ReviewCell communication and signaling : CCS2025
Unraveling the molecular-pathological characteristics and cellular complexity of the tumor immune microenvironment in metastatic non-small cell lung cancer.
Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Recapitulating In Vivo Pharmacokinetics and Size-Dependent Nanomedicine Delivery in a Microfluidic Platform.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ceramide signaling in non-small-cell lung cancer: from dysregulation to targeted therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Inhalable Therapeutics in Lung Cancer: Overcoming Barriers for Effective Treatment.AAPS PharmSciTech · 2026Review
- Ultrasonication-assisted green synthesis, in silico EGFR-binding analysis, and cytotoxic evaluation of nitro-perimidines for non-small cell lung cancer.Journal of computer-aided molecular design · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Metastatic non-small cell lung cancer (mNSCLC) cells carry heterogeneity, not only among different subtypes but also within a single tumor. Most evidence suggests that mNSCLC exploits specific molecular drivers and mechanisms to maintain physiology, metabolism, and immune evasion during tumorigenesis. Genome-wide association studies also revealed particular mutations in the oncogenic drivers supporting tumor cell proliferation and survival, resulting in aggressive and drug-resistant phenotypes of mNSCLC. While significant progress has been made in understanding mNSCLC at the genetic and molecular levels, a considerable gap remains in understanding the dynamic interplay between intrinsic factors-particularly key tumor-associated cells-and tumor immune microenvironment (TIME) during metastasis. Hence, this review highlights histological and genetic characteristics, emphasizes the clinical relevance of metastasis, and the roles of tumor-associated cells in shaping the immunosuppressive tumor microenvironment (TME) in mNSCLC. Understanding these intricate features and mechanisms is crucial for identifying novel therapeutic targets and improving strategies to combat mNSCLC progression in diagnosed patients.
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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.