Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Increased inflammatory lipid metabolism and anaplerotic mitochondrial activation follow acquired resistance to vemurafenib in BRAF-mutant melanoma cells.

British journal of cancer - 1 Jan 2020

Delgado-Goñi Teresa, Galobart Teresa Casals, Wantuch Slawomir, Normantaite Deimante, Leach Martin O, Whittaker Steven R, Beloueche-Babari Mounia

Abstract excerpt

BACKGROUND: BRAF inhibitors, such as vemurafenib, have shown efficacy in BRAF-mutant melanoma treatment but acquired-resistance invariably develops. Unveiling the potential vulnerabilities associated with vemurafenib resistance could provide rational strategies for combinatorial treatment. METHODS: This work investigates the metabolic characteristics and vulnerabilities of acquired resistance to vemurafenib in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Survival
Share to Dinoprostone

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Gefitinib

Share to Melanoma

Share to Proto-Oncogene Proteins B-raf

Share to Skin Neoplasms

Share to Vemurafenib

Source

Open in PubMed Open full text

Identifiers

PMID: 31819183
DOI: 10.1038/s41416-019-0628-x
PMCID: PMC6964672

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Increased inflammatory lipid metabolism and anaplerotic mitochondrial activation follow acquired resistance to vemurafenib in BRAF-mutant melanoma cells.PMID 31819183Read ↗

The BRAF Inhibitor Vemurafenib Activates Mitochondrial Metabolism and Inhibits Hyperpolarized Pyruvate-Lactate Exchange in BRAF-Mutant Human Melanoma Cells.Semantic proximity Read ↗

Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanomaSemantic proximity Read ↗

Relationship between melanoma vemurafenib tolerance thresholds and metabolic pathway choice and Wnt signaling involvementSemantic proximity Read ↗

Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanomaSemantic proximity Read ↗

Therapeutic implications of the metabolic changes associated with BRAF inhibition in melanoma.Semantic proximity Read ↗

New insight into the role of metabolic reprogramming in melanoma cells harboring BRAF mutations.Semantic proximity Read ↗

Dependence On Glycolysis Sensitizes BRAF-mutated Melanomas For Increased Response To Targeted BRAF Inhibition.Semantic proximity Read ↗

Melanoma metabolism contributes to the cellular responses to MAPK/ERK pathway inhibitors.Semantic proximity Read ↗

BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Semantic proximity Read ↗

Simvastatin reprograms lipid metabolism in B16.F10 melanoma cells to favor an early resistant phenotype.Semantic proximity Read ↗

3-Bromopyruvate Suppresses the Malignant Phenotype of Vemurafenib-Resistant Melanoma Cells.Semantic proximity Read ↗

Polyamine and EIF5A hypusination downstream of c-Myc confers targeted therapy resistance in BRAF mutant melanoma.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.