Abstract

BackgroundLung adenocarcinoma (LUAD) is the most prevalent subtype of non-small cell lung cancer. Additionally, disulfidptosis, a newly discovered type of cell death, has been found to be closely associated with the onset and progression of tumors. MethodsThe study first identified genes related to disulfidptosis through correlation analysis. These genes were then screened using univariate cox regression and LASSO regression, and a prognostic model was constructed through multivariate cox regression. A nomogram was also created to predict the prognosis of LUAD. The model was validated in three independent data sets: GSE72094, GSE31210, and GSE37745. Next, patients were grouped based on their median risk score, and differentially expressed genes between the two groups were analyzed. Enrichment analysis, immune infiltration analysis, and drug sensitivity evaluation were also conducted. ResultsIn this study, we examined 21 genes related to disulfidptosis and developed a gene signature that was found to be associated with a poorer prognosis in LUAD. Our model was validated using three independent datasets and showed AUC values greater than 0.5 at 1, 3, and 5 years. Enrichment analysis revealed that the disulfidptosis-related genes signature had a multifaceted impact on LUAD, particularly in relation to tumor development, proliferation, and metastasis. Patients in the high-risk group exhibited higher tumor purity and lower stromal score, ESTIMATE score, and Immune score. ConclusionThis study constructed a gene signature related to disulfidptosis in lung adenocarcinoma and analyzed its impact on the disease and its association with the tumor microenvironment. The findings of this research provide valuable insights into the understanding of lung adenocarcinoma and could potentially lead to the development of new treatment strategies.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.