ArticleNature communications2025
Multi-omics analyses reveal biological and clinical insights in recurrent stage I non-small cell lung cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Genomic instability, postoperative recurrence and therapeutic vulnerabilities in resectable non‑small cell lung cancer (Review).Oncology reports · 2026Review
- Distinct Spatial Immune Architectures in Tumor and Tumor-Adjacent Tissues of Early-Stage Non-Small Cell Lung Cancer.bioRxiv : the preprint server for biology · 2026Article
- Sprayable hydrogel loaded with engineered fusion cellular vesicles for cancer recurrence suppression.Journal of nanobiotechnology · 2026Article
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
- Lobectomy, segmentectomy, and wedge resection for elderly patients with solid-predominant stage I NSCLC: survival, pulmonary function, and postoperative outcomes.Translational lung cancer research · 2026Article
- EZH2 Regulates the Proliferation-Senescence Balance and Tumor-Stromal Signaling in Lung Adenocarcinoma.International journal of molecular sciences · 2026Article
- Multi-omics investigation of per- and polyfluoroalkyl substances in lung adenocarcinoma: comprehensive network toxicology, machine learning and molecular docking experiments.Molecular diversity · 2026Article
- Development of bicistronic plasmids and fusion proteins for clinical translation of tumor immune reprogramming.Molecular therapy. Advances · 2026Article
- Acidic-responsive nano liposomes potentiate in situ dual immunotherapy on lung cancer by codelivering antagonistic peptide and agonist.International journal of pharmaceutics: X · 2026Article
- CSIE: cancer subtyping via inference and ensemble.Briefings in bioinformatics · 2026Article
- DNA methylation heterogeneity in complex tumor microenvironment: Quantitative methods, influencing factors, and clinical implications.Genes & diseases · 2026Review
- DNA hypomethylation-activated PRAME drives early-stage lung adenocarcinoma recurrence via ZNF740 and PI3K/AKT/mTOR signaling.Translational lung cancer research · 2026Article
- Integrating AI-driven single-cell analysis to decode epithelial heterogeneity: A prognostic signature and translational immunotherapy strategy targetingChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026Article
- Single-cell phenotype-associated subpopulation identification via transfer foundation model and statistical ensemble learning.BMC biology · 2026Article
- Article
- Review
- A lung microbial signature for postoperative recurrence in stage I-II non-small cell lung cancer.Respiratory research · 2026Article
- Ensemble learning on serum metabolic fingerprints for early detection of lung adenocarcinoma.NPJ precision oncology · 2026Article
- ITGA8 suppresses proliferation and metastasis of lung adenocarcinoma through the inhibition of glycolysis.Scientific reports · 2026Article
- Prognostic and immunological roles of ammonia-induced cell death-related genes in non-small cell lung cancer.BMC pulmonary medicine · 2026Article
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12 authors.
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Abstract
Post-operative recurrence rates of stage I non-small cell lung cancer (NSCLC) range from 20% to 40%. Nonetheless, the molecular mechanisms underlying recurrence hitherto remain largely elusive. Here, we generate genomic, epigenomic and transcriptomic profiles of paired tumors and adjacent tissues from 122 stage I NSCLC patients, among which 57 patients develop recurrence after surgery during follow-up. Integrated analyses illustrate that the presence of predominantly solid or micropapillary histological subtypes, increased genomic instability, and APOBEC-related signature are associated with recurrence. Furthermore, TP53 missense mutation in DNA-binding domain could contribute to shorter time to recurrence. DNA hypomethylation is pronounced in recurrent NSCLC, and PRAME is the significantly hypomethylated and overexpressed gene in recurrent lung adenocarcinoma (LUAD). Mechanistically, hypomethylation at TEAD1 binding site facilitates the transcriptional activation of PRAME. Inhibition of PRAME restrains the tumor metastasis via downregulation of epithelial-mesenchymal transition-related genes. We also identify that enrichment of AT2 cells with higher copy number variation burden, exhausted CD8 + T cells and Macro_SPP1, along with the reduced interaction between AT2 and immune cells, is essential for the formation of ecosystem in recurrent LUAD. Finally, multi-omics clustering could stratify the NSCLC patients into 4 subclusters with varying recurrence risk and subcluster-specific therapeutic vulnerabilities. Collectively, this study constitutes a promising resource enabling insights into the biological mechanisms and clinical management for post-operative recurrence of stage I NSCLC.
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