ArticleNature communications2025
Clonal evolution and transcriptional plasticity shape metastatic dissemination routes in prostate 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 5 papers.
What it found
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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
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Who cites it
5 citing papers in PubMed.
- Tumor‑immune spatiotemporal co‑evolution: A new paradigm for understanding and overcoming therapy resistance in metastatic castration‑resistant prostate cancer (Review).International journal of molecular medicine · 2026Review
- Single-cell and spatial RNA sequencing in prostate cancer.Nature reviews. Urology · 2026Review
- Melanoma evolution in the lymph node shapes systemic outcomes.bioRxiv : the preprint server for biology · 2026Article
- Phylogeography of Bone Metastasis: Clonal Evolution, Skeletal Niche Adaptation, and Clinical Implications.International journal of molecular sciences · 2026Review
- Exploring the biology of metastatic hormone-sensitive prostate cancer: on the road to precision medicine.The Journal of clinical investigation · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Prostate cancer is a highly heterogeneous disease, driven by genomic and transcriptional changes that impact disease progression and metastatic potential. The interplay between clonal evolution, transcriptional plasticity, and tumour microenvironment is, however, poorly understood. Here, we leverage and integrate single-nuclei RNA sequencing and whole-genome sequencing from 43 spatially distinct tumour samples from five patients with locally advanced prostate cancer to reconstruct clonal evolution trajectories and transcriptional changes driving metastasis at single-cell resolution. We find extensive clonal heterogeneity, including both monophyletic and polyphyletic metastatic dissemination, and ongoing clonal evolution in the primary tumour after metastatic spread. Metastatic seeding converges on disease trajectories involving both genomic and transcriptional changes, including androgen receptor independence and activation of estrogen-, WNT- and JAK-STAT- pathway activity, in spatially distinct areas. Our findings suggest an intricate interplay between clonal evolution and cellular plasticity driving metastatic seeding and point toward more integrative prognostic markers for improved patient management.
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Registered trials
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