ArticleJournal of thoracic disease2025
Research on the correlation between lung adenocarcinoma and necrosis by sodium overload.
Article in Journal of thoracic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Necrosis by Sodium Overload: Mechanisms, Pathophysiological Roles, and Therapeutic Prospects of a Novel Form of Regulated Cell Death.Cell biochemistry and biophysics · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Necrosis by sodium overload (NECSO), a necrotic pathway triggered by sodium overload, has been implicated in various cellular processes. Its link to lung adenocarcinoma (LUAD) remained unexplored; this study investigated the potential relationship between NECSO and LUAD. Methods: We interrogated the interplay between LUAD and NECSO through an integrated multi-omics workflow. First, RNA sequencing (RNA-seq) expression profiles, paired clinical annotations, and somatic mutation data were retrieved from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) and harmonized within R v4.4.1. NECSO-related genes were then mined via co-expression analysis anchored to transient receptor potential melastatin 4 (TRPM4), the established gatekeeper of NECSO. Functional implications were delineated by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Subsequently, a prognostic risk-score model was constructed from survival-associated candidates and rigorously validated through Kaplan-Meier survival analysis, receiver operating characteristic (ROC) assessment, and calibration curves. Finally, we performed immune cell infiltration and drug sensitivity analyses, thereby completing a coherent pipeline from data integration to clinical translation. Results: Our analyses identified multiple potential NECSO-related genes in LUAD. We developed a prognostic model with 10 predictive genes ( Conclusions: This study elucidated the potential mechanisms of NECSO in LUAD and established an effective prognostic model, offering novel insights for the diagnosis and treatment of LUAD.
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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 OpenQuestion graph.