ArticleHereditas2026
TLE1 as a key regulator of osimertinib resistance and EMT in lung adenocarcinoma: implications for prognosis and immunotherapy response.
Article in Hereditas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- 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
6 authors.
Funding
Abstract
backgroundAcquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) poses a considerable challenge for the long-term treatment of non-small cell lung cancer (NSCLC). This study aims to identify a novel biomarker associated with osimertinib resistance and explore its role in EGFR-TKI resistance in lung adenocarcinoma (LUAD).
methodsComprehensive bioinformatics analysis were done using transcriptomic data from the TCGA and GEO databases to identify genes associated with osimertinib tolerance. Candidate genes were further screened against a histone modification-related gene set from MSigDB, leading to the identification of TLE1. The hub gene, TLE1, was further evaluated through survival analysis, GSEA and CIBERSORT analyses. Loss-of-function experiments performed in vitro were utilized to assess the impact of TLE1 on osimertinib resistance in LUAD.
resultsTLE1 was of particularly noteworthy, exhibiting elevated expression in LUAD, especially in stage IV patients, and was associated with poor prognosis. GSEA results showed that mTOR, VEGF and HIF-1 signaling pathways were notably activated in the high TLE1 expression group. CIBERSORT analysis markedly elevated levels of regulatory T cells (Tregs) in the TLE1 high expression group. Additionally, epithelial-mesenchymal transition (EMT) scores were significantly elevated in osimertinib tolerant groups and exhibited a positive correlation with TLE1 expression. Furthermore, TLE1 expression was significantly higher in osimertinib-resistant PC9 cells compared to parental PC9 cells. Downregulation of TLE1 enhanced the sensitivity of osimertinib-resistant PC9 cells to osimertinib.
conclusionsTLE1 was identified as a critical gene associated with osimertinib tolerance, influencing LUAD progression, potentially serving as a novel therapeutic target. CLINICAL TRIAL NUMBER: Not applicable.
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.