Trial reportScientific reports2023
Analysis of long non-coding RNAs associated with disulfidptosis for prognostic signature and immunotherapy response in uterine corpus endometrial carcinoma.
Trial report in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Recent advances in characterizing the immune microenvironment and biomarkers of endometrial carcinoma.Frontiers in immunology · 2026Review
- Comparison of Long Non-Coding RNA Expressions in Endometrial Polyp and Endometrial Cancer Cases.Diagnostics (Basel, Switzerland) · 2025Article
- Disulfide bond-related gene signature development for bladder cancer prognosis prediction and immune microenvironment characterization.Scientific reports · 2025Article
- Article
- Research progress and potential therapeutic targets of a novel disulfide stress-driven cell death-disulfidptosis in gynecological tumors and other gynecological disorders.American journal of cancer research · 2025Review
- Establishment of a prognostic signature and immune infiltration characteristics for uterine corpus endometrial carcinoma based on a disulfidptosis/ferroptosis-associated signature.Frontiers in immunology · 2025Article
- Prognostic value of disulfidptosis-associated genes in gastric cancer: a comprehensive analysis.Frontiers in oncology · 2025Article
- New mechanism of LncRNA: In addition to act as a ceRNA.Non-coding RNA research · 2024Review
- Development of a disulfidptosis-related prognostic model for endometrial cancer with potential therapeutic target.Discover oncology · 2024Article
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 at 3 institutions in 1 country.
Funding
Abstract
Disulfidptosis, the demise of cells caused by the abnormal breakdown of disulfide bonds and actin in the cytoprotein backbone, has attracted attention in studies concerning disulfide-related cell death and its potential implications in cancer treatment. This study utilized bioinformatics to detect disulfidptosis associated lncRNA prognostic markers (DALPMs) with Uterine Corpus Endometrial Carcinoma (UCEC)-related to investigate the correlation between these indicators and the tumor immune microenvironment. The RNA sequencing data and somatic mutation information of patients with UCEC were obtained from the Cancer Genome Atlas (TCGA) database. Patients were randomly divided into Train and Test groups. The findings revealed a potential prognostic model comprising 14 DALPMs. Both univariate and multivariate Cox analyses demonstrated that the model-derived risk score functioned as a standalone prognostic indicator for patients. Significant disparities in survival outcomes were observed between the high- and low-risk groups as defined by the model. Differences in tumor mutational burden (TMB), tumor immune dysfunction and exclusion (TIDE), and tumor microenvironment (TME) stromal cells between patients of the high- and low-risk groups were also observed. The forecast model comprising long non-coding RNAs (lncRNAs) associated with disulfidptosis can effectively anticipate patients' prognoses.
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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 Socratic graph.