Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-24147

ABSTRACT: Transcription profiling of human leukemia cell lines treated with sera from Type I diabetes patients to investigate sera-induced transcriptional signatures.

OTHER RELATED OMICS DATASETS IN: PRJNA130025

PROVIDER: E-GEOD-24147 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-24147-analysis-methods.tsv	Tabular
	E-GEOD-24147-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-24147-configuration.xml	Xml
	E-GEOD-24147-percentile-ranks.tsv	Tabular
	E-GEOD-24147.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 123

Similar Datasets

Homo sapiens

Project description:Sera-induced transcriptional signatures in human leukemia cell lines

| PRJNA130025 | ENA

Project description:Gut microbiota signatures in Type 2 diabetes patients

| PRJNA872293 | ENA

Sera-induced transcriptional signatures in human leukemia cell lines

Project description:Inflammation is common to many disorders and responsible for tissue and organ damage. However, the associated peripheral cytokine milieu is frequently dilute and difficult to measure, necessitating development of more sensitive and informative biomarkers for mechanistic studies, earlier diagnosis, and monitoring therapeutic interventions. Previously, we have shown that sera from type 1 diabetes (T1D) patients induces a unique disease-specific pro-inflammatory transcriptional profile in fresh peripheral blood mononuclear cells (PBMCs) compared to sera of healthy controls. To address the potential variance introduced by heterogeneity in responsiveness of PBMCs from different donors, we evaluated human leukemia cell lines as surrogates for fresh PBMCs. Expression signatures of 7 different cell lines were 1) tested in their power to differentiate sera of T1D patients from healthy controls; and 2) compared to the signature obtained with fresh PBMCs.

2010-09-16 | GSE24147 | GEO

Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes

Project description:This SuperSeries is composed of the following subset Series: GSE35711: Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [CF_S1S3_5Auto_20CF_10HC] GSE35712: Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [H1N1_S5_5Pre_5D0] GSE35716: Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [Pneu_S3S24_10Pneu_4HC] GSE35725: Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [T1D_114] Refer to individual Series

2012-09-01 | E-GEOD-35713 | biostudies-arrayexpress

Transcription profiling of human leukemia cell lines treated with sera from Type I diabetes patients to investigate sera-induced transcriptional signatures.

2010-09-16 | E-GEOD-24147 | biostudies-arrayexpress

Plasma induced signatures reveal an extracellular milieu possessing an immunoregulatory bias in treatment naïve inflammatory bowel disease

Project description:The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we apply this approach to inflammatory bowel disease by examining groups of Crohn's disease (CD) and ulcerative colitus (UC) patients. The induced plasma induced signatures are compared to those of Type 1 diabetes patients (RO T1D) as well as unrelated healthy controls (uHC).

2015-10-01 | GSE71730 | GEO

Type 1 Diabetes DNA Damage Checkpoint Pathway Quantitation

Project description:iTRAQ-based quantitative proteomics and phosphoproteomics analyses of induced pluripotent stem cells (iPSC) from patients with longstanding type 1 diabetes. "Preserved DNA Damage Checkpoint Pathway Protects From Complications in Long-standing Type 1 Diabetes", Cell Metabolism, in press.

2015-07-08 | MSV000079185 | MassIVE

Epigenetic reprogramming in relapsed childhood ALL

Project description:Reversing gene expression signatures in relapsed patient may restore chemosensitivity. We demonstrate that the histone deacetylase inhibitor vorinostat not only reprograms the aberrant gene expression profile of relapsed blasts but is synergistic when applied prior to chemotherapy in primary patient samples and leukemia cell lines Primary patient samples were collected from patients treated at the New York University Medical Center and from the Childrenâs Oncology Group (COG) cell bank,RNA was isolated from three primary patient samples and three B-lineage leukemia cell lines with or without treatment with vorinostat for 24 hours.

2012-06-11 | E-GEOD-34880 | biostudies-arrayexpress

Small RNA-sequencing of plasma exosome-enriched extracellular vesicles derived miRNAs from lactating mothers with type 1 diabetes and lactating healthy mothers

Project description:Previous studies have shown that the circulating miRNA signatures are altered in plasma-derived extracellular vesicles of individuals with type 1 diabetes. These alterations in the miRNA profile could serve as a potential biomarker applicable in clinical practice for monitoring disease status in lactating mothers with type 1 diabetes during the postpartum period. In the present study, we investigate the profiles of extracellular vesicle-derived miRNAs in circulation in a cohort of lactating mothers with and without type 1 diabetes.

2021-09-23 | E-MTAB-10458 | biostudies-arrayexpress

Kevetrin induces apoptosis in TP53 wild-type and mutant acute myeloid leukemia cells

Project description:Tumor protein p53 is a key regulator of several cellular pathways, including DNA repair, cell cycle and angiogenesis. Kevetrin exhibits p53-dependent as well as independent activity in solid tumors, while its effects on leukemic cells remain unknown. We analyzed the response of acute myeloid leukemia (AML) cell lines (TP53 wild-type: OCI-AML3 and MOLM-13; and TP53-mutant: KASUMI-1 and NOMO-1) to kevetrin at a concentration range of 85-340 μM. Kevetrin induced cell growth arrest and apoptosis in all cell lines and in primary cells, with TP53-mutant models displaying a higher sensitivity and p53 induction. Gene expression profiling revealed a common core transcriptional program altered by drug exposure and the downregulation of glycolysis, DNA repair and unfolded protein response signatures. These findings suggest that kevetrin may be a promising therapeutic option for patients with both wild-type and TP53-mutant AML.

2020-09-03 | GSE137574 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data