ReviewCancer metastasis reviews2023
Newly identified form of phenotypic plasticity of cancer: immunogenic mimicry.
Review in Cancer metastasis reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed.
- Exosome-Mediated Bidirectional Signaling Regulates Glioma Stem-Cell Homeostasis and Radiation-Induced Plasticity.bioRxiv : the preprint server for biology · 2026Article
- EPHB2 drives EMT-linked vasculogenic mimicry and cervical cancer progression via an ERK-ETV4 transcriptional program.Journal of translational medicine · 2026Article
- Multiomics integration of serum proteome and autoantibody profiles reveals diagnostic and prognostic biomarkers in glioma.Journal of neuro-oncology · 2026Article
- Capillary constrictions prime cancer cell tumorigenicity through PIEZO1.Nature communications · 2025Article
- Review
- Knockdown of WISP1/DKK1 restrains phenotypic plasticity in esophageal squamous cell carcinoma by suppressing epithelial-mesenchymal transition and stemness.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Phenotypic Plasticity, Non-genetic Mechanisms, and Immune Drug Resistance in Cancer.Cancer treatment and research · 2025Review
- Identification of genetic fingerprint of type I interferon therapy in visceral metastases of melanoma.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer plasticity is now a recognized new hallmark of cancer which is due to disturbances of cell differentiation programs. It is manifested not only in various forms like the best-known epithelial-mesenchymal transition (EMT) but also in vasculogenic and megakaryocytic mimicries regulated by EMT-specific or less-specific transcription factors such as HIF1a or STAT1/2. Studies in the past decades provided ample data that cancer plasticity can be manifested also in the expression of a vast array of immune cell genes; best-known examples are PDL1/CD274, CD47, or IDO, and we termed it immunogenic mimicry (IGM). However, unlike other types of plasticities which are epigenetically regulated, expression of IGM genes are frequently due to gene amplifications. It is important that the majority of the IGM genes are regulated by interferons (IFNs) suggesting that their protein expressions are regulated by the immune microenvironment. Most of the IGM genes have been shown to be involved in immune escape of cancers broadening the repertoire of these mechanisms and offering novel targets for immunotherapeutics.
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Identifiers
What 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.