Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Study of Vemurafenib in Participants With BRAF V600 Mutation-Positive Cancers

ABSTRACT: This open-label, multi-center study will assess the efficacy and safety of vemurafenib in participants with BRAF V600 mutation-positive cancers (solid tumors and multiple myeloma, except melanoma and papillary thyroid cancer) and for whom vemurafenib is deemed the best treatment option in the opinion of the investigator. Participants will receive twice daily oral doses of 960 mg vemurafenib until disease progression, unacceptable toxicity, or withdrawal of consent. The safety and efficacy of vemurafenib in combination with cetuximab in a subset of participants with colorectal cancer will also be assessed.

DISEASE(S): Ovarian Cancer,Solid Tumor,Multiple Myeloma, Neoplasms,Patients With Cancers (excluding Melanoma And Papillary Thyroid cancer) Harboring Braf V600 Mutations As Identified By The routinely Performed Mutation Analysis Assays At Each Individual participating Site,Non-small Cell Lung Cancer,Colorectal Cancer,Breast Cancer,Patients With Cancers (excluding Melanoma And Papillary Thyroidcancer) Harboring Braf V600 Mutations As Identified By Theroutinely Performed Mutation Analysis Assays At Each Individualpartici...,Cholangiocarcinoma,Multiple Myeloma

PROVIDER: 2119744 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Vemurafenib, BRAF inhibitor, Resistance in BRAFV600E Positive Thyroid Cancer cell lines

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of RNAs in BRAFV600E+ thyroid cancer cell lines 8505C and WRO. We generated genome-wide transcriptome maps of 8505C and WRO cells after vemurafenib, BRAF inhibitor, treatment. In addition, we generated genome-wide transcriptome maps of clonally selected vemurafenib-resistant 8505C and WRO cells with or without vemurafenib treatment. Negative control treatment was 0.1% of dimethy solfoxide (DMSO), the diluent used to resuspend vemurafenib. The treatment regine of vemurafenib was 2 µM concentration for 24 hours. We find that both inducible response to BRAFi and acquired BRAFi resistance in thyroid cancer cells showed significant activation of the JAK/STAT pathway. Our study demonstrates that the JAK/STAT-signaling pathway is activated as thyroid cancer cells develop resistance to BRAFi and that this pathway is a potential target for anticancer activity and to overcome drug resistance that commonly develops to treatment with BRAFi in thyroid cancer and potentially in other malignancies.

2023-02-16 | GSE178267 | GEO

RNAseq changes in mouse wound with or without time course treatment by Vemurafenib

Project description:BRAF inhibitors are highly effective therapies for patients with BRAF V600 mutated metastatic melanoma. Patients who receive BRAF inhibitors develop a variety of hyper-proliferative skin conditions, whose pathogenic basis is the paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in BRAF wild-type cells. Most of these hyper-proliferative skin changes improve when a MEK inhibitor is co-administered, as a MEK inhibitor blocks paradoxical MAPK activation. We tested whether we could take advantage of the mechanistic understanding of the skin hyper-proliferative side effects of BRAF inhibitors to accelerate skin wound healing by inducing paradoxical MAPK activation. Here we show that the BRAF inhibitor vemurafenib accelerates human keratinocyte proliferation and migration by increasing ERK phosphorylation and cell cycle progression. Topical treatment with vemurafenib in two wound-healing models in mice accelerated cutaneous wound healing and improved the tensile strength of healing wounds through paradoxical MAPK activation; addition of a MEK inhibitor reversed the benefit of vemurafenib-accelerated wound healing. The same dosing regimen of topical BRAF inhibitor did not increase the incidence of cutaneous squamous cell carcinomas in mice even after the application of a carcinogen. Therefore, topical BRAF inhibitors may have clinical applications in accelerating the healing of skin wounds. Full depth incisional wound mice tissues with/without Vemurafenib treatment were sent for RNAseq analysis on day 2, 6 and 14

2016-07-29 | E-GEOD-74558 | biostudies-arrayexpress

RNAseq changes in mouse wound with or without time course treatment by Vemurafenib

2016-07-29 | GSE74558 | GEO

Giani2019 - Computational modeling to predict MAP3K8 effects as mediator of resistance to vemurafenib in thyroid cancer stem cells

Project description:Computational modeling to predict MAP3K8 effects as mediator of resistance to vemurafenib in thyroid cancer stem cells

2024-09-02 | BIOMD0000000883 | BioModels

Vemurafenib induces a noncanonical senescence-associated secretory phenotype in melanoma cells which promotes vemurafenib resistance

Project description:To explore the characteristics of senescent melanoma cells induced by vemurafenib or cisplatin, melanoma A375 cells were treated with vemurafenib and cisplatin, respectively. The senescent phenotypes were verified by β-gal staining, EdU assay, cell morphology and the senescence-related pathways. RNA-seq was performed to explore the differentially expressed genes in the senescent cells induced by vemurafenib or cisplatin.

2023-07-07 | GSE209769 | GEO

Time-series RNA-seq experiment performed on 10 melanoma cell lines treated with BRAF inhibitor vemurafenib.

Project description:BRAF targeted drug vemurafenib have shown very good clinical benefit in melanoma patient containing BRAF V600E mutation. However, resistance always occurs in patient. Early stage of the resistance development require the tumor cell adapted to the targeted drug. We are trying to study the kinetic of melanoma cell adaptation towards vemurafenib. 10 melanoma cell lines with BRAF mutation are treated with targeted therapy vemurafenib. RNA-seq samples are collected after drug treatment for different time (day3 and day21) to compare with DMSO-treated control samples for each cell line. Except innate resistant cell line M381, all other cell lines shows inhibition of proliferation. However, a small cluster of cell lines (M397, M229 and M263) shows some other unique transcriptomic change. For cell line M397, M229 and M263, we also collected the RNA-seq data for long-term (73day/90day) drug treatment condition where the cells developed resistance to vemurafenib treatment. Dedifferentiation is enriched in these unique transcriptomic change within these 3 cell lines. Similar cell state dedifferentiation phenomenon is also reported to cause resistance towards immunotherpay where the resistant de-differentiated melanoma cells are induced by TNF which is secreted by tumor-infiltrating T cells. We also treat our cultured melanoma cells with TNF and collected the treated sample for RNA-seq experiment.

2019-06-22 | E-MTAB-5493 | biostudies-arrayexpress

DETERMINE Trial Treatment Arm 05: Vemurafenib in Combination With Cobimetinib in Adult Patients With BRAF Positive Cancers.

Project description:This clinical trial is looking at a combination of drugs called vemurafenib and cobimetinib. Vemurafenib is approved as standard of care for adult patients with unresectable or metastatic melanoma. Cobimetinib is approved as standard of care in combination with vemurafenib for the treatment of adult patients with unresectable or metastatic melanoma. Cobimetinib and vemurafenib work in patients with these types of cancers which have certain changes in the cancer cells called BRAF V600 mutation-positive. Investigators now wish to find out if it will be useful in treating patients with other cancer types which are also BRAF V600 mutation-positive. If the results are positive, the study team will work with the NHS and the Cancer Drugs Fund to see if these drugs can be routinely accessed for patients in the future. This trial is part of a trial programme called DETERMINE. The programme will also look at other anti-cancer drugs in the same way, through matching the drug to rare cancer types or ones with specific mutations.

| 11423 | ecrin-mdr-crc

Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

2014-05-20 | GSE42872 | GEO

Vemurafenib, BRAF inhibitor, Resistance in BRAFV600E Positive Thyroid Cancer cell lines

Project description:Vemurafenib, BRAF inhibitor, Resistance in BRAFV600E Positive Thyroid Cancer cell lines

| PRJNA738167 | ENA

Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

Project description:Vemurafenib is a BRAF inhibitor with specificity for the most common BRAF mutant encountered in melanomas (BRAFV600E). Vemurafenib suppresses the proliferation of BRAF mutant human melanoma cells by suppressing downstream activation of the MEK/ERK mitogen activated protein kinases. We used microarrays to examine the transcriptional response of a vemurafenib-sensitive BRAFV600E human melanoma cell line (A375) to vemurafenib in order to further delineate the mechanisms by which BRAFV600E drives cell proliferation and energy metabolism in human melanoma. BRAFV600E A375 human melanoma cells were treated with vehicle (0.1% DMSO) or 10 uM vemurafenib for 24 h after which total RNA was extracted. Cells were prepared and RNA was extracted in 3 separate batches (three different cell stocks on three separate days) providing three independent replicates (n=3). Paired replicates (prepared from the same stock of cells on the same day) are denoted by A, B and C.

2014-05-20 | E-GEOD-42872 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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