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

Copper Chelation as Targeted Therapy in a Mouse Model of Oncogenic BRAF-Driven Papillary Thyroid Cancer.

Clinical cancer research : an official journal of the American Association for Cancer Research - 1 Sept 2018

Xu MengMeng, Casio Michael, Range Danielle E, Sosa Julie A, Counter Christopher M

Abstract excerpt

Purpose: Sixty percent of papillary thyroid cancers (PTC) have an oncogenic (V600E) BRAF mutation. Inhibitors of BRAF and its substrates MEK1/2 are showing clinical promise in BRAFV600E PTC. PTC progression can be decades long, which is challenging in terms of toxicity and cost. We previously found that MEK1/2 require copper (Cu) for kinase activity and can be inhibited with the well-tolerated and economical Cu...

Read the complete abstract on PubMed

Topics

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

Share to Chelating Agents
Share to MAP Kinase Kinase 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Molybdenum

Share to Phenylurea Compounds

Share to Quinolines

Share to Sorafenib

Share to Thyroid Cancer, Papillary

Share to Vemurafenib

Source

Open in PubMed Open full text

Identifiers

PMID: 30065097
DOI: 10.1158/1078-0432.CCR-17-3705
PMCID: PMC6125179

Genes

BRAF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Copper Chelation as Targeted Therapy in a Mouse Model of Oncogenic BRAF-Driven Papillary Thyroid Cancer.PMID 30065097Read ↗

Copper Chelation Inhibits BRAFV600E-Driven Melanomagenesis and Counters Resistance to BRAFV600E and MEK1/2 Inhibitors.Semantic proximity Read ↗

BRAFV600E-Driven Lung Adenocarcinoma Requires Copper to Sustain Autophagic Signaling and ProcessingSemantic proximity Read ↗

Mutationally activated BRAF(V600E) elicits papillary thyroid cancer in the adult mouse.Semantic proximity Read ↗

Metastasis-associated MCL1 and P16 copy number alterations dictate resistance to vemurafenib in a BRAFV600E patient-derived papillary thyroid carcinoma preclinical model.Semantic proximity Read ↗

Role of BRAF in thyroid oncogenesis.Semantic proximity Read ↗

Small-molecule MAPK inhibitors restore radioiodine incorporation in mouse thyroid cancers with conditional BRAF activationSemantic proximity Read ↗

Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiation.Semantic proximity Read ↗

MEK inhibitor PD0325901 significantly reduces the growth of papillary thyroid carcinoma cells in vitro and in vivo.Semantic proximity Read ↗

BRAF-activated ARSI suppressed EREG-mediated ferroptosis to promote BRAFV600E (mutant) papillary thyroid carcinoma progression and sorafenib resistance.Semantic proximity Read ↗

p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer.Semantic proximity Read ↗

Vemurafenib in patients with BRAF(V600E)-positive metastatic or unresectable papillary thyroid cancer refractory to radioactive iodine: a non-randomised, multicentre, open-label, phase 2 trial.Semantic proximity Read ↗

BRAF inhibitors: experience in thyroid cancer and general review of toxicity.Semantic proximity Read ↗

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