ArticlePigment cell & melanoma research2010
PLX4032, a selective BRAF(V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells.
Article in Pigment cell & melanoma research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 184 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
184 citing papers in PubMed, 321 citations in OpenAlex.
- Targeted next generation sequencing identifies clinically actionable mutations in patients with melanoma.Pigment cell & melanoma research · 2014Trial
- Safety and efficacy of vemurafenib in BRAF(V600E) and BRAF(V600K) mutation-positive melanoma (BRIM-3): extended follow-up of a phase 3, randomised, open-label study.The Lancet. Oncology · 2014Trial
- Targeted therapy in BRAF‑mutant melanoma: Advances and challenges (Review).International journal of oncology · 2026Review
- Lipophilic Statins Deplete GPX4 to Promote Ferroptosis and Sensitize Cancer Cells to Immune Checkpoint Blockade.Molecular cancer therapeutics · 2026Article
- The GENEVA platform models tumor mosaicism to reveal variations of responses to KRAS inhibitors and identify improved drug combinations.Nature cancer · 2026Article
- Article
- Combination of the Novel RAF Dimer Inhibitor Brimarafenib With the MEK Inhibitor Mirdametinib Is Effective Against NRAS Mutant Melanoma.Pigment cell & melanoma research · 2025Article
- Sustained Response to Pan-BRAF Inhibitor Plixorafenib (FORE8394, PLX8394) in a Young Adult With Neurodegenerative Langerhans Cell Histiocytosis.JCO precision oncology · 2025Article
- Xanthohumol Sensitizes Melanoma Cells to Vemurafenib by Lowering Membrane Cholesterol and Increasing Membrane Fluidity.International journal of molecular sciences · 2025Article
- Targeted therapy of cancer stem cells: inhibition of mTOR in pre-clinical and clinical research.Cell death & disease · 2024Review
- GP100 expression is variable in intensity in melanoma.Cancer immunology, immunotherapy : CII · 2024Article
- A topical BRAF inhibitor (LUT-014) for treatment of radiodermatitis among women with breast cancer.JAAD international · 2024Article
- Melanocortin-1 Receptor Expression as a Marker of Progression in Melanoma.JCO precision oncology · 2024Article
- Potential role of immunotherapy and targeted therapy in the treatment of cancer: A contemporary nursing practice.Heliyon · 2024Review
- Inhibition of TGF-β signaling, invasion, and growth of cutaneous squamous cell carcinoma by PLX8394.Oncogene · 2023Article
- Compression drives diverse transcriptomic and phenotypic adaptations in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Vemurafenib Inhibits Acute and Chronic Enterovirus Infection by Affecting Cellular Kinase Phosphatidylinositol 4-Kinase Type IIIβ.Microbiology spectrum · 2023Article
- In Silico Studies of Novel Vemurafenib Derivatives as BRAF Kinase Inhibitors.Molecules (Basel, Switzerland) · 2023Article
- Shared hotspot mutations in oncogenes position dogs as an unparalleled comparative model for precision therapeutics.Scientific reports · 2023Article
- Impairment of SK-MEL-28 Development-A Human Melanoma Cell Line-By theInternational journal of molecular sciences · 2023Article
124 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
BRAF(V600E/K) is a frequent mutationally active tumor-specific kinase in melanomas that is currently targeted for therapy by the specific inhibitor PLX4032. Our studies with melanoma tumor cells that are BRAF(V600E/K) and BRAF(WT) showed that, paradoxically, while PLX4032 inhibited ERK1/2 in the highly sensitive BRAF(V600E/K), it activated the pathway in the resistant BRAF(WT) cells, via RAF1 activation, regardless of the status of mutations in NRAS or PTEN. The persistently active ERK1/2 triggered downstream effectors in BRAF(WT) melanoma cells and induced changes in the expression of a wide-spectrum of genes associated with cell cycle control. Furthermore, PLX4032 increased the rate of proliferation of growth factor-dependent NRAS Q61L mutant primary melanoma cells, reduced cell adherence and increased mobility of cells from advanced lesions. The results suggest that the drug can confer an advantage to BRAF(WT) primary and metastatic tumor cells in vivo and provide markers for monitoring clinical responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.