Rhabdomyosarcoma (RMS) is the most common paediatric soft-tissue
Genomic imbalances in rhabdomyosarcoma cell lines affect expression of genes frequently altered in primary tumors: an approach to identify candidate genes involved in tumor development.
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BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.
Sex, Age, Subject
View SamplesSamples were taken from surgically resected tumor specimens from patients with colorectal cancer. The expression profiles were determined using the Affymetrix GeneChip Human Exon 1.0 ST Array version 2. Gene mutation status was determined using Sanger sequencing.
BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.
Sex, Age, Subject
View SamplesmRNA from 59 primary colorectal tumour samples were extracted and hybridized to HG-U133Plus 2.0 expression arrays. Mutation status for several genes were determined using Sanger sequencing.
BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.
Sex, Age, Subject
View SamplesDoxycycline-inducible YAP1 S127A-driven rhabdomyosarcoma (RMS) tumors, control skeletal muscle and regressed tumors following YAP1 normalization by doxycycline withdrawal were compared to determine the YAP1-regulated gene expression profile relevant to RMS formation.
The Hippo transducer YAP1 transforms activated satellite cells and is a potent effector of embryonal rhabdomyosarcoma formation.
Specimen part
View SamplesThe objective was to identify the molecular mechanisms responsible for in vitro and in vivo efficacy of an anti-MYCN peptide nucleic acid on a preclinical model of alveolar rhabdomyosarcoma. Cells treated with a anti-MYCN PNA exhibit growth arrest and apoptosis, and in vivo tumor growth is blocked.
Antitumor activity of sustained N-myc reduction in rhabdomyosarcomas and transcriptional block by antigene therapy.
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View SamplesThe S. aureus transcriptome was assessed for strains Newman (wild type) and Newman (sarZ) during both exponential (2hr) and early stationary (5hr) cell growth.
A new oxidative sensing and regulation pathway mediated by the MgrA homologue SarZ in Staphylococcus aureus.
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View SamplesPlants exhibit a robust transcriptional response to gamma radiation which includes the induction of transcripts required for homologous recombination and the suppression of transcripts that promote cell cycle progression. Various DNA damaging agents induce different spectra of DNA damage as well as collateral damage to other cellular components and therefore are not expected to provoke identical responses by the cell.
High atomic weight, high-energy radiation (HZE) induces transcriptional responses shared with conventional stresses in addition to a core "DSB" response specific to clastogenic treatments.
Age, Time
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Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
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View SamplesGenome-wide identification of bona fide targets of transcription factors in mammalian cells is still a challenge. We present a novel integrated computational and experimental approach to identify direct targets of a transcription factor. This consists in measuring time-course (dynamic) gene expression profiles upon perturbation of the transcription factor under study, and in applying a novel reverse-engineering algorithm (TSNI) to rank genes according to their probability of being direct targets. Using primary keratinocytes as a model system, we identified novel transcriptional target genes of Trp63, a crucial regulator of skin development. TSNI-predicted Trp63 target genes were validated by Trp63 knockdown and by ChIP-chip to identify Trp63-bound regions in vivo. Our study revealed that short sampling times, in the order of minutes, are needed to capture the dynamics of gene expression in mammalian cells. We show that Trp63 transiently regulates a subset of its direct targets, thus highlighting the importance of considering temporal dynamics when identifying transcriptional targets. Using this approach, we uncovered a previously unsuspected transient regulation of the AP-1 complex by Trp63, through direct regulation of a subset of AP-1 components. The integrated experimental and computational approach described here is readily applicable to other transcription factors in mammalian systems and is complementary to genome-wide identification of transcription factor binding sites.
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
No sample metadata fields
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