Browse
Submit Data
Databases
API
Help

Dataset Information

4 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigation of the blood levels at a reduced dose of erlotinib with the addition of ritonavir compared to the normal dose of erlotinib

ABSTRACT: Primary objectives: Effect of the highly potent CYP3A4 inhibitor ritonavir on the pharmacokinetics (PK) of erlotinib, measured as AUC0-24h, AUCmean, Cmax and Cmin Primary endpoints: The effect of the highly potent CYP3A4 inhibitor ritonavir on the pharmacokinetics (PK) of erlotinib, measured as AUC0-24h, Cmax and Cmin.

DISEASE(S): Non-small Cell Lung Cancer Stage Iv,Advanced Egfr Mutation Positive Non Small Cell Lung Cancer, Pancreatic Carcinoma, Colorectal Cancer And Biliary Cancer,Gevorderd Egfr Mutatie Positief Niet-kleincellig Longkanker, Pancreascarcinoom, Colorectaal Kanker En Galwegkanker

PROVIDER: 2538815 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

Project description:The non-small cell lung cancer (NSCLC) cell line HCC827 harbors an activating EGFR mutation (exon 19 deletion) that confers sensitivity to the FDA-approved EGFR inhibitor erlotinib. By applying the ClonTracer barcoding system, we were able to show the presence of pre-existing sub-populations in HCC827 that contribute to erlotinib resistance. Prior studies implicated that MET amplification confers resistance to erlotinib in this cell line. Therefore we examined the effects of the c-Met inhibitor crizotinib on the barcoded HCC827 population when treated either sequentially or simultaneously with both inhibitors. Despite the significant reduction in barcode complexity, the erlotinib/crizotinib combination treatment failed to eradicate all of the resistant clones implying the presence of an erlotinib/crizotinib dual resistant subpopulation. We performed transcriptome profiling (RNA-seq) to elucidate the potential resistance mechanisms of the dual resistant subpopulation in comparison to vehicle-treated or single agent erlotinib-resistant HCC827 cell populations as controls. mRNA profiling of the subpopulations of human NSCLC cell line HCC827 that contribute to EGFR inhibitor erlotinib and MET inhibitor crizotinib resistance

2014-10-07 | E-GEOD-62118 | biostudies-arrayexpress

Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

2014-10-07 | GSE62118 | GEO

Differential Gene Expression in Erlotinib-Treated Fibroblasts

Project description:Analysis of human, adult, dermal fibroblasts following treatment with 100nM or 1 uM of erlotinib, a tryrosine kinase inhibitor (TKI) that targets the epidermal growth factor receptor (EGFR) inhibiting EGFR activation and signaling. Erlotinib is widely used to effectively treat patients with advanced non-small cell lung cancer but treatment with erlotinib and other EGFR TKIs are associated with a painful skin rash. Results identified significantly differentially expressed genes in fibroblasts treated with erlotinib providing insight into how the drug alters the transcriptome in ways that may contribute to the TKI-related rash.

2019-01-01 | GSE106151 | GEO

Expression data from human hepatocarcinoma HCC-1.2 cell line treated by erlotinib

Project description:Tyrosine kinase inhibitors represent a new generation of targeted drugs for cancer treatment and chemoprevention. The EGF receptor inhibitor erlotinib is under discussion for chemoprevention of hepatocellular carcinoma. A comprehensive analysis of gene expression and respective pathways regulated by erlotinib is needed.

2017-10-26 | GSE67545 | GEO

microRNA profiling of H358 non-small cell lung cancer cells selected for resistance against erlotinib or wild-type

2015-09-15 | E-MTAB-3391 | biostudies-arrayexpress

Gene expression profiling of erlotinib-resistant PC9 cells.

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. To better understand gene expression changes in cells that survived the inhibitor treatment, we treated the EGFR-mutant PC9 cells with erlotinib, isolated RNA, and performed RNA-seq analysis. We were able to identify genes that are differentially expressed in erlotinib-treated cells compared to untreated. The results of this study will be integrated with single cell RNA-seq to address the utility of bulk RNA versus single cell RNA strategies in identifying biomarkers of drug resistance.

2020-12-19 | GSE148465 | GEO

Gene expression analysis of H358 non-small cell lung cancer cells selected for resistance against erlotinib or wild-type

2015-09-15 | E-MTAB-3387 | biostudies-arrayexpress

Whole transcriptome analysis of erlotinib treatment in EGFR-mutant cells

Project description:We were interested in characterizing the transcriptional changes that occur on a genome-wide scale following treatment of EGFR-mutant lung cancer cells with targeted therapies. HCC827 human lung cancer cells harboring an amplified EGFR allele with an activating in frame deletion of 15 nucleotides in exon 19 were treated in triplicate with 1uM erlotinib (EGFR inhibitor), AZD-6244 (MEK inhibitor) or BEZ-235 (PI3-Kinase/mTOR inhibitor) for 6 hours, followed by total mRNA isolation and whole transcriptome analysis using Affymetrix U133 Plus 2.0 expression arrays.

2015-02-25 | E-GEOD-51212 | biostudies-arrayexpress

Quinacrine Overcomes Resistance to Erlotinib by Inhibiting FACT, Nuclear Factor-kappa B and Cell Cycle Progression in Non-Small Cell Lung Cancer

Project description:Erlotinib is a tyrosine kinase inhibitor (TKI) that is approved as a second-line monotherapy in patients with advanced non-small cell lung cancer (NSCLC). In these patients, erlotinib prolongs survival but its benefit remains modest since many tumors express wild-type EGF receptor (wtEGFR) lacking a TKI-sensitizing mutation, develop a second-site EGFR mutation, e.g., EGFR-L858R/T790M, or activate an alternate receptor tyrosine kinase, e.g., through MET amplification. To test potential drug combinations that could improve the efficacy of erlotinib, we combined erlotinib with quinacrine, which inhibits the FACT (facilitates chromatin transcription) complex that is required for nuclear factor-κB (NF-κB) transcriptional activity. In A549 (wtEGFR), H1975 (EGFR-L858R/T790M) and H1993 (MET amplification) NSCLC cells, the combination of erlotinib and quinacrine was highly synergistic, as quantified by Chou-Talalay combination indices. The combination inhibited colony formation, induced cell cycle arrest and apoptosis, and slowed xenograft tumor growth. Quinacrine decreased the level of active FACT subunit SSRP1 and suppressed NF-κB-dependent luciferase activity. Knockdown of SSRP1 decreased cell growth and sensitized cells to erlotinib. Transcriptomic profiling showed that quinacrine, alone or in combination with erlotinib, significantly affected cell cycle-related genes that contain binding sites for transcription factors that regulate SSRP1 target genes. As potential biomarkers of drug synergy, we identified genes that were more strongly suppressed by the combination than by either single treatment, and whose increased expression predicted poorer survival in lung adenocarcinoma patients. Combination of quinacrine and erlotinib is synergistic in NSCLC through suppression of FACT, resulting in inhibition of cell cycle progression.

2014-06-19 | GSE57422 | GEO

Gene expression profiling of Erlotinib sensitive and resistant human non small cell lung cancer (NSCLC) cell lines

Project description:We characterized the gene expression profile of Epithelial Growth Factor Receptor (EGFR) inhibitor (Erlotinib)-sensitive and resistant human NSCLC cell lines. Total RNA was extracted from the cell lines and expression profiles were studied by Agilent microarray analysis. Wide changes in gene expression profiles occur in the Erlotinib-resistant cell lines when compared with their parental cell lines (HCC827 and HCC4006).

2017-09-23 | GSE80344 | GEO

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