Sort   by:  
 Page size 
TranscriptomicsSpectrum, clinical correlates and clinical implications of BRAF-inhibitor resistance mechanisms in melanoma
Multiple BRAF inhibitor resistance mechanisms have been described, however their relative frequency, clinical correlates, and effect on subsequent therapy have not been assessed in patients with metastatic melanoma. Excised progressing BRAFV600 mutant melanoma metastases (Prog) from patients treated...
ORGANISM(S): Homo sapiens 
2014-02-19 | E-GEOD-50509 | biostudies-arrayexpress
TranscriptomicsExpression data from BRAF-mutant melanoma cell lines
Melanoma cell lines were assessed for differences in gene expression patterns between the lines sensitive and resistant to BRAF and MEK inhibitor drugs. 22 BRAF-mutant melanoma cell lines were assessed for response to BRAF and MEK inhibitors in a 3 day drug treatment dose response assay. Based on t...
ORGANISM(S): Homo sapiens 
2015-08-26 | E-GEOD-45558 | biostudies-arrayexpress
TranscriptomicsNew compounds triggering endoplasmic reticulum stress exert anti-melanoma effects and overcome BRAF inhibitor resistance
We discovered and developed a new series of molecules (thiazole benzenesulfonamides). HA15, the lead compound of this series, displayed anti-cancerous activity on all tested melanoma cells including those isolated from patients and those that developed resistance to BRAF inhibitors. Our molecule dis...
ORGANISM(S): Homo sapiens 
2016-06-01 | E-GEOD-79071 | biostudies-arrayexpress
TranscriptomicsPredominance of MAPK reactivation in early resistance to debrafenib/trametinib combination therapy of BRAF mutant metastatic melanoma.
One third of BRAF-mutant metastatic melanoma patients treated with combined BRAF and MEK inhibition progress within six months. Treatment options for these patients remain limited. Here we analyse twenty BRAFV600 mutant melanoma metastases derived from 10 patients treated with the combination of deb...
ORGANISM(S): Homo sapiens 
2014-12-03 | E-GEOD-61992 | biostudies-arrayexpress
TranscriptomicsWnt5A Enhances Resistance of Melanoma Cells to Targeted BRAF Inhibitors
About half of all melanomas harbor a constitutively active mutant BRAFV600E/K kinase that can be selectively inhibited by targeted BRAF inhibitors (BRAFi). While patients treated with BRAFi initially exhibit measurable clinical improvement, the majority of patients eventually develop drug resistance...
ORGANISM(S): Homo sapiens 
2014-03-06 | E-GEOD-55583 | biostudies-arrayexpress
TranscriptomicsHuman BRAF-V600E melanoma cell lines drug sensitive vs drug resistant
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 resista...
ORGANISM(S): Homo sapiens 
2014-04-21 | E-GEOD-49430 | biostudies-arrayexpress
ProteomicsBRAF inhibitor resistance in melanoma cell lines
LC-MS/MS analysis of cell lines with induced resistance to BRAF inhibitors
ORGANISM(S): Homo sapiens (Human) 
2018-10-19 | PXD001682 | Pride
Braf resistance Melanoma 
TranscriptomicsRNA-seq melanoma
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 A...
ORGANISM(S): Homo sapiens 
2014-01-04 | E-GEOD-50535 | biostudies-arrayexpress
ProteomicsExpression Proteomics of BRAF Inhibitor Resistance in Melanoma Cell Lines
To investigate mechanisms of resistance to BRAF inhibitor therapy in melanoma, BRAF mutant cell lines have been chronically exposed to BRAFi to create phenotypes with acquired drug resistance. Expression proteomics is used to examine the differences between naive and drug-resistant cells.
ORGANISM(S): Homo sapiens (Human) 
2016-12-13 | PXD004342 | Pride
Kinase inhibitor Tmt Melanoma Braf Drug resistance 
GenomicsDiscovery of resistance mechanisms to the BRAF inhibitor vemurafenib in metastatic BRAF mutant melanoma
Discovery of resistance mechanisms to the BRAF inhibitor vemurafenib in metastatic BRAF mutant melanoma by massively-parallel sequencing of tumour samples. Comparison of genomic characteristics of pretreatment ‘sensitive’ to recurrence ‘resistant’ tumours to identify the genetics of drug resistance.
EGAS00001000551 | EGA
Sort   by:  
 Page size