ReviewCells2019
The Vicious Cross-Talk between Tumor Cells with an EMT Phenotype and Cells of the Immune System.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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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
64 citing papers in PubMed.
- Epithelial-Mesenchymal Transition, Immune Response, and Extracellular Matrix Remodelling in Oral Cancer.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026Article
- Review
- Targeting Tumour Heterogeneity through sequential timing of anti-hallmark combination therapies -a hypothesis for implementation.Frontiers in immunology · 2026Review
- C5orf46: a promising prognosis risk indicator with implication in the remodeling of KIRC and pan-cancer tumor microenvironments.Frontiers in oncology · 2026Article
- Identification and validation of prognostic genes for lung adenocarcinoma prognosis based on PANoptosis-related genes.Discover oncology · 2025Article
- Oxidative and Glycolytic Metabolism: Their Reciprocal Regulation and Dysregulation in Cancer.Cells · 2025Review
- The role of platelets in tumor immune evasion and metastasis: mechanisms and therapeutic implications.Cancer cell international · 2025Review
- Starfysh integrates spatial transcriptomic and histologic data to reveal heterogeneous tumor-immune hubs.Nature biotechnology · 2025Article
- OTU deubiquitinases in cancer pathogenesis and precision therapy.American journal of cancer research · 2025Review
- Cancer-associated Fibroblasts (CAFs) Regulate Lung Cancer Malignant Progression by Transferring SERPINE2 (PN1) via Exosomes.Current molecular medicine · 2025Article
- Comprehensive Computational Assessment of SNAI1 and SNAI2 in Gastric Cancer: Linking EMT, Tumor Microenvironment, and Survival Outcomes.Cancer informatics · 2025Article
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- Fluorofenidone enhances cisplatin efficacy in non-small cell lung cancer: a novel approach to inhibiting cancer progression.Translational lung cancer research · 2024Article
- Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer Management: Opportunities and Challenges.Biomolecules · 2024Review
- miR-200a-3p promotes the malignancy of endometrial carcinoma through negative regulation of epithelial-mesenchymal transition.Discover oncology · 2024Article
- Tissue factor overexpression promotes resistance to KRAS-G12C inhibition in non-small cell lung cancer.Oncogene · 2024Article
- The synergistic effects of anoikis-related genes and EMT-related genes in the prognostic prediction of Wilms tumor.Frontiers in molecular biosciences · 2024Article
- Role of Histone Deacetylase 6 and Histone Deacetylase 6 Inhibition in Colorectal Cancer.Pharmaceutics · 2023Review
- Cancer CD39 drives metabolic adaption and mal-differentiation of CD4Cell death & disease · 2023Article
- EMT-induced immune evasion: connecting the dots from mechanisms to therapy.Clinical and experimental medicine · 2023Review
4 more citing papers are in PubMed but not listed here.
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
No grant is acknowledged in the PubMed record.
Abstract
Carcinoma cells that undergo an epithelial-mesenchymal transition (EMT) and display a predominantly mesenchymal phenotype (hereafter EMT tumor cells) are associated with immune exclusion and immune deviation in the tumor microenvironment (TME). A large body of evidence has shown that EMT tumor cells and immune cells can reciprocally influence each other, with EMT cells promoting immune exclusion and deviation and immune cells promoting, under certain circumstances, the induction of EMT in tumor cells. This cross-talk between EMT tumor cells and immune cells can occur both between EMT tumor cells and cells of either the native or adaptive immune system. In this article, we review this evidence and the functional consequences of it. We also discuss some recent evidence showing that tumor cells and cells of the immune system respond to similar stimuli, activate the expression of partially overlapping gene sets, and acquire, at least in part, identical functionalities such as migration and invasion. The possible significance of these symmetrical changes in the cross-talk between EMT tumor cells and immune cells is addressed. Eventually, we also discuss possible therapeutic opportunities that may derive from disrupting this cross-talk.
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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.