Newly identified form of phenotypic plasticity of cancer: immunogenic mimicry

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.

Automated summary

Cancer plasticity, characterized by disturbances of cell differentiation programs, is a recognized hallmark of cancer. It includes various forms such as epithelial-mesenchymal transition (EMT), vasculogenic mimicry, and megakaryocytic mimicry. Immunogenic mimicry (IGM), a type of cancer plasticity, involves the expression of immune cell genes regulated by interferons (IFNs), often due to gene amplifications. These IGM genes play a role in immune escape of cancers and offer potential targets for immunotherapeutics.