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Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping [RNA-seq]

ABSTRACT: Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping [RNA-seq]

PROVIDER: PRJNA841360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19349906_1.fastq.gz	Fastqsanger.gz
	SRR19349906_2.fastq.gz	Fastqsanger.gz
	SRR19349907_1.fastq.gz	Fastqsanger.gz
	SRR19349907_2.fastq.gz	Fastqsanger.gz
	SRR19349908_1.fastq.gz	Fastqsanger.gz

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Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping

Project description:Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping

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Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping

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Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping

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Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping

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Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping [RNA-seq]

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Discovery of resistance mechanisms to the BRAF inhibitor vemurafenib in metastatic BRAF mutant melanoma

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Targeting MUC1-C sensitizes colorectal cancer cells to BRAF inhibitor

Project description:BRAF mutant colorectal cancer has a poor prognosis and gets resistant to BRAF inhibitors quickly. This study aims to clarify the mechanism of resistance to BRAFi. We found MCU1-C is overexpressed in BRAF mutant colorectal cancer and targeting MUC1-C genetically and pharmacologically sensitized Colorectal cancer cells to BRAF inhibitor. This finding suggests that MUC1-C could be a new therapeutic target for BRAF mutant colorectal cancer.

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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.

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