ReviewMolecular biomedicine2026
BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.
Review in Molecular biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Exploring the apoptotic potential of Prunus spinosa Trigno extract in BRAF-mutated melanoma cells.Molecular biology reports · 2026Article
- Elucidating the Nexus of Mitochondrial Dysfunction and Oncometabolite Accumulation in Tumorigenesis.Nigerian medical journal : journal of the Nigeria Medical AssociationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
BRAF inhibitors (BRAFi) have transformed the treatment of BRAF mutant melanoma, but inherent and acquired resistance remains a major barrier to curative outcomes. Resistance arises from interconnected mechanisms: genetic alterations reactivating the MAPK pathway or bypass cascades (e.g., PI3K/AKT/RTK), epigenetic modulation, metabolic reprogramming, and the tumor microenvironment (TME) remodeling. Despite extensive research into these mechanisms, a cohesive framework linking each resistance module to targeted therapeutic strategies is lacking. This review systematically categorizes resistance into intrinsic and acquired subtypes: intrinsic resistance is driven by constitutive molecular traits of BRAF mutant melanoma (e.g., persistent MAPK activation, baseline PI3K/AKT hyperactivity), while acquired resistance emerges via therapeutic pressure-induced genetic mutations, epigenetic shifts, metabolic reprogramming, or TME modifications. For each identified resistance mechanism, we provide a detailed examination of corresponding therapeutic advancements. These encompass the development of next-generation BRAFi, strategically designed combination therapies, epigenetic modulators, immunotherapeutic approaches, and RNA-based therapeutic agents. Furthermore, we underscore the pivotal role of state-of-the-art technologies, such as liquid biopsies, single-cell multi-omics analyses, and artificial intelligence, in facilitating precise resistance monitoring and personalized therapy selection. By integrating these insights, we present a structured, translationally focused framework to guide basic research and clinical decision-making, ultimately advancing precision salvage therapy and trials aimed at preventing or overcoming BRAFi resistance.
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What Socratic 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 Socratic graph.