ReviewMolecular cancer2026
Tumor microenvironment dynamics in gastric cancer pathogenesis and therapeutic resistance.
Review in Molecular cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Single-Cell Transcriptomic Analysis Identifies an OLFM4-Associated Gastric Cancer Cell State with Palmitoylation-Related Signatures and Altered Metabolic Activities.Biomolecules · 2026Article
- Multi-omics exploration of hypoxia in gastric cancer.World journal of surgical oncology · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer remains a significant global health challenge due to its high incidence and mortality, and limited treatment options in advanced stages. Notably, gastric cancer exhibits a complex tumor microenvironment (TME) with substantial cellular and spatial heterogeneity, which profoundly impacts disease pathogenesis and therapeutic resistance. Genetic mutations and chronic inflammation contribute to its development by promoting abnormal cell proliferation and creating an immunosuppressive TME. The TME comprises various cellular and acellular components—including tumor-infiltrating lymphocytes, myeloid lineage cells such as tumor-associated macrophages and myeloid-derived suppressor cells, cancer-associated fibroblasts, extracellular matrix, and peripheral nerves—that interact with cancer cells, influencing tumor initiation, progression, immune evasion, and resistance to therapy. These elements modulate immune responses, remodel the extracellular matrix, and facilitate tumor growth and metastasis, thereby adding to the complexity of the TME. Moreover, the TME plays a critical role in therapeutic resistance through mechanisms involving angiogenesis, fibrosis, and metabolic reprogramming. Understanding the dynamic interactions within the TME offers opportunities to develop novel therapeutic strategies. Emerging approaches targeting the TME—including modulation of immune components, inhibition of fibrosis, normalization of angiogenesis, and disruption of metabolic pathways—hold promise in overcoming therapeutic resistance. Advances in technologies such as single-cell sequencing and spatial transcriptomics further enhance our understanding of TME heterogeneity, paving the way for personalized medicine in gastric cancer treatment. This review summarized the current knowledge of the cellular and molecular composition of the TME of gastric cancer, its role in disease pathogenesis and therapy resistance, and explores potential therapeutic strategies targeting TME components.
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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 Socratic graph.