ArticleClinical and translational medicine2025
BRAF
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Recent Developments and Structure-Activity Relationships of BRAF Inhibitors for Cancer Drug Discovery.Archiv der Pharmazie · 2026Review
- Development of PROTACs for targeted degradation of oncogenic TRK fusions.RSC chemical biology · 2026Article
- Review
- BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Molecular biomedicine · 2026Review
- PROTAC-based protein degradation: a window of opportunity for melanoma therapy.Journal of biomedical science · 2026Review
- Lessons learned in linking PROTACs from discovery to the clinic.Nature reviews. Chemistry · 2026Review
- Development of PROTACs for targeted degradation of oncogenic TRK fusions.bioRxiv : the preprint server for biology · 2025Article
- BRAFClinical and translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
aimsThis study compares the suppression of Mitogen-activated protein kinase (MAPK) signalling and early resistance potential between a proteolysis-targeting chimera (PROTAC) and inhibitors targeting BRAF
methodsWe performed a detailed in silico analysis of the transcriptomic landscape of the A375 melanoma cell line treated with a PROTAC and BRAF
resultsPROTAC-treated cells showed significantly lower MAPK pathway activity, strong cell cycle arrest and elevated apoptotic gene expression compared to inhibitor-treated cells, with no effect on the PI3K/AKT pathway. A high microphtalmia-associated transcription factor (MITF)/Tyrosine-Protein Kinase Receptor (AXL) ratio in PROTAC-treated cells indicated reduced early drug resistance. BRAF degradation induced a melanocytic-transitory phenotype. Although PROTAC and inhibitor treatments caused overlapping transcriptomic changes, key differences were observed. PROTAC treatment enriched processes such as epithelial‒mesenchymal transition, inflammatory responses, and Tumor necrosis factor-Alpha (TNF-α) and IL2/STAT5 signalling.
conclusionPROTAC-targeting BRAF
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Identifiers
What OpenQuestion holds
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.