ArticleScientific reports2023
A bioinformatics approach to identify a disulfidptosis-related gene signature for prognostic implication in colon adenocarcinoma.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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
47 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- The emerging roles of disulfidptosis in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- The emerging roles of disulfidptosis in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- Disulfidptosis contributes to rotenone-induced dopaminergic neuron damage.Neural regeneration research · 2026Article
- An m6A-programmed cell death signature predicts prognosis and identifies STK25 as a therapeutic target in colon adenocarcinoma.Oncology letters · 2026Article
- Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms.Cancer cell international · 2026Article
- ZDHHC9-mediated KLF5 palmitoylation enhances the cAMP/PKA/CREB axis to promote colorectal cancer progression.Oncogene · 2026Article
- Disulfidptosis-related genes signature predicts prognosis and immune microenvironment in colon cancer.Frontiers in molecular biosciences · 2026Article
- Disulfidptosis in cancer: from redox stress to therapeutic strategy.Cancer gene therapy · 2026Review
- MRPL3 is identified as a prognostic biomarker and therapeutic target in lung adenocarcinoma via a lactylation-disulfidptosis gene signature model and experimental validation.Frontiers in immunology · 2026Article
- Development and experimental validation of an osteoporosis diagnosis model based on disulfidoptosis-related genes and immune infiltration analysis.Frontiers in immunology · 2026Article
- Disulfidptosis OXSM serves as a potential prognostic biomarker and correlates with immune infiltrates in glioma.Discover oncology · 2025Article
- Article
- Expanding the Knowledge of the Molecular Effects and Therapeutic Potential of Incomptine A for the Treatment of Non-Hodgkin Lymphoma: In Vivo and Bioinformatics Studies, Part III.Pharmaceuticals (Basel, Switzerland) · 2025Article
- FLNA, a disulfidptosis-related gene, modulates tumor immunity and progression in colorectal cancer.Cellular & molecular biology letters · 2025Article
- Cellular senescence and disulfide death-related genes as biological markers of breast cancer prognosis.Discover oncology · 2025Article
- Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025Review
- NCAPG2 is a diagnostic biomarker associated with immune infiltration in cholangiocarcinoma.Discover oncology · 2025Article
- Pancancer analysis of DNA damage repair gene mutations and their impact on immune regulatory gene expression.Scientific reports · 2025Article
- Target oxidative stress-induced disulfidptosis: novel therapeutic avenues in Parkinson's disease.Molecular brain · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon adenocarcinoma (COAD) is a type of cancer that arises from the glandular epithelial cells that produce mucus in the colon. COAD is influenced by various factors, including genetics, environment and lifestyle. The outcome of COAD is determined by the tumor stage, location, molecular characteristics and treatment. Disulfidptosis is a new mode of cell death that may affect cancer development. We discovered genes associated with disulfidptosis in colon adenocarcinoma and proposed them as novel biomarkers and therapeutic targets for COAD. We analyzed the mRNA expression data and clinical information of COAD patients from The Cancer Genome Atlas (TCGA) database and Xena databases, extracted disulfidptosis-related genes from the latest reports on disulfidptosis. We used machine learning to select key features and build a signature and validated the risk model using data from the Gene Expression Omnibus (GEO) database and Human Protein Atlas (HPA). We also explored the potential biological functions and therapeutic implications of the disulfidptosis-related genes using CIBERSORTx and GDSC2 databases. We identified four disulfidptosis-related genes: TRIP6, OXSM, MYH3 and MYH4. These genes predicted COAD patient survival and modulated the tumor microenvironment, drug sensitivity and immune microenvironment. Our study reveals the importance of disulfidptosis-related genes for COAD prognosis and therapy. Immune infiltration and drug susceptibility results provide important clues for finding new personalized treatment options for COAD. These findings may facilitate personalized cancer treatment.
Indexed as
Identifiers
What 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.