ArticleDiscover oncology2025
Tumor microenvironment and drug resistance in lung adenocarcinoma: molecular mechanisms, prognostic implications, and therapeutic strategies.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Metabolic signature of phosphoethanolamine and arginine pathways predicts prognosis and immunotherapy resistance in lung adenocarcinoma.Translational cancer research · 2026Article
- Integrative In Silico Identification of TP53-Associated Drug Repurposing Candidates in Lung Adenocarcinoma.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The tumor microenvironment in lung cancer: Heterogeneity, therapeutic resistance and emerging treatment strategies (Review).International journal of oncology · 2026Review
- Inflammatory cytokine-associated cisplatin resistance in non-small cell lung cancer and re-sensitization through interleukin-6 receptor blockade.World journal of clinical oncology · 2025Article
- Construction and validation of a lung adenocarcinoma prognostic model based on neutrophil extracellular traps and oxidative stress-related genes.European journal of medical research · 2025Article
- NK cell-related genes-driven novel molecular subtyping and prognostic signatures for Wilms tumor: uncovering the therapeutic potential of TGX-221 and biomarker role of HS2ST1.Frontiers in oncology · 2025Article
- Integrating Bulk RNA and Single-cell transcriptome to explore the role of glycan-related genes in lung adenocarcinoma.Journal of Cancer · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fight against lung adenocarcinoma (LUAD) is challenged by tumor microenvironment (TME)-mediated drug resistance, which limits effective treatment. This study examines the LUAD TME and identifies four distinct subtypes through multi-omics profiling: immune-rich, immune-exhausted, stromal-dominant, and TME-desert. Each subtype has unique molecular features, tumor diversity, and links to clinical outcomes. Immune-rich subtypes respond better to immune checkpoint inhibitors, while stromal-dominant and TME-desert subtypes show resistance to treatment and poor prognosis. Molecular analysis uncovers subtype-specific mutations, chromosomal instability, and altered signaling pathways, pointing to potential therapeutic targets. In silico drug screening identifies promising treatments for resistant subtypes. These findings, validated in independent cohorts, highlight the critical role of the TME in drug resistance and treatment response, providing insights for personalized treatment strategies in 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.