ReviewMolecular oncology2017
New insights into the role of EMT in tumor immune escape.
Review in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 285 papers, 1 of them a synthesis that pooled it.
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
285 citing papers in PubMed, 1 synthesis or guideline pooled it, 412 citations in OpenAlex.
- Immunotherapy in Esophagogastric Cancer: Treatment Landscape, Challenges, and New Directions.Journal of gastrointestinal cancer · 2024Pooled it
- The ARTEMIS trial identifies immune activation as a key predictor of neoadjuvant chemotherapy response in triple-negative breast cancer.Breast cancer research : BCR · 2026Trial
- Pembrolizumab plus chemotherapy in frontline treatment of advanced ovarian cancer: Clinical and translational results from a phase 2 trial.Med (New York, N.Y.) · 2025Trial
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
- Alzheimer's disease through the lens of mesenchymal drift: the collapse of cellular identity.BMB reports · 2026Review
- Adaptive epithelial-mesenchymal bi-directional transition: A key invasive plasticity for tumor metastasis.iScience · 2026Review
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Evaluation of Serum HIF-1α as a Hypoxia-Related Biomarker in Patients with Malignant Salivary Gland Neoplasms.Biomedicines · 2026Article
- Epithelial-mesenchymal transition is associated with altered immune composition and cytotoxic function in triple-negative breast cancer.Breast cancer research : BCR · 2026Article
- Aging increases ovarian cancer growth, metastasis, and immunosuppression that can be alleviated by inhibiting hedgehog signaling.bioRxiv : the preprint server for biology · 2026Article
- Epithelial-Mesenchymal Plasticity in Cancer: Transcriptional Regulation, Biomarker Challenges, and Emerging Therapeutic Opportunities.Cell biochemistry and function · 2026Review
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Epithelial-mesenchymal transition and immunosuppression: Two sides of the same coin.Cellular and molecular life sciences : CMLS · 2026Review
- CD4+ T Cells Sensitize Quasimesenchymal Breast Tumors Lacking CD73 to Anti-CTLA4 Immune Checkpoint Blockade Therapy.Cancer research communications · 2026Article
- Unveiling LAIR1: a prognostic biomarker associated with gastric cancer progression and metastasis.Translational cancer research · 2026Article
- MFAP2 promotes metastasis and drug resistance by regulating epithelial-to-mesenchymal transition through EGFR signaling pathway in colorectal cancer cells.Genes & diseases · 2026Article
- TBX20 regulates epithelial-mesenchymal transition, maintains tumor stemness and immune factor expression, and promotes immune escape in lung cancer.Oncology letters · 2026Article
- Single-cell and spatial transcriptome analysis reveals the potential therapeutic targets for testicular sex cord-stromal cell tumor.Biomarker research · 2026Article
- Integrative bioinformatics and molecular simulations identify HMGB3 as a key immune modulator in triple negative breast cancer.Discover oncology · 2026Article
- Article
225 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
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Novel immunotherapy approaches have provided durable remission in a significant number of cancer patients with cancers previously considered rapidly lethal. Nonetheless, the high degree of nonresponders, and in some cases the emergence of resistance in patients who do initially respond, represents a significant challenge in the field of cancer immunotherapy. These issues prompt much more extensive studies to better understand how cancer cells escape immune surveillance and resist immune attacks. Here, we review the current knowledge of how cellular heterogeneity and plasticity could be involved in shaping the tumor microenvironment (TME) and in controlling antitumor immunity. Indeed, recent findings have led to increased interest in the mechanisms by which cancer cells undergoing epithelial-mesenchymal transition (EMT), or oscillating within the EMT spectrum, might contribute to immune escape through multiple routes. This includes shaping of the TME and decreased susceptibility to immune effector cells. Although much remains to be learned on the mechanisms at play, cancer cell clones with mesenchymal features emerging from the TME seem to be primed to face immune attacks by specialized killer cells of the immune system, the natural killer cells, and the cytotoxic T lymphocytes. Recent studies investigating patient tumors have suggested EMT as a candidate predictive marker to be explored for immunotherapy outcome. Promising data also exist on the potential utility of targeting these cancer cell populations to at least partly overcome such resistance. Research is now underway which may lead to considerable progress in optimization of treatments.
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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.