ArticleFrontiers in immunology2026
The role of disulfidptosis-driven tumor microenvironment remodeling in pancreatic cancer progression.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- The ferroptosis-cuproptosis crosstalk in hematological malignancies: multi-omics insights into gene-regulated cell death and emerging therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Programmed cell death and metastatic evolution in breast cancer: the role of anoikis, necroptosis, and ferroptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Disulfidptosis as an immunometabolic rheostat in gastrointestinal cancers: tuning the balance between T Cell exhaustion and immunogenic cell death.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) continues to pose a significant clinical challenge due to its high mortality rate and limited treatment efficacy. The role of disulfidptosis, a recently discovered mode of regulatory cell death, in pancreatic cancer progression and tumor immunity remains poorly understood. Methods: We developed and validated a disulfidptosis-related prognostic signature based on 13 pivotal genes. Integrated multi-omics approaches, incorporating bulk and single-cell transcriptomics, spatial transcriptomics, and functional assays, were employed to investigate the association between disulfidptosis and key biological processes. Results: The prognostic signature effectively stratified PDAC patients into distinct risk categories with markedly different clinical outcomes and exhibited consistent predictive accuracy across multiple independent cohorts. It informed personalized treatment strategies, revealing differential sensitivity to therapeutic agents including dasatinib and UMI-77. Multi-omics analyses revealed that disulfidptosis is closely associated with redox homeostasis, cytoskeletal organization, and immune evasion. The high-risk subgroup displayed an immunosuppressive tumor microenvironment, characterized by diminished CD8 Conclusion: Our study develops a novel prognostic framework for patient stratification based on disulfidptosis-related genes in PDAC. Integrated multi-omics analyses reveal a strong association between disulfidptosis and an immunosuppressive tumor microenvironment, positioning it as a candidate metabolic vulnerability that warrants further functional investigation. These findings offer correlative insights into the involvement of disulfidptosis in immune regulation and suggest that further exploration of this pathway may inform future immunotherapeutic strategies.
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