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GenomicsRNA-seq studies in dabrafenib treated endothelial cells
RNA-seq studies in dabrafenib treated endothelial cells
PRJNA1462056 | ENA
GenomicsDabrafenib alters MDSC differentiation and function by activation of GCN2
Dabrafenib alters MDSC differentiation and function by activation of GCN2
PRJNA999590 | ENA
GenomicsMelanoma resistance to combination dabrafenib/trametinib therapy
Acquired resistance to combination dabrafenib/trametinib therapy in BRAF mutant metastatic melanoma
PRJEB7503 | ENA
TranscriptomicsRNA-seq studies in dabrafenib treated endothelial cells
Cerebral Cavernous Malformations (CCM) constitute the second most common type of intracranial vascular malformations. Cavernomas arise due to somatic or autosomal dominant inherited loss-of-function mutations in KRIT1 (CCM1), CCM2, or PDCD10 (CCM3), forming fragile mulberry-like malformed blood vess...
ORGANISM(S): Homo sapiens 
2026-07-15 | GSE329903 | GEO
GenomicsWhole Exome Sequencing Data of Dabrafenib Resistant HT-29 Cell Line
Whole Exome Sequencing Data of Dabrafenib Resistant HT-29 Cell Line
PRJEB65911 | ENA
GenomicsBarcode Sequencing Data of Dabrafenib Resistant HT-29 Cell Line
Barcode Sequencing Data of Dabrafenib Resistant HT-29 Cell Line
PRJEB62610 | ENA
GenomicsH3K4me3 Epigenetic remodelling after Dabrafenib treatment
The data depicts H3k4me3-CHIP SEQ results done on WM164 cells before treatment and after 50 days treatment with Dabrafenib
ORGANISM(S): Homo sapiens 
2017-06-24 | GSE100439 | GEO
TranscriptomicsDabrafenib alters MDSC differentiation and function by activation of GCN2
The BRAF inhibitor dabrafenib has been reported to activate the integrated stress response (ISR) kinase GCN2, and the therapeutic effect has been partially attributed to GCN2 activation. Since ISR signaling is a key component of myeloid-derived suppressor cell (MDSC) development and function, we mea...
ORGANISM(S): Mus musculus 
2024-03-20 | GSE239496 | GEO
GenomicSingle Patient BRAF Mutant Brain Tumor, Pre- and Post-dabrafenib WES.

A single adolescent patient with a BRAF V600E mutated brain tumor was treated with dabrafenib and had a complete response, followed by progression. The pre-treatment and post-progression tumors were both sequenced in order to identify potential drivers of resistance.

phs001629 | dbGaP
ProteomicsEffect of PTEN knockout on dabrafenib-trametinib treatment in A375 melanoma cells - replicate 2
Approximately 50% of melanomas harbor an activating BRAFV600E mutation. Standard of care involves a combination of inhibitors targeting mutant BRAF and MEK1/2, the substrate for BRAF in the MAPK pathway. PTEN loss of function mutations occur in 40% of BRAFV600E melanomas, resulting in increased PI3K...
ORGANISM(S): Homo sapiens (Human) 
2024-04-23 | PXD033921 | Pride
A375 Kinase inhibitor Braf Melanoma Mek Kinome 
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