Newly identified form of phenotypic plasticity of cancer : immunogenic mimicry
(2023) In Cancer and Metastasis Reviews 42(1). p.323-334- Abstract
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... (More)
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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- author
- Tímár, József ; Honn, Kenneth V. ; Hendrix, Mary J.C. ; Marko-Varga, György LU and Jalkanen, Sirpa
- organization
- publishing date
- 2023
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Cancer plasticity, Epithelial mesenchymal transition, Immunogenic mimicry, Megakaryocytic mimicry, Vasculogenic mimicry
- in
- Cancer and Metastasis Reviews
- volume
- 42
- issue
- 1
- pages
- 323 - 334
- publisher
- Springer
- external identifiers
-
- scopus:85147719051
- pmid:36754910
- ISSN
- 0167-7659
- DOI
- 10.1007/s10555-023-10087-1
- language
- English
- LU publication?
- yes
- id
- df39026e-3619-4cc4-aa04-dd742d72b6ef
- date added to LUP
- 2023-02-23 15:48:58
- date last changed
- 2024-06-14 00:14:37
@article{df39026e-3619-4cc4-aa04-dd742d72b6ef,
abstract = {{<p>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.</p>}},
author = {{Tímár, József and Honn, Kenneth V. and Hendrix, Mary J.C. and Marko-Varga, György and Jalkanen, Sirpa}},
issn = {{0167-7659}},
keywords = {{Cancer plasticity; Epithelial mesenchymal transition; Immunogenic mimicry; Megakaryocytic mimicry; Vasculogenic mimicry}},
language = {{eng}},
number = {{1}},
pages = {{323--334}},
publisher = {{Springer}},
series = {{Cancer and Metastasis Reviews}},
title = {{Newly identified form of phenotypic plasticity of cancer : immunogenic mimicry}},
url = {{http://dx.doi.org/10.1007/s10555-023-10087-1}},
doi = {{10.1007/s10555-023-10087-1}},
volume = {{42}},
year = {{2023}},
}