ArticleHeliyon2024
Identification of disulfidptosis-related clusters and construction of a disulfidptosis-related gene prognostic signature in triple-negative breast cancer.
Article in Heliyon, 2024. 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.
- Disulfidptosis-related genes define a prognostic signature and novel therapeutic targets in Ewing's sarcoma through transcriptomic analysis and experimental validation.Frontiers in immunology · 2026Article
- Advances in novel cell death mechanisms in breast cancer: intersecting perspectives on ferroptosis, cuproptosis, disulfidptosis, and pyroptosis.Molecular cancer · 2025Review
- Identification of Molecular Subtypes and Prognostic Features for Triple-Negative Breast Cancer Based on Golgi Apparatus-Related Gene Signature.Oncology research · 2025Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aimed to explore disulfidptosis-related clusters of triple-negative breast cancer (TNBC) and build a reliable disulfidptosis-related gene signature for forecasting TNBC prognosis. Methods: The disulfidptosis-related clusters of TNBC were identified based on public datasets, and a comparative analysis was conducted to assess their differences in the overall survival (OS) and immune cell infiltration. Morever, the differentially expressed genes (DEGs) between clusters were recognized. Then, the prognostic DEGs were then chosen. A prognostic signature was constructed by the prognostic DEGs, followed by nomogram construction, drug sensitivity, immune correlation, immunotherapy response prediction, and cluster association analyses. Results: Two disulfidptosis-related clusters of TNBC were identified, which had different OS and macrophage infiltration. Moreover, 235 DEGs were identified between two clusters. A prognostic signature was then constructed by five prognostic DEGs including HLA-DQA2, CCL13, GBP1, LAMP3, and SLC7A11. This signature was highly valuable in predicting prognosis. A nomogram was built by risk score and AJCC stage, which could forecast OS accurately. Moreover, patients with high-risk scores exhibited greater sensitivity to chemotherapy drugs such as lapatinib and had a lower immunotherapy response. Conclusions: Two TNBC clusters linked to disulfidptosis were identified, with different OS and immune cell infiltration. Moreover, a five-disulfidptosis-related gene signature may be a powerful prognostic biomarker for TNBC.
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