ReviewMedical oncology (Northwood, London, England)2025
Contribution of tumor microenvironment (TME) to tumor apoptosis, angiogenesis, metastasis, and drug resistance.
Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
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- RNF research trends and an RNF43-based prognostic model for colorectal cancer with immune microenvironment analysis.Discover oncology · 2026Article
- ViMST: vision transformer-based dual modality multi-task graph contrastive network for spatial transcriptomics microenvironments investigation.BMC biology · 2026Article
- 1,5-Disubstituted Tetrazoles as Promising Anticancer Resistance Agents: A Chemoinformatic Characterization.ACS omega · 2026Article
- Polymeric Nano Drug Delivery Systems for Overcoming Tumor Microenvironment-Mediated Drug Resistance.Pharmaceutics · 2026Review
- Digital Pathology and the AI-Based Quantification of the Tumor Microenvironment in Gastrointestinal Cancer: From Tumor Budding and Tumor-Infiltrating Lymphocytes to Tertiary Lymphoid Structures.International journal of molecular sciences · 2026Review
- Co-Delivery of Glucose Oxidase and Iron-Doped ZIF-8 as a pH-Responsive Ferroptosis and Starvation Agent for Triple-Negative Breast Cancer Therapy.Nanomaterials (Basel, Switzerland) · 2026Article
- The interplay between autophagy and immunogenic cell death: nanomaterial-based strategies for cancer immunotherapy.Journal of nanobiotechnology · 2026Review
- Review
- Nanomedicine-based lactate metabolism and lactylation regulation for exploring new therapeutic strategies in cancer.Materials today. Bio · 2026Review
- Research Progress on Anticancer Mechanism of Ginsenoside Regulating Tumor Microenvironment.Current issues in molecular biology · 2026Review
- ARNTL deregulation promotes ovarian cancer progression and metastasis by activating cancer-associated fibroblasts.Journal of ovarian research · 2026Article
- Cytoplasmic LIM domain only 2 enhances tumor endothelial cell migration through integrin β1-mediated focal adhesion signaling.Acta neuropathologica communications · 2026Article
- Insights into oncovirus-driven tumor dynamics: a perspective from intravital imaging.Frontiers in cell and developmental biology · 2026Review
- The Prospects of Palmitylethanolamide in Tumor Prevention and Treatment.Journal of inflammation research · 2026Review
- The mechanism of lncRNA PVT1 in oral squamous cell carcinoma.Frontiers in oncology · 2026Review
- CAF-derived exosomes: orchestrators of dysregulated signaling pathways in breast cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer.Iranian journal of basic medical sciences · 2026Review
- Evaluation of ARHGAP26 expression, prognostic significance, and immune infiltration in clear cell renal cell carcinoma.Journal, genetic engineering & biotechnology · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) contains tumor cells, surrounding cells, and secreted factors. It provides a favorable environment for the maintenance of cancer stem cells (CSCs), the spread of cancer cells to metastatic sites, angiogenesis, and apoptosis, as well as the growth, proliferation, invasion, and drug resistance of cancer cells. Cancer cells rely on the activation of oncogenes, inactivation of tumor suppressors, and the support of a normal stroma for their growth, proliferation, and survival, all of which are provided by the TME. The TME is characterized by the presence of various cells, including cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), CD8 + cytotoxic T cells (CTLs), regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), mesenchymal stem cells (MSCs), endothelial cells, adipocytes, and neuroendocrine (NE) cells. The high expression of inflammatory cytokines, angiogenic factors, and anti-apoptotic factors, as well as drug resistance mechanisms in the TME, contributes to the poor therapeutic efficacy of anticancer drugs and tumor progression. Hence, this review describes the mechanisms through which the TME is involved in apoptosis, angiogenesis, metastasis, and drug resistance in tumor cells.
Indexed as
Identifiers
40087196What 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.