ArticleNature cancer2025
Tumor antigens preferentially derive from unmutated genomic sequences in melanoma and non-small cell lung cancer.
Article in Nature cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed.
- Mapping the functional dark proteome in cancer.Nature reviews. Cancer · 2026Review
- Receptor-defined targeting of a genomically unique melanoma-enriched noncanonical antigen.Signal transduction and targeted therapy · 2026Article
- Normal-immunopeptidome denominator: a safety atlas for immunotherapies targeting non-canonical and aberrantly expressed tumor antigens.Journal for immunotherapy of cancer · 2026Article
- T cells are blind to the dark mechanics of tumors.Trends open · 2026Review
- Clinical attribute-based risk matrix for prognostication in immunotherapy-treated non-small cell lung cancer.Nature communications · 2026Article
- Review
- Immune Spatial Organization Predicts Distant Metastasis Risk in Aggressive Localized Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Universal off-the-shelf TGF-Acta pharmaceutica Sinica. B · 2026Article
- DEA hypothesis: disinhibition, enhancing recognition, and alerting the host are the three pillars of effective cancer immunotherapy.Journal for immunotherapy of cancer · 2026Review
- Multiplexed cytokine and antigen mRNA administration generates durable anti-tumor immunity against pancreatic cancer.Nature communications · 2026Article
- A Platform for High-throughput and Ultrasensitive Immunopeptidomics.Molecular & cellular proteomics : MCP · 2026Article
- Noncanonical Transcription and Splicing Shape the Colorectal Cancer Immunopeptidome in MSI and MSS Tumors.Molecular & cellular proteomics : MCP · 2026Article
- Article
- Advances in predicting T cell epitope recognition for cancer immunotherapy.Nature cancer · 2026Review
- The promises and challenges of neoantigen cancer vaccines.Nature biotechnology · 2026Review
- Next-generation neoantigen mRNA vaccines: Immuno-engineering strategies for precision cancer immunotherapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Oocyte-inspired universal whole-cell vaccines against tumor heterogeneity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Immune modulatory vaccines targeting tumor microenvironment antigens: recent advances in oncology and beyond.Signal transduction and targeted therapy · 2026Review
- Bright side of the dark genome: antigens for next-gen cancer vaccines.Journal for immunotherapy of cancer · 2026Review
- Pipe dream to pipeline: Journey of cancer vaccines and the road ahead.Cell reports. Medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors.
Funding
Abstract
Melanoma and non-small cell lung cancer (NSCLC) display exceptionally high mutational burdens. Hence, immune targeting in these cancers has primarily focused on tumor antigens (TAs) predicted to derive from nonsynonymous mutations. Using comprehensive proteogenomic analyses, we identified 589 TAs in cutaneous melanoma (n = 505) and NSCLC (n = 90). Of these, only 1% were derived from mutated sequences, which was explained by a low RNA expression of most nonsynonymous mutations and their localization outside genomic regions proficient for major histocompatibility complex (MHC) class I-associated peptide generation. By contrast, 99% of TAs originated from unmutated genomic sequences specific to cancer (aberrantly expressed tumor-specific antigens (aeTSAs), n = 220), overexpressed in cancer (tumor-associated antigens (TAAs), n = 165) or specific to the cell lineage of origin (lineage-specific antigens (LSAs), n = 198). Expression of aeTSAs was epigenetically regulated, and most were encoded by noncanonical genomic sequences. aeTSAs were shared among tumor samples, were immunogenic and could contribute to the response to immune checkpoint blockade observed in previous studies, supporting their immune targeting across cancers.
Indexed as
Identifiers
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.