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BRAF inhibitor resistance in melanoma cell lines

ABSTRACT: LC-MS/MS analysis of cell lines with induced resistance to BRAF inhibitors

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Melanocyte, Cell Culture

DISEASE(S): Melanoma

SUBMITTER: Maria Pernemalm

LAB HEAD: Janne Lehtiö

PROVIDER: PXD001682 | Pride | 2018-10-19

REPOSITORIES: Pride

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			Action	DRS
	120330_Maria_Melanoma_poolA_fr01-72_sequest-percolator_swissprot-human.msf	Msf
	120330_Maria_Melanoma_poolA_fr01-72_sequest-percolator_swissprot-human.pep.xml	Pepxml
	120330_Maria_Melanoma_poolA_fr01-72_sequest-percolator_swissprot-human.prot.xml	Xml
	120330_Maria_Melanoma_poolA_fr01.raw	Raw
	120330_Maria_Melanoma_poolA_fr02.raw	Raw

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1 - 5 of 150

Publications

Silencing FLI or targeting CD13/ANPEP lead to dephosphorylation of EPHA2, a mediator of BRAF inhibitor resistance, and induce growth arrest or apoptosis in melanoma cells.

Azimi Alireza A Tuominen Rainer R Costa Svedman Fernanda F Caramuta Stefano S Pernemalm Maria M Frostvik Stolt Marianne M Kanter Lena L Kharaziha Pedram P Lehtiö Janne J Hertzman Johansson Carolina C Höiom Veronica V Hansson Johan J Egyhazi Brage Suzanne S

Cell death & disease 20170831 8

A majority of patients with BRAF-mutated metastatic melanoma respond to therapy with BRAF inhibitors (BRAFi), but relapses are common owing to acquired resistance. To unravel BRAFi resistance mechanisms we have performed gene expression and mass spectrometry based proteome profiling of the sensitive parental A375 BRAF V600E-mutated human melanoma cell line and of daughter cell lines with induced BRAFi resistance. Increased expression of two novel resistance candidates, aminopeptidase-N (CD13/ANP ...[more]

PMID: 29048432

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Expression Proteomics of BRAF Inhibitor Resistance in Melanoma Cell Lines

Project description: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.

2016-12-13 | PXD004342 | Pride

Activity-Based Protein Profiling of BRAF Inhibitor Resistance in Melanoma Cell Lines

Project description: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. Activity-based protein profiling with desthiobiotinylating ATP probes (ActivX, Thermo) is used to examine the differences between naive and drug-resistant cells.

2016-12-13 | PXD004343 | Pride

protein levels in BRAF inhibitor resistance melanoma cells treated with PF3758309

Project description:11 BRAF inhibitor resistance melanoma cells were treated with PAK inhibitor PF3758309 for 48 hr, the cell lysis were analyzed by RPPA profiling by protein array (RPPA)

2017-07-31 | GSE96753 | GEO

Identification of Resistance Genes to BRAF Inhibitor in Melanoma by piggyBac Transposon Activation Mutagenesis Screen

Project description:Genotype directed anti-cancer therapies such BRAF inhibitor in BRAF mutant melanoma can show remarkable clinical efficacy but resistance limits their benefit. We show that a transposon activation screen efficiently identifies resistance genes to BRAF and captures a number of previously uncharacterized resistance mechanisms, including an E3 ubiquitin ligase NEDD4L and the Hippo pathway effector WWTR1 (TAZ). Resistance can be reversed by combining BRAF inhibition with tyrosine kinase inhibitors as observed previously for other resistance genes. Moreover, an integrative analysis of several gain- and loss-of-function genetic screens performed in the same context reveals smaller functional diversity of resistance mechanisms to MAPK inhibition than suggested by the broad range of resistance genes identified, implying common therapeutic strategies. A375 cells with lentiviral vector controls or WWTR1 cDNA plasmid.

2016-07-01 | E-GEOD-73470 | biostudies-arrayexpress

Identification of Resistance Genes to BRAF Inhibitor in Melanoma by piggyBac Transposon Activation Mutagenesis Screen

2016-07-01 | GSE73470 | GEO

protein levels in BRAF/MEK inhibitor resistance melanoma cells treated with PF3758309 [CR]

Project description:3 BRAF/MEK inhibitor resistance melanoma cells were treated with PAK inhibitor PF3758309 for 48 hr, the cell lysis were analyzed by RPPA profiling by protein array (RPPA)

2017-07-31 | GSE96902 | GEO

Spectrum, clinical correlates and clinical implications of BRAF-inhibitor resistance mechanisms in melanoma

Project description: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 with dabrafenib (n=22) or vemurafenib (n=8) were analyzed for known resistance mechanisms. Oncogenic signaling in Prog and matched pre-treatment tumors was examined using gene expression analysis. Resistance mechanisms were correlated with clinicopathologic features and outcome. A resistance mechanism was identified in 21/38 (55%) Prog samples from 30 patients; BRAF splice variants (n=12, 32%), N-RAS mutations (n=3, 8%), BRAF amplification (n=3, 8%), MEK1/2 mutations (n=3, 8%) and an AKT1 mutation (n=1, 3%). Four Progs tumours displayed multiple resistance mechanisms, and four patients with multiple Progs demonstrated inter-tumoral heterogeneity of resistance mechanisms. Six (21%) of 29 Progs showed loss of MAPK activity by gene expression analysis. These MAPK-inhibited Progs had unknown resistance mechanisms, and these patients had a shorter progression-free survival than patients with MAPK re-activated Progs. There were no responses to subsequent targeted therapy, even when the identified mechanism of resistance was predicted to be responsive. Heterogeneity of resistance mechanisms was common between patients, within patients and within individual tumors. The MAPK pathway remained inhibited in a subset of resistant tumors with unknown mechanisms of resistance, and the outcomes of patients with these tumors are poor. The use of sequential targeted therapies based on the molecular characteristics of a single progressing biopsy is unlikely to provide improved clinical outcomes. Total RNA was obtained from fresh-frozen melanoma tumour samples from patients before commencing treatment with dabrafenib or vemurafenib and at time of tumour progression.

2014-02-19 | E-GEOD-50509 | biostudies-arrayexpress

Expression data from BRAF-mutant melanoma cell lines

Project description: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 the IC50, 18 lines were found to be responsive to BRAF or MEK inhibition and 4 were resistant. Normalised gene expression data generated from experimental replicate affymetrix arrays was assessed to identify differential patterns of inherent gene expression between the cell lines grouped as drug-responsive or drug-resistant. This were used to idenify specific candidate genes and pathways associated with inherent BRAF/MEK inhibitor drug resistance in melanoma cells.

2015-08-26 | E-GEOD-45558 | biostudies-arrayexpress

microRNA expression profiling of melanoma cell lines with acquired resistance to the BRAF inhibitor PLX4032 compared to the parental sensitive counterparts

Project description:microRNA expression profiles show altered patterns in cell lines with acquired resistance to the BRAF inhibitor compared to the parental cell lines, and common miRNAs regulated in the resistant variants

2020-10-02 | GSE141314 | GEO

Gene expression profiling of melanoma cell lines with acquired resistance to the BRAF inhibitor PLX4032 and the parental sensitive counterparts and of melanoma cell lines intrinsically resistant.

Project description:Targeted therapy with small molecules inhibiting BRAF and MEK kinase represents a therapeutic option in advanced metastatic melanoma although drug resistance limits the achievement of persistent cures. The genomic analyses of tumors from patients developing treatment resistance indicate that drug tolerance may result from non-mutational events occurring in the tumor microenvironment. To identify tumor specific transcriptional changes related to resistance to the BRAF-inhibitor PLX4032, cell lines with acquired resistance to PLX4032 were generated from six sensitive melanoma lines by chronic in vitro drug exposure (Vergani E, Oncotarget 2016) and analyzed for gene expression profiles; in addition a set of cell lines with intrinsic resistance was included for comparison. Cell lines were obtained from metastatic surgical specimens and were previously genetically characterized (Daniotti M, Oncogene 2004; Vergani E, JID 2022, accepted).

2022-06-17 | GSE201913 | GEO

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