ArticleNature communications2019
Epithelial tumor suppressor ELF3 is a lineage-specific amplified oncogene in lung adenocarcinoma.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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
46 citing papers in PubMed, 70 citations in OpenAlex.
- From Glycan Biology to Drug Candidates: An Integrated Sialylation Niche Index and AI-Guided Therapeutic Framework for Head and Neck Squamous Cell Carcinoma.Biomedicines · 2026Article
- Discovery of a Small-Molecule Inhibitor Targeting the ELF3-HSP27 Interaction to Suppress Breast Cancer Progression.Pharmaceuticals (Basel, Switzerland) · 2026Article
- A machine learning framework predicts oncogenic driver mutations from SNP profiles in lung adenocarcinoma.Discover oncology · 2026Article
- Exploring phenotype-related single-cells through attention-enhanced representation learning.Genome medicine · 2026Article
- Article
- AI-Guided Chemotherapy Optimization in Lung Cancer Using Genomic and Survival Data.Journal of personalized medicine · 2025Article
- PRSS3 is a potential prognostic biomarker for lung adenocarcinoma.Translational cancer research · 2025Article
- TNBC response to paclitaxel phenocopies interferon response which reveals cell cycle-associated resistance mechanisms.Scientific reports · 2025Article
- ETS Family Transcription Factors in Gastric Cancer and the Role of ELF3 in the Core Metaplasia Transcription Factor Network.Oncology research · 2025Article
- Overexpression of ELF3 in the PTEN-deficient lung epithelium promotes lung cancer development by inhibiting ferroptosis.Cell death & disease · 2024Article
- Hypomethylation-associated ELF3 helps nasopharyngeal carcinoma to escape immune surveillance via MUC16-mediated glycolytic metabolic reprogramming.American journal of physiology. Cell physiology · 2024Article
- Post-Transcriptional Modifications to miRNAs Undergo Widespread Alterations, Creating a Unique Lung Adenocarcinoma IsomiRome.Cancers · 2024Article
- High-throughput characterization of functional variants highlights heterogeneity and polygenicity underlying lung cancer susceptibility.American journal of human genetics · 2024Article
- TNBC response to paclitaxel phenocopies interferon response which reveals cell cycle-associated resistance mechanisms.bioRxiv : the preprint server for biology · 2024Article
- Switch of ELF3 and ATF4 transcriptional axis programs the amino acid insufficiency-linked epithelial-to-mesenchymal transition.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- DeepGRNCS: deep learning-based framework for jointly inferring gene regulatory networks across cell subpopulations.Briefings in bioinformatics · 2024Article
- Decoding the basis of histological variation in human cancer.Nature reviews. Cancer · 2024Review
- Huaier suppresses cell viability, migration and invasion in human non-small cell lung cancer via lncRNA DLEU2/miR-212-5p/ELF3 axis.International journal of medical sciences · 2024Article
- Actionable Driver Events in Small Cell Lung Cancer.International journal of molecular sciences · 2023Review
- Methionine-producing tumor micro(be) environment fuels growth of solid tumors.Cellular oncology (Dordrecht, Netherlands) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 7 institutions in 2 countries.
Funding
Abstract
Gene function in cancer is often cell type-specific. The epithelial cell-specific transcription factor ELF3 is a documented tumor suppressor in many epithelial tumors yet displays oncogenic properties in others. Here, we show that ELF3 is an oncogene in the adenocarcinoma subtype of lung cancer (LUAD), providing genetic, functional, and clinical evidence of subtype specificity. We discover a region of focal amplification at chromosome 1q32.1 encompassing the ELF3 locus in LUAD which is absent in the squamous subtype. Gene dosage and promoter hypomethylation affect the locus in up to 80% of LUAD analyzed. ELF3 expression was required for tumor growth and a pan-cancer expression network analysis supports its subtype and tissue specificity. We further show that ELF3 displays strong prognostic value in LUAD but not LUSC. We conclude that, contrary to many other tumors of epithelial origin, ELF3 is an oncogene and putative therapeutic target in 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.