ReviewDiscover oncology2026
Role of tumor microenvironment in regulator of tumor progression and immunotherapy.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Radiomic analysis of the peritumoral zone identifies imaging signatures of glioma invasion associated with HSP70 expression.Frontiers in 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) is a pivotal regulator of carcinogenesis, progression, and therapeutic response. This complex niche, comprised of immune cells, cancer-associated fibroblasts, extracellular matrix, and signaling molecules, fosters immunosuppression and facilitates immune evasion through the recruitment and activation of cells like tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). A key mechanism of this evasion is the expression of immune checkpoint molecules, including PD-1(programmed death receptor-1)/PD-L1(programmed death ligand-1) and CTLA-4, which inhibit anti-tumor immunity. Although immune checkpoint inhibitors have demonstrated remarkable clinical success, their efficacy is variable and often hampered by the high heterogeneity and adaptive resistance of the TME. Emerging strategies, such as targeting metabolic pathways, gut microbiota, and employing combination therapies, are being explored to reprogram the TME and overcome resistance. This review comprehensively outlines the composition of the TME, its role in driving tumor progression and immunotherapy response, and discusses future directions, emphasizing that a deeper understanding of the TME is essential for developing novel and personalized cancer immunotherapies.
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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.