ArticleNature medicine2023
Multi-organ landscape of therapy-resistant melanoma.
Article in Nature medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed.
- Folate metabolism in tumor-associated macrophages drives immunosuppressive function to promote tumor growth.bioRxiv : the preprint server for biology · 2026Article
- PredictedInternational journal of molecular sciences · 2026Article
- 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
- TFAP2A links drug resistance to antitumor immunity.bioRxiv : the preprint server for biology · 2026Article
- Genomic copy-number variants drive apoptotic evasion underlying acquired resistance to immune checkpoint inhibitors.Immunity · 2025Article
- Targeting TAZ-TEAD in minimal residual disease enhances the duration of targeted therapy in melanoma models.Nature communications · 2025Article
- Genome instability and crosstalk with the immune response.Genome medicine · 2025Review
- Metastases in patients with adjuvant therapies: How to proceed?Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Article
- Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025Review
- Carbon Dot-Linked Hydrogel for TAMs Transform: Spatiotemporal Manipulation to Reshape Tumor Microenvironment.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Evodiamine encapsulated by hyaluronic acid modified zeolitic imidazolate framework-8 for tumor targeted therapy.Drug delivery and translational research · 2025Article
- Clinical development prospects of siRNA drugs for tumor therapy: analysis of clinical trial registration data from 2004 to 2024.Frontiers in pharmacology · 2025Article
- Targeting ferroptosis, pyroptosis and necroptosis for cancer immunotherapy in melanoma: mechanistic insights and clinical perspectives.Frontiers in immunology · 2025Review
- A novel patient-derived cutaneous melanoma cell line reveals key features of metastatic melanoma.Frontiers in oncology · 2025Article
- The Fanconi anemia pathway induces chromothripsis and ecDNA-driven cancer drug resistance.Cell · 2024Article
- Leptomeningeal metastases from solid tumors: A Society for Neuro-Oncology and American Society of Clinical Oncology consensus review on clinical management and future directions.Neuro-oncology · 2024Review
- Interferon signaling and ferroptosis in tumor immunology and therapy.NPJ precision oncology · 2024Article
- ALDH1A3-acetaldehyde metabolism potentiates transcriptional heterogeneity in melanoma.Cell reports · 2024Article
- RNAi-based drug design: considerations and future directions.Nature reviews. Drug discovery · 2024Review
- Functional analysis of recurrent CDC20 promoter variants in human melanoma.Communications biology · 2023Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Metastasis and failure of present-day therapies represent the most common causes of mortality in patients with cutaneous melanoma. To identify the underlying genetic and transcriptomic landscapes, in this study we analyzed multi-organ metastases and tumor-adjacent tissues from 11 rapid autopsies after treatment with MAPK inhibitor (MAPKi) and/or immune checkpoint blockade (ICB) and death due to acquired resistance. Either treatment elicits shared genetic alterations that suggest immune-evasive, cross-therapy resistance mechanisms. Large, non-clustered deletions, inversions and inter-chromosomal translocations dominate rearrangements. Analyzing data from separate melanoma cohorts including 345 therapy-naive patients and 35 patients with patient-matched pre-treatment and post-acquired resistance tumor samples, we performed cross-cohort analyses to identify MAPKi and ICB as respective contributors to gene amplifications and deletions enriched in autopsy versus therapy-naive tumors. In the autopsy cohort, private/late mutations and structural variants display shifted mutational and rearrangement signatures, with MAPKi specifically selecting for signatures of defective homologous-recombination, mismatch and base-excision repair. Transcriptomic signatures and crosstalks with tumor-adjacent macroenvironments nominated organ-specific adaptive pathways. An immune-desert, CD8
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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.