Newly identified form of phenotypic plasticity of cancer: immunogenic mimicry

Cancer and Metastasis Reviews - Tập 42 - Trang 323-334 - 2023
József Tímár1, Kenneth V. Honn2,3, Mary J. C. Hendrix4, György Marko-Varga5, Sirpa Jalkanen6,7
1Department of Pathology, Forensic and Insurance Medicine, Semmelweis University, Budapest, Hungary
2Departments of Pathology, Oncology and Chemistry, Wayne State University, Detroit, USA
3Barbara Ann Karmanos Cancer Institute, Detroit, USA
4Department of Biology, Shepherd University, Shepherdstown, USA
5Clinical Protein Science and Imaging, Biomedical Centre, Department of Biomedical Engineering, Lund University, Lund, Sweden
6Medicity Research Laboratories, Turku/Finland
7InFLAMES Flagship, University of Turku, Turku, Finland

Tóm tắt

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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