Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

16 prostatic cancer cell lines and sensitivity to an anticancer tumor agent dasatinib

ABSTRACT: Transcriptional profiling was conducted on RNA from 16 prostatic cancer cell lines to identify genes whose expression level correlate with sensitivity of an anti-tumor agent (dasatinib). Keywords: comparison of sensitive group versus resistant group of cell lines to agent

ORGANISM(S): Homo sapiens

PROVIDER: GSE9633 | GEO | 2007/12/01

SECONDARY ACCESSION(S): PRJNA103487

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of human prostatic cancer cell lines and sensitivity to an anticancer tumor agent

Project description:Transcriptional profiling was conducted on RNA from 16 prostatic cancer cell lines to identify genes whose expression level correlate with sensitivity of an anti-tumor agent Experiment Overall Design: Baseline gene expression profiling was performed using 16 prostatic cancer cell lines to identify expression signatures highly correlated with in vitro sensitivity to a particular agent

2008-06-16 | E-GEOD-9633 | biostudies-arrayexpress

Gene expression profiles of dasatinib-resistant and dasatinib-sensitive pancreatic cancer cell lines

Project description:Gene profiles from three dasatinib-resistant and three dasatinib-sensitive pancreatic cancer cell lines were compared by microarray analysis.

2015-02-24 | GSE59357 | GEO

Gene expression profiles of dasatinib-resistant and dasatinib-sensitive pancreatic cancer cell lines

Project description:Gene profiles from three dasatinib-resistant and three dasatinib-sensitive pancreatic cancer cell lines were compared by microarray analysis. RNA from three dasatinib-resistant (MiaPaCa2, Panc1, SU8686) and three dasatinib-sensitive (Panc0504, Panc0403, Panc1005) pancreatic cancer cell lines were extracted. Biological triplicates were employed for each cell line. Complementary DNA microarray analysis was performed using Illumina Human HT-12 v4 BeadChip (Illumina, San Diego, CA) at the National University of Singapore Core Facility following the manufacturer’s instructions.

2015-02-24 | E-GEOD-59357 | biostudies-arrayexpress

Homo sapiens

Project description:16 prostatic cancer cell lines and sensitivity to an anticancer tumor agent dasatinib

| PRJNA103487 | ENA

Global gene expression profile of dasatinib-resistant RCH-ACV cells

Project description:Purpose: Several ALL subtypes have been described depending on their karyotype, cell type, immunophenotype and gene-expression profile. Recently, a novel ALL subtype has been described and is characterized by expression of the pre-B cell receptor (pre-BCR). Interestingly, half of the cases is associated with the chromosomal translocation t(1:19), coding for the chimeric fusion protein E2A-PBX1, which is present in about 5% of pediatric and adult ALL. Using preclinical models, we and other groups have shown very promising preclinical activity of dasatinib in pre-BCR+ ALL and early clinical evidence supports our observations. To study mechanism of acquired dasatinib resistance, we generated dasatinib-resistant pre-BCR+/E2A-PBX1+ cell lines through multiple passages in the presence of increasing drug concentrations. Whole transcriptome analysis of dasatinib-sensitive and resistant ALL cells were performed to detect systematically differentially expressed genes and enriched pathways involved in dasatinib resistance.

2018-09-18 | GSE97352 | GEO

Transcription profiling of human breast cancer cell lines treated with dasatinib and herceptin

Project description:effect on gene expression with the treatment of dasatinib and herceptin on breast cancer cell lines

2010-09-21 | E-MEXP-2065 | biostudies-arrayexpress

Expression data from a reversible dasatinib-resistant state in long-term dasatinib-treated c-KIT-mutated Kasumi-1 cell line

Project description:Long-term treatment of Kasumi-1 cells at clinically attained doses of dasatinib led to decreased drug-sensitivity by means of IC50 values (relative to treatment-naive cells). Changes were paralled by profound alterations in c-KIT expression and cell signaling signatures. Upon brief discontinuation of dasatinib treatment, these alterations reversed and drug sensitivity was restored. We used gene expression profiling to examine reversal of dasatinib-resistance at the molecular/expression level. Kasumi-1 cells were either treated with dasatinib for 12 weeks (R48) or left untreated (K). Subsequently, dasatinib was withdrawn from R48 cells for 1 week (PR48). RNA was extracted from R48 and K cells and hybridized on Affymetrix microarrays after 12 weeks and PR48 after a total time span of 13 weeks.

2013-11-27 | E-GEOD-39073 | biostudies-arrayexpress

RNAseq of rhabdomyosarcoma cells after treatment with SGI-110 and/or Dasatinib

Project description:Patients with metastatic or recurrent rhabdomyosarcoma, the most common childhood soft tissue sarcoma, continue to do poorly and new treatments are needed. In this study we evaluated a novel combination therapy using a dna methyltransferase inhibitor, SGI-110, and the SRC family kinase inhibitor, Dasatinib. To understand the transcriptional changes that occur after treatment with SGI-110 with and without Dasatinib we performed RNAseq on two human RMS cell lines (Rh30 and RD) after 5 days of drug treatment.

2021-04-30 | GSE147240 | GEO

Dasatinib enhances anti-tumor efficacy of chimeric antigen receptor T cells by inhibiting cell differentiation and exhaustion

Project description:CD19-targeted Chimeric antigen receptor T cells (CART) cells have shown remarkable promise in various B cell malignancies. Sustained tonic signaling and antigen exposure drives CART cell differentiation and exhaustion, which limits the therapeutic potency and persistence of CART cells and is a major cause of CD19-expressing leukemia relapse after CD19-targeted CART cells treatment in ALL. Here, we systematically screened FDA approved tyrosine kinase inhibitors, and identified dasatinib as the best candidate to prevent or reverse both CD28/CART and 4-1BB/CART cells from differentiation and exhaustion during ex vivo expansion, which enhanced the therapeutic efficacy and in vivo persistence. Using RNA-seq, we identified the differentially expressed genes between dasatinib treated group and Nalm6 stimulated group, and found that memory-associated transcription factors TCF7 and naive/memory-associated cell surface marker CCR7 were upregulated, whereas exhaustion-related regulators (NR4A1, BATF3, ATF4 and FOS) and inhibitory receptors (PD1, LAG3) were down-regulated in dasatinib treated CAR T cells. Moreover, T cell activation associated signaling pathways (T cell receptor, Jak-STAT, MAPK and PI3K-Akt) which were upregulated in Nalm6 stimulated CART cells, showed fundamental downregulation in dasatinib treated CART cells. These findings imply that dasatinib played important roles in CART cell differentiation and exhaustion by inhibition of T cell activation pathways.

2021-06-03 | GSE151774 | GEO

Kinome profiling of diffuse large B-cell lymphoma cells in response to dasatinib

Project description:Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease, with at least one-third of its patients not responding to the current chemotherapy regimen, R-CHOP. By gene expression profiling, patients with DLBCL can be categorized into two clinically relevant subtypes: activated B-cell (ABC) DLBCL and germinal center B-cell (GCB). Patients with ABC DLBCL have a worse prognosis, and are defined by chronic, overactive signaling through the B-cell receptor and NF-κB pathways. We examined the effects of the Src family kinase (SFK) inhibitor dasatinib in a panel of ABC and GCB DLBCL cell lines, and found that the ABC DLBCL cell lines are much more sensitive to dasatinib than the GCB DLBCL cell lines. However, using multiplexed inhibitor bead coupled to mass spectrometry (MIB/MS) kinome profiling competition and western blot analysis, both subtypes display inhibition of the SFKs in response to dasatinib after both short- and long-term treatment. MIB/MS analyses revealed several cell cycle kinases, including CDK4, CDK6, and the Aurora kinases, are inhibited by dasatinib treatment in the ABC DLBCL subtype, but not in the GCB DLBCL subtype. The present findings have important implications for the clinical use of dasatinib for the treatment of ABC DLBCL, either alone or in combination with other agents.

2018-12-14 | PXD009380 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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