ArticleScientific reports2026
Identification and validation of prognostic genes associated with integrative stress response in lung adenocarcinoma and construction of the risk models.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
Integrated stress response (ISR) genes are implicated in lung adenocarcinoma (LUAD) prognosis, but their clinical utility remains unexplored. This study aims to identify ISR-related prognostic genes and construct a risk model for LUAD survival prediction. LUAD transcriptomic and clinical data were retrieved from public databases. ISR-related genes (ISR-RGs) were screened via differential expression and regression analysis. A risk model and a nomogram integrating clinical indicators were built and validated. Functional enrichment, immune cell infiltration, and RT-qPCR in clinical samples were performed. Five prognostic genes (AGER, GPX3, CCNA2, KCNK3, and CHEK1) were identified. High-risk patients exhibited poorer survival. The nomogram was able to forecast the survival of LUAD well. Genes were functionally linked to cell cycle and DNA replication and correlated with immune cells (e.g., CCNA2 positively with CD4⁺ T cells [cor = 0.52]; CHEK1 negatively with memory B cells [cor = - 0.40]). RT-qPCR confirmed dysregulation: AGER, GPX3, and KCNK3 downregulated and CHEK1 and CCNA2 upregulated versus controls. The five prognostic genes pertinent to both LUAD and ISR were identified, and a risk model was constructed for the good prediction of LUAD survival, which offered a fresh outlook for alleviating the poor prognosis of LUAD.
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.