ReviewMedComm2025
Polarization of Tumor Cells and Tumor-Associated Macrophages: Molecular Mechanisms and Therapeutic Targets.
Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Modulation of Antitumor Immunity and the Tumor Microenvironment byInternational journal of molecular sciences · 2026Review
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Monocarboxylate Transporter 2 (MCT2) Reduction Is Associated with Increased Lung Tumor Growth and Alterations in the Immune Microenvironment in a Subcutaneous Tumor Model.International journal of molecular sciences · 2026Article
- SMAD7-Associated Glycolytic Regulation Promotes Lactate-Dependent Macrophage Phenotype Modulation in Colorectal Cancer.Cancers · 2026Article
- Review
- Review
- Molecular Insights and Novel Therapies for Lymphoproliferative Disorders.International journal of molecular sciences · 2026Review
- Leveraging Macrophage Metabolic Reprogramming for Enhanced Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- SLAMF8 promotes tumor growth of gastric cancer by enhancing M2 polarization of tumor-associated macrophages.Journal of translational medicine · 2026Article
- Metabolic pattern changes of macrophages during cancer development and progression.Journal of translational medicine · 2026Review
- The promising role of cathepsins as biomarkers and therapeutic targets in glioblastoma.Discover oncology · 2026Review
- Optimizing next-generation CAR-macrophages against solid tumors: challenges and potential strategies.Journal of hematology & oncology · 2026Review
- HOXD13-mediated immune crosstalk between cancer cells and tumor-associated macrophages drives colorectal cancer progression.Journal for immunotherapy of cancer · 2026Article
- Immune and Tumor Microenvironment Mechanisms ofCancers · 2026Review
- Review
- Nanomedicines Reshape the Tumor Microenvironment: Multidimensional Strategies from Modulating "Barriers" to Metabolic Intervention.International journal of nanomedicine · 2026Review
- Macrophage-based therapeutic strategies in glioblastoma: advancements in drug delivery and immunotherapy.Frontiers in oncology · 2026Review
- The link between macrophage polarization and response to radiotherapy in cancers: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Polarization of Tumor Cells and Tumor-Associated Macrophages: Molecular Mechanisms and Therapeutic Targets.MedComm · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages (TAMs) are prominent constituents of solid tumors, and their prevalence is often associated with poor clinical outcomes. These highly adaptable immune cells undergo dynamic functional changes within the immunosuppressive tumor microenvironment (TME), engaging in reciprocal interactions with malignant cells. This bidirectional communication facilitates concurrent phenotypic transformation: tumor cells shift toward invasive mesenchymal states, whereas TAMs develop immunosuppressive, pro-tumorigenic traits. Increasing evidence highlights metabolic reprogramming, characterized by dysregulation of lipid metabolism, amino acid utilization, and glycolytic activity, as the fundamental molecular basis orchestrating this pathological symbiosis. However, a comprehensive understanding of how metabolic reprogramming specifically coordinates the mutual polarization of tumor cells and TAMs is lacking. This review thoroughly examines the molecular mechanisms governing this co-polarization process, detailing critical transcriptional regulators, essential signaling pathways, and the maintenance of adaptive phenotypes within the TME. Furthermore, this review critically assesses promising therapeutic strategies aimed at disrupting this alliance, including the use of metabolically targeted agents, engineered chimeric antigen receptor macrophages, and TAM-selective nanoparticle delivery systems. These insights provide a crucial foundation for the development of next-generation cancer immunotherapies focused on reprogramming pathological polarization dynamics to overcome treatment resistance and improve clinical outcomes.
Indexed as
Identifiers
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.