ArticleThe Journal of clinical investigation2015
Co-clinical assessment identifies patterns of BRAF inhibitor resistance in melanoma.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
What it found
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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
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.
- Brain metastases: A Society for Neuro-Oncology (SNO) consensus review on current management and future directions.Neuro-oncology · 2022Guideline
- Co-clinical FDG-PET radiomic signature in predicting response to neoadjuvant chemotherapy in triple-negative breast cancer.European journal of nuclear medicine and molecular imaging · 2022Trial
- Tumor-associated B-cells induce tumor heterogeneity and therapy resistance.Nature communications · 2017Trial
- Clinical, Molecular, and Immune Analysis of Dabrafenib-Trametinib Combination Treatment for BRAF Inhibitor-Refractory Metastatic Melanoma: A Phase 2 Clinical Trial.JAMA oncology · 2016Trial
- Genome-Wide CRISPR Screen Identifies a microRNA Orchestrating Pleiotropic Resistance to Targeted Therapy and T Cell Immunity in Melanoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PSGL-1 blockade delays relapse to BRAF/MEK inhibition in cutaneous melanoma.bioRxiv : the preprint server for biology · 2026Article
- Sequential transcriptional waves and NF-κB-driven chromatin remodeling direct drug-induced dedifferentiation in cancer.Nature communications · 2026Article
- Article
- DNA fragmentation factor B suppresses interferon to enable cancer persister cell regrowth.Nature cell biology · 2025Article
- Elevated NR2F1 underlies the persistence of invasive disease after treatment of BRAF-mutant melanoma.The Journal of clinical investigation · 2025Article
- Transcriptome-wide decoding the roles of aberrant splicing in melanoma MAPK-targeted resistance evolution.EMBO reports · 2025Article
- MelanoDB: A dataset of clinical and molecular features of patients with advanced melanoma treated with MAPK inhibitors.Scientific data · 2025Article
- Sensitivity to immune checkpoint inhibitors in BRAF/MEK inhibitor refractory melanoma.Journal for immunotherapy of cancer · 2025Article
- Transposon mediated functional genomic screening for BRAF inhibitor resistance reveals convergent Hippo and MAPK pathway activation events.Scientific reports · 2025Article
- UBA1 inhibition sensitizes cancer cells to PARP inhibitors.Cell reports. Medicine · 2024Article
- A Next-Generation BRAF Inhibitor Overcomes Resistance to BRAF Inhibition in Patients with BRAF-Mutant Cancers Using Pharmacokinetics-Informed Dose Escalation.Cancer discovery · 2024Article
- Article
- Harnessing the potential of reverse-phase protein array technology: Advancing precision oncology strategies.Cancer science · 2024Review
- Cost and time-efficient construction of a 3'-end mRNA library from unpurified bulk RNA in a single tube.Experimental & molecular medicine · 2024Article
- Telomere dysfunction in Tert knockout mice delays BrafInternational journal of cancer · 2024Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
Multiple mechanisms have been described that confer BRAF inhibitor resistance to melanomas, yet the basis of this resistance remains undefined in a sizable portion of patient samples. Here, we characterized samples from a set of patients with melanoma that included individuals at baseline diagnosis, on BRAF inhibitor treatment, and with resistant tumors at both the protein and RNA levels. Using RNA and DNA sequencing, we identified known resistance-conferring mutations in 50% (6 of 12) of the resistant samples. In parallel, targeted proteomic analysis by protein array categorized the resistant samples into 3 stable groups, 2 of which were characterized by reactivation of MAPK signaling to different levels and 1 that was MAPK independent. The molecular relevance of these classifications identified in patients was supported by both mutation data and the similarity of resistance patterns that emerged during a co-clinical trial in a genetically engineered mouse (GEM) model of melanoma that recapitulates the development of BRAF inhibitor resistance. Additionally, we defined candidate biomarkers in pre- and early-treatment patient samples that have potential for predicting clinical responses. On the basis of these observations, we suggest that BRAF inhibitor-resistant melanomas can be actionably classified using protein expression patterns, even without identification of the underlying genetic alteration.
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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.