ArticleThe oncologist2025
Integrative multiomic and immune profiling of lung adenocarcinoma: molecular landscapes, gene expression, and treatment response insights.
Article in The oncologist, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 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
3 citing papers in PubMed.
- Characterizing ex vivo models for studying lipid metabolism in triple negative breast cancer.Journal of lipid research · 2026Article
- Decades of omics in lung cancer research: a bibliometric analysis and visualization from 2004 to 2024.Journal of thoracic disease · 2026Article
- The multifaceted roles of microRNAs in nonalcoholic steatohepatitis: from pathogenic mechanisms to diagnostic and therapeutic opportunities.Frontiers in genetics · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
backgroundLung adenocarcinoma (LUAD) is a major cause of cancer death. Traditional histopathological classification overlooks molecular heterogeneity, limiting personalized treatment. This study used multiomic data to define LUAD subtypes, assess prognostic significance, and analyze immune features, aiming to improve targeted therapy and clinical outcomes.
methodsThis study used Consensus Clustering and Gap Statistics to analyze LUAD multiomic data, including mRNA, lncRNA, miRNA, DNA methylation, and mutations. Clustering was validated by silhouette plots and heatmaps. Molecular characterization involved regulon activity, immune and metabolic profiling. Functional assays (qPCR, WB, CCK-8, flow cytometry) assessed neuronal differentiation factor (NDNF)'s role in LUAD.
resultsTwo molecular LUAD subtypes showed distinct clustering and survival outcomes. One subtype had worse prognosis and unique immune features, including checkpoint expression and microenvironment differences. Gene signatures and metabolism varied by subtype. Neuronal differentiation factor was downregulated in tumors; its overexpression suppressed LUAD cell viability and promoted apoptosis, suggesting tumor-suppressive function.
conclusionsThis study identifies 2 LUAD subtypes with distinct molecular and immune features linked to prognosis and therapy response. Neuronal differentiation factor downregulation and its tumor-suppressive effects highlight its therapeutic potential. These findings support improved LUAD stratification and personalized treatment strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.