Vertaisarvioitu katsausartikkeli tieteellisessä aikakauslehdessä (A2)

Newly identified form of phenotypic plasticity of cancer: immunogenic mimicry




Julkaisun tekijätTima Jozsef, Honn Kenneth V., Hendrix Mary J. C., Marko-Varga Gyorgy, Jalkanen Sirpa

KustantajaSPRINGER

Julkaisuvuosi2023

JournalCancer and Metastasis Reviews

Tietokannassa oleva lehden nimiCANCER AND METASTASIS REVIEWS

Lehden akronyymiCANCER METAST REV

Volyymi42

Julkaisunumero1

Aloitussivu323

Lopetussivun numero334

Sivujen määrä12

ISSN0167-7659

eISSN1573-7233

DOIhttp://dx.doi.org/10.1007/s10555-023-10087-1

Verkko-osoitehttps://link.springer.com/article/10.1007/s10555-023-10087-1

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/178990215


Tiivistelmä

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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Last updated on 2023-31-03 at 15:31