Pan-cancer clinicopathological and genomic characteristics of peritoneal metastasis

  • NPJ Precis Oncol. 2025 Dec 13. doi: 10.1038/s41698-025-01227-7.
Tianwei Chen  #  1  2 ,  Yebin Yang  #  3 ,  Xiaoli Liu  #  4 ,  Fanhe Dong  3 ,  Liang Wang  3 ,  Yuqiang Shan  5 ,  Xiang Wang  6
Affiliations
  • 1. Zhejiang Key Laboratory of Zero Magnetic Medicine, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China. [email protected].
  • 2. Department of Gastrointestinal Surgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China. [email protected].
  • 3. Department of Gastrointestinal Surgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China.
  • 4. The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou First People's Hospital, Hangzhou, China.
  • 5. Department of Gastrointestinal Surgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China. [email protected].
  • 6. Zhejiang Key Laboratory of Zero Magnetic Medicine, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China. [email protected].
  • # Contributed equally.
PMID: 41390696 DOI: 10.1038/s41698-025-01227-7
Abstract

Peritoneal metastasis (PM) poses a significant clinical challenge, yet the patient characteristics and genomic drivers underlying PM remain poorly characterized. Leveraging the MSK-MetTropism cohort (n = 25,755), our pan-cancer analysis reveals PM occurs in 29% of metastatic patients with extreme incidence variation (1% in THPA to 92% in HGSOC), and digestive/gynecologic malignancies exhibit the highest PM propensity with significant sex disparities. PM confers worse survival in 11/39 subtypes. Genomic profiling of 5,942 PM patients identifies enriched mutations in ESR1, TCF7L2, and FBXW7, pathway-level of TGF-Beta mutation, and subtype-specific drivers, including RET mutations in gastric PM. Mutational signatures implicate ROS (SBS18), HR deficiency (SBS3), and SBS8 across ≥9 Cancer types. These results establish foundational insights into PM biology, though future PM tissue profiling is warranted to overcome primary tumor bias in genomic data.

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