Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

21 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human BRAF-V600E melanoma cell lines drug sensitive vs drug resistant

ABSTRACT: aCGH of human melanoma cell lines comparing parental (drug sensitve) vs isogenic drug resistant-derived subline Two condition experiment: two BRAF-V600E mutant cell lines (drug sensitive - parental baseline) vs two derived sublines after chronic exposure to the MEK inhibitor trametinib (drug resistant) are compared

ORGANISM(S): Homo sapiens

SUBMITTER: Katherine Nathanson

PROVIDER: E-GEOD-49430 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Concurrent MEK2 mutation and BRAF amplification confer resistance to BRAF and MEK inhibitors in melanoma.

Villanueva Jessie J Infante Jeffrey R JR Krepler Clemens C Reyes-Uribe Patricia P Samanta Minu M Chen Hsin-Yi HY Li Bin B Swoboda Rolf K RK Wilson Melissa M Vultur Adina A Fukunaba-Kalabis Mizuho M Wubbenhorst Bradley B Chen Thomas Y TY Liu Qin Q Sproesser Katrin K DeMarini Douglas J DJ Gilmer Tona M TM Martin Anne-Marie AM Marmorstein Ronen R Schultz David C DC Speicher David W DW Karakousis Giorgos C GC Xu Wei W Amaravadi Ravi K RK Xu Xiaowei X Schuchter Lynn M LM Herlyn Meenhard M Nathanson Katherine L KL

Cell reports 20130919 6

Although BRAF and MEK inhibitors have proven clinical benefits in melanoma, most patients develop resistance. We report a de novo MEK2-Q60P mutation and BRAF gain in a melanoma from a patient who progressed on the MEK inhibitor trametinib and did not respond to the BRAF inhibitor dabrafenib. We also identified the same MEK2-Q60P mutation along with BRAF amplification in a xenograft tumor derived from a second melanoma patient resistant to the combination of dabrafenib and trametinib. Melanoma ce ...[more]

PMID: 24055054

Similar Datasets

Human BRAF-V600E melanoma cell lines drug sensitive vs drug resistant

Project description:aCGH of human melanoma cell lines comparing parental (drug sensitve) vs isogenic drug resistant-derived subline

2014-04-21 | GSE49430 | GEO

Drug tolerant persister cells of EGFR-mutant cell line under kinase-inhibitor combination

Project description:Drug tolerant persister cells of EGFR-mutant PC9 cell lines surviving treatment with kinase inhibitor combination. Cells were treated with combination of erlotinib, osimertinib, trametinib and dasatinib and surviving cells were harvested for RNA extraction. 3' UTR RNA-seq profiles were compared to parental control cells and to outgrowing cells after treatment had been removed

2023-06-30 | E-MTAB-13045 | biostudies-arrayexpress

3' RNAseq of EGFR mutant lung cancer cell line overexpressing BRAF V600E treated with inhibitors

Project description:In the human EGFR mutant adenocarcinoma cell line PC9 pBabe empty vector (EV) or BRAF V600E were overexpressed. RNA was extracted from EV, BRAF V600E overexpressing or osimertinib-resistant BRAF V600E expressing cells after 48h treatment with osimertinib, trametinib, a combination of both or vehicle controls. RNA was subjected to 3' UTR RNA sequencing.

2021-10-20 | E-MTAB-11004 | biostudies-arrayexpress

Transcription profiling of 5 human parental cell lines and 3 drug resistant variants by culturing the former continuously in the presence of cytotoxic drug doxorubicin

Project description:Title: Analysis of gene expression changes involved in the development of acquired drug resistance.<br> Description: In vitro model of drug resistance consisting of 5 parental cell lines and 3 drug resistant variants by culturing the former continuously in the presence of cytotoxic drug doxorubicin. Model used to identify genes involved in the drug resistant phenotype.

2006-09-01 | E-MIMR-11 | biostudies-arrayexpress

Analysis of Drug Resistant Cell Lines

Project description:Analysis of Drug transports as a mechanism of resistance to aurora kinase inhibition Parental and Taxol-resistant cell lines are compared for gene expression profile differences.

2013-06-22 | GSE47435 | GEO

Analysis of Drug Resistant Cell Lines

2013-06-22 | E-GEOD-47435 | biostudies-arrayexpress

MicroRNA expression data from leukemia and breast cancer cell lines with/without treatment with microparticles

Project description:Microparticles (MPs) comprise the major source of systemic RNA including microRNA (miRNA), the aberrant expression of which appears to be associated with stage, progression and spread of many cancers. We have shown MPs to transfer multidrug resistance proteins accross both haematological and and non-haematological cancers. using microarray miRNA profiling analysis we now analyze changes in miRNA profiles of both cancer types following microparticle transfer. We identified certain upregulated miRNAs in both cancer types. Total RNA was extracted and pooled from duplicate experiments for hybridization on Affymetrix microarrays from (i) the parental drug sensitive leukaemia (CEM) or breast cancer (MCF-7) cells, (ii) their Multidrug Resistant strains leukaemia (VLB100) or breast cancer ( DX cells), (iii) the microparticles isolated from the resistant cells: VLBMP or DXMP, and (iv) the cocultured samples: sensitive cell co-incubated with MPs from their resistant cells ( leukaemia: CEM+VLBMP) or(breast cancer: MCF-7+DXMP). We sought to examine the miRNA profiles of the drug sensitve cells after MP transfer from drug resistant cells across leukaemia nd breact cancer cell lines.

2012-06-08 | E-GEOD-34560 | biostudies-arrayexpress

Multi-omics characterization of MEK inhibitor resistant pancreatic cancer based on a genetically engineered mouse model-derived in vitro system

Project description:Tumor heterogeneity and therapy resistance are hallmarks of pancreatic ductal adenocarcinoma (PDAC). Emerging evidence supports treatment-induced resistance to be a multifactorial process mediated by cellular plasticity involving epigenetic regulation. Here, we used a multi-omics approach to analyze in detail molecular mechanisms underlying MEK inhibitor (MEKi) resistance. Therefore, we characterized different cell stages (parental, MEKi resistant, reverted after different passages of drug withdrawal) in primary cell lines derived from a genetic PDAC mouse model, thereby minimizing inter-individual heterogeneity that could distort genome-wide analyses.

2024-01-26 | PXD018093 | Pride

Genetic and molecular basis of drug resistance and species-specific drug action in Schistosome parasites

Project description:Oxamniquine resistance evolved in the human blood fluke (Schistosoma mansoni) in Brazil in the 1970s. We crossed parental parasites differing ~500-fold in drug response, determined drug sensitivity and marker segregation in clonally-derived F2s, and identified a single QTL (LOD=31) on chromosome 6. A sulfotransferase was identified as the causative gene using RNAi knockdown and biochemical complementation assays and we subsequently demonstrated independent origins of loss-of-function mutations in field-derived and laboratory-selected resistant parasites. These results demonstrate the utility of linkage mapping in a human helminth parasite, while crystallographic analyses of protein-drug interactions illuminate the mode of drug action and provide a framework for rational design of oxamniquine derivatives that kill both S. mansoni and S. haematobium, the two species responsible for >99% of schistosomiasis cases worldwide. mRNA profiles from adult worms resistant (HR, 3 replicates) and susceptible (LE, 2 replicates) to the oxamniquine drug were compared to identify differential expression in genes related to drug resistance

2013-12-05 | E-GEOD-51847 | biostudies-arrayexpress

RNA-seq melanoma

Project description:Using a chromatin regulator-focused shRNA library, we found that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes resistance to BRAF and MEK inhibitors. To investigate how SOX10 loss leads to drug resistance, we performed transcriptome sequencing (RNAseq) of both parental A375 (Ctrl. PLKO) and A375-SOX10KD (shSOX10-1, shSOX10-2) cells. To ask directly whether SOX10 is involved indrug resistance in BRAF(V600E) melanoma patients, we isolated RNA from paired biopsies from melanoma patients (pre- and post- treatment) , that had gained BRAF or MEK inhibitor resistance . We performed RNAseq analysis to determine changes in transcriptome upon drug resistance. Investigate genes regulated by SOX10 and differntial gene expression between pre- and post-treatment biopsies. We use short hairpin RNA to suppression SOX10 in A375 cells and cells were harvested with trizol reagent for RNA isolation. For paired biopsies (patient samples) we collected the first biopsy before the initiation of treatment and the second biopsy after drug resistance developed. RNA was isolated from FFPE samples and subjected for RNA sequencing.

2014-01-04 | E-GEOD-50535 | biostudies-arrayexpress

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