ArticleNature genetics2025
Passenger mutations link cellular origin and transcriptional identity in human lung adenocarcinomas.
Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- Article
- Late-stage dedifferentiation and epigenetic memory of cancer stem cells in hepatocellular carcinoma.Journal of translational medicine · 2026Article
- A Multi-Level miRNA Regulatory Network Associated with IRF1 Expression in Non-Small Cell Lung Cancer: In Silico Identification of Candidate Biomarkers for Immunotherapy Response.International journal of molecular sciences · 2026Article
- TriosCompass: a snakemake workflow for integrated detection of SNVs, indels, STRs, and structural de novo variants in parent-child trios.Bioinformatics (Oxford, England) · 2026Article
- The impact of obesity-related systemic inflammation on the efficacy, toxicity, and biomarkers of immune checkpoint inhibitors in lung cancer: from mechanisms to clinical management.Frontiers in immunology · 2026Review
- Passenger mutations link cellular origin and transcriptional identity in human lung adenocarcinomas.Nature genetics · 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
17 authors.
Funding
Abstract
DNA damage is preferentially repaired in expressed genes; thus, genome-wide correlations between somatic mutation patterns and normal cell transcription may reflect tumor cell origins. Accordingly, we found that aggregate lung adenocarcinoma (LUAD) and squamous cancer (LUSC) somatic mutation density associated most strongly with distal (alveolar) and proximal (basal) lung cell-type-specific gene expression, respectively, consistent with presumed LUAD and LUSC cell origins. Analyzing individual genomes, 21% of LUADs bore mutational footprints of proximal airway origins, with 38% classified as ambiguous. Distal origin LUADs, enriched for KRAS and STK11 drivers, occurred mainly in smokers; proximal origin LUADs, enriched for EGFR drivers, were more common in never-smokers. Ambiguous origin LUADs showed APOBEC signatures and SMARCA4 alterations. TP53 mutant LUADs with non-distal cell origins preferentially exhibited non-distal transcriptional identity. Our study reveals a complex interplay between lineage and identity in LUAD evolution and offers a scalable strategy to infer tumor origins in human cancers.
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Registered trials
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