Centrosome defects are a common feature of many cancers. Surprisingly, flies can proceed through the majority of development without centrosomes or with amplified centrosomes in most of their cells. It is unclear whether this is because centrosome defects do not cause many problems in Drosophila cells, or because they can adapt to cope with any problems that arise. Indeed, centrosome loss and centrosome amplification predispose fly brain cells to form tumours. Here we assess how centrosome loss or centrosome amplification perturbs cell physiology by profiling the global transcriptome of Drosophila larval brains and imaginal discs that either lack centrosomes or have too many centrosomes.
Centrosome loss or amplification does not dramatically perturb global gene expression in Drosophila.
Specimen part
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Glioblastoma stem-like cells give rise to tumour endothelium.
Sex, Age, Specimen part
View SamplesTranscriptome analysis of RNAs from brain tumor
Glioblastoma stem-like cells give rise to tumour endothelium.
Sex, Age, Specimen part
View SamplesEwing sarcoma family of tumors (ESFT) are aggressive bone and soft tissue tumors of unknown cellular origin. Most ESFT express EWS-FLI1, a chimeric protein which functions as a growth-promoting oncogene in ESFT but is toxic to most normal cells. A major difficulty in understanding EWS-FLI1 function has been the lack of an adequate model in which to study EWS-FLI1-induced transformation. Although the cell of origin of ESFT remains elusive, both mesenchymal (MSC) and neural crest (NCSC) have been implicated. We recently developed the tools to generate NCSC from human embryonic stem cells (hNCSC). In the current study we used this model to test the hypothesis that neural crest-derived stem cells are the cells of origin of ESFT and to evaluate the consequences of EWS-FLI1 expression on human neural crest biology.
Modeling initiation of Ewing sarcoma in human neural crest cells.
Specimen part
View SamplesGBM is a heterogenous brain tumor with hyperproliferation of endothelial cells. In order to understand the cellular mechanism of vasculogenesis in GBM, four fractions of cells are seperated. Microarray assays was performed to examine the potential lineage relationship and the signal pathways involved in determining the cell identity and function.
Glioblastoma stem-like cells give rise to tumour endothelium.
Sex, Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MCL-1 Is a Key Determinant of Breast Cancer Cell Survival: Validation of MCL-1 Dependency Utilizing a Highly Selective Small Molecule Inhibitor.
Cell line
View SamplesmRNA expression profile of cultured Breast Cancer cell line measured by Affymetrix microarrays
MCL-1 Is a Key Determinant of Breast Cancer Cell Survival: Validation of MCL-1 Dependency Utilizing a Highly Selective Small Molecule Inhibitor.
Cell line
View SamplesTranscript profiling analysis of csn3-1, csn4-1 and csn5 (csn5a-2 csn5b) light grown and dark grown mutant seedlings compared to light grown and dark grown wild type using Arabidopsis ATH1 GeneChip array
The Arabidopsis COP9 signalosome is essential for G2 phase progression and genomic stability.
No sample metadata fields
View SamplesUsing oligonucleotide microarray analysis, we identified 56 genes that were transcriptionally up-regulated and 69 that were suppressed upon exposure of endothelial cells to C. albicans. Among the regulated genes those attributed to the categories chemotaxis, signaling, and transcription and translation were remarkably overrepresented.
Candida albicans triggers activation of distinct signaling pathways to establish a proinflammatory gene expression program in primary human endothelial cells.
No sample metadata fields
View SamplesRNAi mediated knockdown of BTG1 in the acute lymphoblastic cell line RS4;11 causes this cell line to become resistant to prednisolone treatment when compared to control cells.
BTG1 regulates glucocorticoid receptor autoinduction in acute lymphoblastic leukemia.
Specimen part, Cell line, Treatment
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