Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chapter 3 - Anna Tribe - BCL6 is a context-dependent mediator of the glioblastoma therapy response

ABSTRACT: Whole proteome analysis of LN18 cell treated with one of five DNA-damaging treatments (fractionated irradiation (IRM), temozolomide (TMZ), acute irradiation 24 hours (IRS 24h), acute irradiation 48 hours (IRS 48h) or doxorubicin (Dox)) +/- the BCL6 inhibitor FX1.

INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive Plus

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Melanie McConnell Paul Teesdale-Spittle

PROVIDER: MSV000090274 | MassIVE |

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Magnetic-Targeted Doxorubicin in Treating Patients With Cancer Metastatic to the Liver

Project description:MTC-DOX is Doxorubicin or DOX, a chemotherapy drug, that is adsorbed, or made to "stick", to magnetic beads (MTCs). MTCs are tiny, microscopic particles of iron and carbon. When DOX is added to MTCs, DOX attaches to the carbon part of the MTCs. MTC-DOX is directed to and deposited in the area of a tumor, where it is thought that it then "leaks" through the blood vessel walls. Once in the surrounding tissues, it is thought that Doxorubicin becomes "free from" the magnetic beads and will then be able to act against the tumor cells. The iron component of the particle has magnetic properties, making it possible to direct MTC-DOX to specific tumor sites in the liver by placing a magnet on the body surface. It is hoped that MTC-DOX used with the magnet may target the chemotherapy drug directly to liver tumors and provide a treatment to patients with cancers that have spread to the liver.

| 2007949 | ecrin-mdr-crc

Gene Expression upon Doxorubicin Treatments

Project description:Murine C26 tumor xenografts displayed different responses to the treatments of PBS, Doxorubicin (Dox), and chimeric polypeptide (CP)-Dox conjugates. We used microarrays to globally study gene expression underlying these different responses and identified distinct classes of up-regulated or down-regulated genes upon treatment. C26 murine colon carcinoma xenografts were analyzed at 48 hours after treatment with CP-Dox, free Dox, and PBS (control). This study involved four replicates of each treatment.

2010-07-15 | E-GEOD-17115 | biostudies-arrayexpress

MicroRNA profiling of the failing heart after myocardial infarction induction and doxorubicin treatment

Project description:The use of anthracycline antibiotics such as doxorubicin (DOX) has greatly improved the mortality and morbidity of cancer patients. However, the associated risk of cardiomyopathy has limited their clinical application. DOX-associated cardiotoxicity is irreversible and progresses to heart failure (HF). For this reason, a better understanding of the molecular mechanisms underlying these adverse cardiac effects is essential to develop improved regimes that include cardioprotective strategies. MicroRNAs (miRNAs) are short non-coding RNAs that are able to post-trascriptionally regulate gene expression. MiRNAs have been demonstrated to be involved in both cancer and cardiovascular disease. Therefore, we were interested in unveiling the potential role of miRNAs in chemotherapy-induced HF. We used a combination of three different models to recreate this cardiac toxicity (acute in vitro DOX treatment, DOX-induced HF in vivo and a myocardial infarction -MI- leading to failure model) to study the pattern of dysregulated miRNAs. Using RNA from all three conditions, miRNA microarray profiling was performed and a common miRNA signature was identified. Interestingly, these dysregulated miRNAs have been previously identified as involved in the failing heart. Our results suggest that DOX is able to alter the expression of miRNAs implicated in HF, in vitro as well as in vivo. The present study is a microRNA profiling of the damaged cardiac muscle (cardiomyocyte cell population), following either myocardial infarction (MI) induction or doxorubicin (DOX) treatment. Two DOX-treated models were included: ARC exposed to DOX in vitro and a validated DOX-induced heart failure model generated by repeated administration of DOX injections.

2013-01-29 | E-GEOD-36239 | biostudies-arrayexpress

Chemotherapeutic agent doxorubicin alters uterine gene expression in response to estrogen in ovariectomized CD-1 adult mice

Project description:Chemotherapy can potentially impair fertility in premenopausal cancer patients. Female fertility preservation has been mainly focused on the ovarian aspects and benefited greatly from assisted reproductive technologies, such as in vitro fertilization (IVF). The rate-limiting step for the success of IVF is embryo implantation in the uterus. Doxorubicin (DOX) is a widely used chemotherapeutic agent with ovarian toxicity. It remains unknown if the uterus is a direct target of DOX. To circumvent the indirect uterine effect from ovarian toxicity of DOX and to investigate potential long-term impact of DOX on the uterus, young adult ovariectomized CD-1 mice were given an intraperitoneal injection once with PBS or DOX (10 mg/kg, a human relevant chemotherapeutic dose), and 30 days later, each set of mice was randomly assigned into three groups and subcutaneously injected with oil, 17β-estradiol (E2, for 6 hours), and progesterone (P4, for 54 hours), respectively. Uterine transcriptomic profiles were determined using RNA-seq. Principal component analysis of the uterine transcriptomes revealed four clusters from the six treatment groups: PBS-oil & DOX-oil, PBS-P4 & DOX-P4, PBS-E2, and DOX-E2, indicating that DOX treatment did not affect the overall uterine transcriptomic profiles in the oil and P4-treated mice but altered uterine responses to E2 treatment. These data demonstrate that DOX can directly target the uterus and has a long-term impact on uterine responses to E2.

2019-01-07 | GSE123950 | GEO

Effect of doxorubicin and SPEDOX-6 on human iPSC-derived cardiac spheroids comprised of cardiomyocytes, endothelial cells, and fibroblasts.

Project description:The chemotherapeutic doxorubicin (DOX) detrimentally impacts the heart during cancer treatment. This necessitates development of non-cardiotoxic delivery systems that retain DOX anticancer efficacy. We utilized human induced pluripotent stem cell-derived multi-lineage cardiac spheroids (hiPSC-CSs) to compare the anticancer efficacy and reduced cardiotoxicity of single protein encapsulated doxorubicin (SPEDOX-6), to standard unformulated (UF) DOX using RNA-sequencing. The cardiac spheroids are comprised of hiPSC-derived cardiomyocytes (hiPSC-CMs), hiPSC-derived endothelial cells (ECs), and hiPSC-derived cardiac fibroblasts (CFs) at an 8:1:1 ratio.

2023-07-01 | GSE235470 | GEO

Selective elimination of leukemia cells by reprogramming factors

Project description:To investigate the molecular mechanism for the elimination of leukemia cells after Dox induced OSKM expression, we sorted MLL-AF9 leukemia cells from Dox untreated and treated groups (48h and 72h) leukemic mice for gene expression profiling analysis.

2019-09-23 | GSE64414 | GEO

miRNA Expression Profiles in Isolated Ventricular Cardiomyocytes: Insights into Doxorubicin-Induced Cardiotoxicity

Project description:Doxorubicin (DOX) is a first-line chemotherapeutic agent widely used in the treatment of various cancers, but its clinical efficacy is limited by its early and late cardiotoxic effects. Prior to the visible morphological manifestation of lesions in cardiomyocytes after exposure to DOX, they can detect damage and initiate a complex cascade of responses, including the modulation of gene expression, including the regulation of microRNAs (miRNAs).In this study, we used small RNA sequencing to evaluate miRNA expression levels in cardiomyocytes exposed to DOX at a concentration of 10 μM for periods of 1 and 22 hours, compared to unexposed cells. By analyzing the normalized data and using DESeq2, we identified significant changes in the expression of certain miRNAs in DOX-treated cells. These miRNAs emerge as promising biomarker candidates that, if further investigated, could provide a valuable early detection tool for DOX sensitivity and guide the timely administration of cardioprotective agents.

2024-04-15 | GSE263950 | GEO

The expression profiles of human lymphoma H9 cells after exposure to doxorubicin

Project description:doxorubicin is commonly used for hematological malignancies. Since some of PTCL patients resistance to dox and die due to refractory disease or relapse, enhanced knowledge about drug response mechanisms is required to improve treatment outcome. we found an increased expression of HDAC3 in T lymphoma H9 cells following dox exprosure, we compared the gene expression profiles of H9 cells pre/post treated with doxorubicin to explore the potential mechanism of the high expression of HDAC3

2024-04-18 | GSE260756 | GEO

Transcriptional analysis of doxorubicin-induced cardiotoxicity

Project description:Doxorubicin (Dox) is an effective chemotherapeutic agent against a broad range of tumors. However, a threshold dose of doxorubicin causes an unacceptably high incidence of heart failure and limits its clinical utility. We have established two models of doxorubicin cardiotoxicity in mice: 1) in an acute model, mice are treated with 15mg/kg of doxorubicin once; 2) in a chronic model, they receive 3mg/kg weekly for the first 12 of a total of 18 weeks. Using echocardiography, we have monitored left ventricular function of the mouse hearts during treatment in chronic model and seen the expected development of dilated cardiomyopathy (DCM). Treated mice showed histological abnormalities similar to those seen in patients with doxorubicin cardiomyopathy. To investigate transcriptional regulation in these models, we used a microarray we generated with over 5000 independent cDNA clones from murine heart and skeletal muscle. We have identified genes that respond to doxorubicin exposure in both model systems, and confirmed these results using real-time PCR. In the acute model, a set of genes is regulated early and rapidly returns to baseline levels, consistent with the half-life of doxorubicin. In the chronic model, which mimics the clinical situation much more closely, we identified dysregulated genes that implicate specific mechanisms of cardiac toxicity and may serve as biomarkers of doxorubicin induced dilated cardiomyopathy. Keywords: time course

2005-07-22 | GSE2965 | GEO

Genome-wide map of H3K4me3 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide H3K4me3 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of H3K4me3 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle

2014-11-14 | E-GEOD-51713 | biostudies-arrayexpress

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