Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-19136

ABSTRACT: Gene expression response to implanted drug (paclitaxel)-eluting or bare metal stents in denuded human LIMA arteries

PROVIDER: E-GEOD-19136 | ExpressionAtlas | 2015-09-08

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-19136-analysis-methods.tsv	Tabular
	E-GEOD-19136-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-19136-configuration.xml	Xml
	E-GEOD-19136-percentile-ranks.tsv	Tabular
	E-GEOD-19136.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 70

Similar Datasets

HLA peptides (LC-MSMS) induced by Decitabine in Glioblastoma cell lines

Project description:Treatment of cancer cells with anti-cancer drugs often fails to achieve complete remission. Yet, such drug treatments may induce alteration in the tumor’s gene expression patterns, including those of Cancer/Testis Antigens (CTA). The degradation products of such antigens can be presented as HLA peptides on the surface of the tumor cells and be developed into anti-cancer immunotherapeutics. For example, the DNA methyl transferase inhibitor, 5-aza-2'-deoxycytidine (Decitabine) has limited anti-tumor efficacy, yet it induces the expression of many genes, including CTAs that are normally silenced in the healthy adult tissues. In this study, the presentation of many new HLA peptides derived from CTAs and induced by Decitabine was demonstrated in three human Glioblastoma cell lines. Such presentation of CTA-derived HLA peptides can be exploited for development of new treatment modalities, combining drug treatment with anti-CTA targeted immunotherapy. The Decitabine-induced HLA peptidomes include many CTAs that are not normally detected in healthy tissues or in cancer cells, unless treated with the drug. In addition, the study included large-scale analyses of the simultaneous effects of Decitabine on the transcriptomes, proteomes and HLA peptidomes of the human Glioblastoma cells. It demonstrates the poor correlations between these three levels of gene expression, both in their total levels and in their response to the drug.

2017-03-31 | MSV000080843 | MassIVE

Homo sapiens

Project description:Treatment-specific changes in gene expression discriminate in vivo drug response in human leukemia cells

| PRJNA84963 | ENA

Biomarks of Resistance to Cetuximab in Colorectal Cancer

Project description:Interventions: A group:Before using cetuximab;B group:After progression of disease:no Primary outcome(s): KRAS gene sequence;NRAS gene sequence;BRAF gene sequence;PIK3CA gene sequence;EGFR gene sequence;EGFR gene copy numbers;EGFR expression;Her2 expression;c-Met expression;PTEN expression Study Design: historical control

| 2671639 | ecrin-mdr-crc

Genetic Analysis of Human Traits In-Vitro: Drug Response and Gene Expression in Lymphoblastoid Cell Lines

Project description:Genetic Analysis of Human Traits In-Vitro: Drug Response and Gene Expression in Lymphoblastoid Cell Lines

| PRJNA106213 | ENA

Biomarker Directed Treatment in Metastatic Colorectal Cancer

Project description:This pilot study is being mounted to assess whether treatment assignment by ERCC-1 gene expression status suggests better clinical results from historical experience in metastatic colorectal cancer (mCRC). In wild type KRAS mCRC patients treated with either FOLFOX or FOLFIRI in combination with cetuximab the median response rate is approximately 60-65%. Biomarker directed treatment in this study may demonstrate that patients with low ERCC-1 treated with FOLFOX and cetuximab, and those with high ERCC-1 treated with FOLFIRI and cetuximab, will improve response rate to 70-75%. KRAS wild type patients will be treated with 6 cycles of one of the following regimens chosen for optimization based on patient characteristics (primary treatment phase). Patients with ERCC-1 < 1.7 relative gene expression of ERCC-1 over ß-actin (ERCC-1 low) will be assigned to treatment with mFOLFOX6 in combination with Cetuximab. Patients with ERCC-1 gene expression > 1.7 relative gene expression of ERCC-1 over over ß-actin (ERCC-1 high) will be assigned to treatment with FOLFIRI in combination with Cetuximab.

| 2133316 | ecrin-mdr-crc

The impact of extracellular matrix on the precision medicine utility of pancreatic cancer patient-derived organoids

Project description:Organoids are cultivated in extracellular matrix from different basement membrane extracts (BMEs) that are most commonly acquired commercially. However, the impact of different sources and lots of BMEs on organoid drug response is unknown. Here, we tested the impact of BME source and lot on proliferation, chemotherapy and targeted therapy drug response, and global gene expression in mouse and human pancreatic ductal adenocarcinoma organoids. Both mouse and human organoids displayed increased proliferation in Matrigel (Corning) compared to Cultrex (RnD) and UltiMatrix (RnD). However, we observed no substantial impact on drug response when organoids were cultured in Matrigel, Cultrex, or UltiMatrix. We also did not observe major shifts in gene expression across the different BME sources.

2023-05-10 | GSE232170 | GEO

Decrypting the molecular basis of cellular drug phenotypes by dose-resolved expression proteomics

Project description:Proteomics is making important contributions to drug discovery - from target deconvolution to mechanism of action (MoA) elucidation and the identification of biomarkers of drug response. Here, we introduce decryptE, a proteome-wide approach that measures the full dose-response characteristics of drug-induced protein expression changes which informs cellular drug MoA. Assaying 144 clinical drugs and research compounds against 8,000 proteins resulted in >1 million dose-response curves that can be interactively explored online in ProteomicsDB and a custom-built ShinyApp. Analysis of the collective data provided molecular explanations for known phenotypic drug effects and uncovered novel aspects of the MoAs of human medicines. Most notable, HDAC inhibitors potently and strongly down-regulated the T-cell receptor complex resulting in impaired human T-cell activation in-vitro and ex-vivo. This not only offers a rational explanation for the efficacy of HDAC inhibitors in certain lymphomas and autoimmune diseases but also their poor performance in treating solid tumors.

2023-12-13 | MSV000093659 | MassIVE

Homo sapiens

Project description:Gene expression response to implanted drug (paclitaxel)-eluting or bare metal stents in denuded human LIMA arteries

| PRJNA120751 | ENA

Expression Data from 24 orthotopic tumors grown in the pancreas of mice +/- MEK inhibitor PD0325901

Project description:Analysis of mRNA profiles after MEK1/2 inhibition in human pancreatic cancer cell lines reveals pathways involved in drug sensitivity. We used microarrays to find gene expression patterns associated with drug response and also identified genes regulated by the MAP kinase pathway

2013-04-04 | GSE45758 | GEO

Expression Data from 22 human pancreatic cancer cell lines grown in triplicates +/- MEK inhibitor CI-1040

2013-04-04 | GSE45757 | GEO