Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular dynamics of acquired vemurafenib-resistance in dogs with naturally ocurring BRAF-mutated Urothelial Carcinoma

ABSTRACT: Dogs treated with Vemurafenib were surveyed for naturally aquired drug resistance using proteomics and phosphoproteomics

INSTRUMENT(S):

ORGANISM(S): Canis Familiaris (dog) (canis Lupus Familiaris)

TISSUE(S): Bladder

DISEASE(S): Bladder Transitional Cell Carcinoma

SUBMITTER: Rodrigo Mohallem

LAB HEAD: Uma K Aryal

PROVIDER: PXD062194 | Pride | 2026-01-01

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Knapp-Global-A10_1_A.raw	Raw
	Knapp-Global-A1_1_A.raw	Raw
	Knapp-Global-A2_1_A.raw	Raw
	Knapp-Global-A3_1_A.raw	Raw
	Knapp-Global-A4_1_A.raw	Raw

Items per page:

1 - 5 of 109

Similar Datasets

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

Ezrin inhibition overcomes acquired resistance to vemurafenib in BRAFV600E-mutated colon cancer and melanoma cells in vitro

Project description:In spite of the advancements in targeted therapy for BRAFV600E-mutated metastatic colorectal cancer (mCRC), the development of resistance to BRAFV600E inhibition limits the response rate and durability of the treatment. Better understanding of the resistance mechanisms to BRAF inhibitors will facilitate the design of novel pharmacological strategies for BRAF-mutated mCRC. The aim of this study was to identify novel protein candidates involved in acquired resistance to BRAFV600E inhibitor vemurafenib in BRAFV600E-mutated colon cancer cells using an integrated proteomics approach. Our study suggests a role of ezrin in acquired resistance to vemurafenib in colon cancer and melanoma cells carrying BRAFV600E mutation and supports further pre-clinical and clinical studies to explore the benefits of combined BRAF inhibitors and actin-targeting drugs as a potential therapeutic approach for BRAFV600E-mutated cancers.

2023-08-29 | PXD042499 | Pride

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

2014-05-20 | GSE42872 | GEO

Propranolol overcomes vemurafenib resistance in melanoma by upregulating CDK11 and inducing cell cycle arrest

Project description:Acquired resistance to the BRAF inhibitor vemurafenib remains a major obstacle in melanoma therapy. Drug repurposing offers a promising strategy to overcome such resistance. Here, we investigated the β-blocker propranolol as a sensitizer to vemurafenib in resistant melanoma. Using vemurafenib-resistant cell lines (A375-VR and patient-derived P-8-VR), we found that propranolol restored vemurafenib sensitivity both in vitro and in vivo. RNA sequencing revealed that propranolol significantly upregulated CDK11A and CDK11B. Functional studies demonstrated that knockdown of CDK11 attenuated the pro-apoptotic and cell cycle arrest effects of propranolol and vemurafenib. Mechanistically, propranolol induced G1/S phase arrest and apoptosis without affecting MAPK or AKT pathway reactivation. In a xenograft model, the combination of propranolol and vemurafenib significantly suppressed tumor growth and improved survival. Our study identifies CDK11 upregulation as a novel mechanism by which propranolol reverses vemurafenib resistance, supporting the clinical potential of this drug combination in resistant melanoma.

2026-01-19 | GSE316499 | GEO

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

Serum proteome profiling of naturally acquired Babesia rossi infection in dogs.

Project description: Not available

| S-EPMC10290096 | biostudies-literature

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

Vemurafenib acts as molecular switch in Langerhans Cell Histiocytosis

Project description:Langerhans cell histiocytosis (LCH) is a neoplasm marked by the accumulation of CD1a+CD207+ cells. It is most commonly driven by a somatic activating mutation in the BRAF kinase (BRAFV600E). Multisystem disease with risk-organ involvement requires intensive chemotherapy, making BRAF-inhibitors an attractive option. Here, we present a comprehensive analysis of the course of an LCH patient treated with the combination of vemurafenib with salvage chemotherapy who achieved complete clinical and molecular remission. We conclusively show that there is no relationship between blood-BRAF levels and clinical presentation during treatment with vemurafenib, but that vemurafenib leads to a fast, efficient, but reversible inhibition of clinical manifestations of high-risk LCH such as cytopenia, fever, and hypoproteinemia. In line, serum levels of inflammatory cytokines exactly mirror vemurafenib administration. Genotyping for the BRAFV600E mutation shows its presence in multiple hematopoietic cell types, including NK cells and granulocytes. Single-cell transcriptome analysis of peripheral blood and bone marrow cells at time of diagnosis and during treatment indicate that RAF-inhibition abrogates the expression of inflammatory cytokines previously implicated in LCH. Together, our data suggest that while the CD1a+CD207+ histiocytes are the hallmark of LCH, other BRAF-mutated cells themselves contribute significantly to morbidity in patients with multisystem LCH.

2021-09-23 | GSE175480 | GEO

Profiling melanoma cell line M14 treated with vemurafenib

Project description:The BRAFV600E mutant melanoma cell line M14 responds to the BRAF inhibitor vemurafenib, however, the differences in response between individual cells are underlying resistance. To highlight the underlying mechanisms, we performed treatment of M14 cells with vemurafenib, followed by Drop-seq. We were able to clearly distinguish cells that were treated with the drug from untreated cells, and we discovered different cell populations within the treated cells, likely reflecting heterogeneity of drug resistant cells. We were able to identify specific biomarkers, as preferentially expressed genes, for each cell population. The results of our study will address preexisting and acquired drug resistance that limits clinical usefulness of targeted strategies.

2020-12-19 | GSE134838 | GEO

Honokiol Bis-Dichloroacetate (Honokiol DCA) Demonstrates Activity in Vemurafenib-Resistant Melanoma in Vivo.

Project description:The majority of human melanomas bears BRAF mutations and thus is treated with inhibitors of BRAF, such as vemurafenib. While patients with BRAF mutations often demonstrate an initial dramatic response to vemurafenib, relapse is extremely common. Thus, novel agents are needed for the treatment of these aggressive melanomas. Honokiol is a small molecule compound derived from Magnolia grandiflora that has activity against solid tumors and hematopoietic neoplasms. In order to increase the lipophilicity of honokiol, we have synthesized honokiol DCA, the dichloroacetate ester of honokiol. In addition, we synthesized a novel fluorinated honokiol analog, bis-trifluoromethyl-bis-(4-hydroxy-3-allylphenyl) methane (hexafluoro). Both compounds exhibited activity against A375 melanoma in vivo, but honokiol DCA was more active. Gene arrays comparing treated with vehicle control tumors demonstrated induction of the respiratory enzyme succinate dehydrogenase B (SDHB) by treatment, suggesting that our honokiol analogs induce respiration in vivo. We then examined its effect against a pair of melanomas, LM36 and LM36R, in which LM36R differs from LM36 in that LM36R has acquired vemurafenib resistance. Honokiol DCA demonstrated in vivo activity against LM36R (vemurafenib resistant) but not against parental LM36. Honokiol DCA and hexafluoro inhibited the phosphorylation of DRP1, thus stimulating a phenotype suggestive of respiration through mitochondrial normalization. Honokiol DCA may act in vemurafenib resistant melanomas to increase both respiration and reactive oxygen generation, leading to activity against aggressive melanoma in vivo.

2016-01-20 | GSE76956 | GEO

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