AI Article Synopsis
- - The enhancer of zeste inhibitory protein (EZHIP) plays a role in germ cell development and is recognized as a cancer-testis antigen (CTA) in various cancers, including diffuse midline gliomas (DMGs), where 4% show aberrant expression.
- - Both EZHIP and the H3 K27M mutation—common in DMGs—act as negative regulators of the polycomb repressive complex 2 (PRC2), causing significant changes in the genome's epigenetic regulation.
- - This opinion piece discusses the similarities and differences between EZHIP-DMGs and H3K27M-DMGs, examining their PRC2 inhibition, genetic landscapes, potential cell origins, and future research
Article Abstract
The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy.
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| http://dx.doi.org/10.1016/j.trecan.2024.09.002 | DOI Listing |
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