Elevated SAMD3 expression in T cells predicts improved survival in pancreatic ductal adenocarcinoma patients

Cancer Immunol Immunother. 2025 Feb 1;74(3):93. doi: 10.1007/s00262-025-03948-x.

Abstract

Objective: Pancreatic ductal adenocarcinoma (PDAC) has an immune-suppressive tumor microenvironment that contributes to resistance to immunotherapy. This study aimed to demonstrate that elevated sterile alpha motif domain-containing protein 3 (SAMD3) expression in effector CD8+ T cells was associated with improved survival in PDAC patients.

Design: We investigated the heterogeneity and gene expression profiles of T cells using a single-cell RNA sequencing (sc-RNA-seq) dataset comprised of human PDAC samples. SAMD3 mRNA expression was further evaluated in a tumor-specific OT-I/ovalbumin (OVA) mouse model. SAMD3 levels and their clinical significance were evaluated via immunohistochemistry (IHC) analysis.

Results: SAMD3 was highly expressed in cytotoxic CD8+ T cells, with expression significantly downregulated during T cell exhaustion. SAMD3 levels were positively correlated with CD8+ T cell function. In PDAC patients, high SAMD3 levels in T cells were associated with improved overall survival (OS), disease-free survival (DFS), and T cell infiltration. A patient exhibiting partial response to combination immunotherapy also showed high SAMD3 levels in T cells.

Conclusion: SAMD3 is a biomarker of T cell function, with elevated expression in T cells predicting improved survival. These findings highlight the potential of precision immunotherapy approaches for treating PDAC.

Keywords: Pancreatic ductal adenocarcinoma; SAMD3; Single-cell RNA sequencing; T cell.

MeSH terms

  • Animals
  • Biomarkers, Tumor* / genetics
  • Biomarkers, Tumor* / metabolism
  • CD8-Positive T-Lymphocytes* / immunology
  • CD8-Positive T-Lymphocytes* / metabolism
  • Carcinoma, Pancreatic Ductal* / genetics
  • Carcinoma, Pancreatic Ductal* / immunology
  • Carcinoma, Pancreatic Ductal* / metabolism
  • Carcinoma, Pancreatic Ductal* / mortality
  • Carcinoma, Pancreatic Ductal* / pathology
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lymphocytes, Tumor-Infiltrating / immunology
  • Male
  • Mice
  • Middle Aged
  • Pancreatic Neoplasms* / genetics
  • Pancreatic Neoplasms* / immunology
  • Pancreatic Neoplasms* / metabolism
  • Pancreatic Neoplasms* / mortality
  • Pancreatic Neoplasms* / pathology
  • Prognosis
  • Tumor Microenvironment / immunology

Substances

  • Biomarkers, Tumor