ArticleAging2023
Unravelling diagnostic clusters and immune landscapes of disulfidptosis patterns in gastric cancer through bioinformatic assay.
Article in Aging, 2023. 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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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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Integrated machine learning and multi-omics analysis identifies CYP1B1 as a candidate target of orientin in intervertebral disc degeneration-associated low back pain.Frontiers in pain research (Lausanne, Switzerland) · 2026Article
- Disulfidptosis: A Metabolic Cell Death Mechanism with Therapeutic Potential in Cancer.Oncology research · 2026Review
- Advances in the study of disulfidptosis in digestive tract tumors.Discover oncology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disulfidptosis is a novel type of cell death mediated by SLC7A11-induced disulfide stress. Gastric cancer (GC) is a common malignant gastrointestinal tumor. Existing evidence shows that SLC7A11 can regulate cell death and improve the progression of GC, suggesting disulfidptosis may exist in the pathological process of GC. However, the underlying functions of disulfidptosis regulators in GC remain unknown. The dataset of GSE54129 was screened to comprehensively investigate the disulfidptosis-related diagnostic clusters and immune landscapes in GC. Totally 15 significant disulfidptosis regulators were identified via difference analysis between GC samples and controls. Then random forest model was utilized to assess their importance score (mean decrease Gini). Then a nomogram model was constructed, which could offer benefit to patients based on our subsequent decision curve analysis. All the included GC patients were divided into 2 disulfidptosis subgroups (clusterA and clusterB) according to the significant disulfidptosis regulators in virtue of consensus clustering analysis. The disulfidptosis score of each sample was calculated through PCA algorithms to quantify the disulfidptosis subtypes. Patients from clusterB exhibited lower disulfidptosis scores than those of patients in clusterA. In addition, we found that the cases in clusterB were closely associated with the immunity of activated CD4 T cell, etc., while clusterA was linked to immature dendritic cell, mast cell, natural killer T cell, natural killer cell, etc., which has a higher disulfidptosis score. Therefore, disulfidptosis regulators play an important role in the pathological process of GC, providing a promising marker and an immunotherapeutic strategy for future GC therapy.
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Registered trials
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