to the normalized gene expression data across samples using the R module pvclust (Suzuki and Shimodaira, Bioinformatics 22, 1540-1542, 2006). Hierarchical clustering showed a close similarity in gene expression between all ten immortalized lines, compared with two normal NSCs. We then compared their gene expression profiles to those present in the brain transcriptome database (Cahoy et al., J Neurosci 28, 264-278, 2008). Using five gene sets that are associated with neurons, oligodendrocytes, OPCs, astrocytes and cultured astroglial cells, GSEA enrichment scores were calculated for the ten immortalized NSCs lines against two control normal NSCs. GSEA enrichment analysis was performed using GSEA software v. 2.07 (http://www.broadinstitute.org/gsea). We found a strong enrichment for genes that are differentially expressed in the cultured astroglial cells. Twelve tumors (six WT and six p53 mutant tumors) and three control subcutaneous tissues were used for RNA extraction and hybridization on Affymetrix microarrays. CEL files were processed using the RMA algorithm to normalize the data. Unsupervised hierarchical clustering was applied to the normalized gene expression data across samples using the R module pvclust (Suzuki and Shimodaira, Bioinformatics 22, 1540-1542, 2006). Hierarchical clustering of 12 tumors showed a close similarity between the tumors, compared with three control subcutaneous tissues. We next performed GSEA analysis on the tumors. Using gene sets specific to the four defined GBM subtypes (Verhaak et al., Cancer Cell 17, 98-110, 2010), a GSEA enrichment score was then calculated for the twelve tumor samples against three control subcutaneous tissue samples. GSEA enrichment analysis was performed using GSEA software v. 2.07 (http://www.broadinstitute.org/gsea). This analysis showed that the mouse tumors were significantly enriched for genes specific for the mesenchymal GBM. Immortalized cell lines and tumors were used for RNA extraction and hybridization on Affymetrix microarrays. Ten immortalized lines (Line 3, 28, 31, 59, 95, 116, 119, 120, 123, 331) were compared with two normal NSCs. Twelve tumors were generated from four lines (1, 31, 59, 123) and compared with three subcutaneous tissues (SubQ).
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2011-09-13 | E-GEOD-32078 | biostudies-arrayexpress
Project description:How organ size and form are controlled during development is a major question of biology. Blood vessels have been shown to be essential for early development of the liver and pancreas, and are fundamental to normal and pathological tissue growth. Here we report that non-nutritional signals from blood vessels surprisingly act to restrain pancreas growth. Elimination of endothelial cells increases the size of embryonic pancreatic buds. Conversely, VEGF-induced hypervascularization decreases pancreas size. The growth phenotype results from vascular restriction of pancreatic tip cell formation, lateral branching and differentiation of the pancreatic epithelium into endocrine and acinar cells. The effects are seen both in vivo and ex vivo, indicating a perfusion-independent mechanism. Thus the vasculature controls pancreas morphogenesis and growth by reducing branching and differentiation of primitive epithelial cells. For transcriptome analysis, RNA was isolated using QIAGEN RNeasy micro Kit from pancreatic buds of Pdx1-tTA (n=3) and littermate Pdx1-tTA; TET-VEGF (n=3) e12.5 embryos, or from e12.5 wild type pancreatic buds explanted and treated with VEGFR2i (n=5) or vehicle (n=5) for 2 days. Pooled samples were hybridized to Affymetrix mouse gene 1.0 st arrays. The arrays were RMA normalized using Partek Genomic Suite 6.5. Differentially regulated genes were selected based on p-values and ratios using t-test.
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Project description:While blood transcriptional profiling has improved diagnosis and understanding of disease pathogenesis of adult tuberculosis (TB), no studies applying gene expression profiling of children with TB have been described so far. In this study, we have compared whole blood gene expression in childhood TB patients, as well as in healthy latently infected (LTBI) and uninfected (HC) children in a cohort of Warao Amerindians in the Delta Amacuro in Venezuela. We identified a 116-gene signature set by means of random forest analysis that showed an average prediction error of 11% for TB vs. LTBI and for TB vs. LTBI vs. HC in our dataset. Furthermore, a minimal set of only 9 genes showed a significant predictive value for all previously published adult studies using whole blood gene expression, with average prediction errors between 17% and 23%. 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