ReviewCancer gene therapy2026
Disulfidptosis in cancer: from redox stress to therapeutic strategy.
Review in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Experimental Detection Methods and Clinical Translational Challenges of Disulfidptosis in Cancer.Cells · 2026Review
- Review
- Disulfidptosis and androgenic cancers: from molecular mechanisms to clinical applications and future translational research.Frontiers in endocrinology · 2026Review
- The role of disulfidptosis-driven tumor microenvironment remodeling in pancreatic cancer progression.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disulfidptosis, a recently identified form of disulfide-dependent cell death, has emerged as a key regulator of cancer progression and therapy resistance. This review examines the molecular mechanisms connecting the redox balance within the tumor microenvironment (TME), outlines its crosstalk with traditional cell death pathways, and highlights its promise as a therapeutic strategy. Current evidence indicates that disulfidptosis is driven by glutathione (GSH) depletion and thiol-disulfide exchange imbalance, leading to endoplasmic reticulum stress and tumor cell vulnerability. Translational applications-including small-molecule activators and combination therapies-are discussed, alongside challenges in clinical translation and future research directions.
Indexed as
Identifiers
41152588What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.