Phenotypic plasticity and immunogenic mimicry of cancer

Tímár József (1), Kenneth V. Honn (2), Mary J. C. Hendrix (3), Marko-Varga György (4), Sirpa Jalkanen (5)
(1) Semmelweis Egyetem, Patológiai, Igazságügyi és Biztosításorvostani Intézete, Budapest
(2) Wayne State University, Detroit, MI
(3) Sepherd University, Sepherdtown, WV
(4) Lund University, Lund, Svédország
(5) University of Turku, Turku, Finnország

It is a newly recognized hallmark of cancer, the phenotypic plasticity comprising of (epithelial) mesenchymal transition, vasculogenic- and megakariocytic mimicries. It is well known that immune escape of cancers may relay on the ectopic expression of PDL1 (or CTLA4). Recently we have found in melanoma lung metastases the serial amplification of immune cell genes and consequent protein expressions. Systematic analysis of the literature revealed documentation of ectopic expressions of 26 immune cell genes in tumor cells of various cancer types, which was termed immunogenic mimicry. Most of these genes are regulated by IFN and are involved in immune checkpoint regulation. The clinical potential of these mimicry genes can be demonstrated not only by the success of immunoncology drugs registered recently but also by the new trials where the targets are mimicry genes such as CD27, CD47, CD166, CD172 or IDO.

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