Vertaisarvioitu katsausartikkeli tieteellisessä aikakauslehdessä (A2)
Newly identified form of phenotypic plasticity of cancer: immunogenic mimicry
Julkaisun tekijät: Tima Jozsef, Honn Kenneth V., Hendrix Mary J. C., Marko-Varga Gyorgy, Jalkanen Sirpa
Kustantaja: SPRINGER
Julkaisuvuosi: 2023
Journal: Cancer and Metastasis Reviews
Tietokannassa oleva lehden nimi: CANCER AND METASTASIS REVIEWS
Lehden akronyymi: CANCER METAST REV
Volyymi: 42
Julkaisunumero: 1
Aloitussivu: 323
Lopetussivun numero: 334
Sivujen määrä: 12
ISSN: 0167-7659
eISSN: 1573-7233
DOI: http://dx.doi.org/10.1007/s10555-023-10087-1
Verkko-osoite: https://link.springer.com/article/10.1007/s10555-023-10087-1
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/178990215
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.
Ladattava julkaisu This is an electronic reprint of the original article. |