Please use this identifier to cite or link to this item: https://doi.org/10.1186/s13045-019-0814-6
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dc.titleEZH2 abnormalities in lymphoid malignancies: Underlying mechanisms and therapeutic implications
dc.contributor.authorLi, B.
dc.contributor.authorChng, W.-J.
dc.date.accessioned2021-12-16T07:46:04Z
dc.date.available2021-12-16T07:46:04Z
dc.date.issued2019
dc.identifier.citationLi, B., Chng, W.-J. (2019). EZH2 abnormalities in lymphoid malignancies: Underlying mechanisms and therapeutic implications. Journal of Hematology and Oncology 12 (1) : 118. ScholarBank@NUS Repository. https://doi.org/10.1186/s13045-019-0814-6
dc.identifier.issn17568722
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/210718
dc.description.abstractEZH2 is the catalytic subunit of the polycomb repressive complex 2 (PRC2), which along with other PRC2 components mediates gene expression suppression via the methylation of Histone H3 at lysine 27. Recent studies have revealed a dichotomous role of EZH2 in physiology and in the pathogenesis of cancer. While it plays an essential role in the development of the lymphoid system, its deregulation, whether due to genetic or non-genetic causes, promotes B cell-and T cell-related lymphoma or leukemia. These findings triggered a boom in the development of therapeutic EZH2 inhibitors in recent years. Here, we discuss physiologic and pathogenic function of EZH2 in lymphoid context, various internal causes of EZH2 aberrance and how EZH2 modulates lymphomagenesis through epigenetic silencing, post-translational modifications (PTMs), orchestrating with surrounding tumor micro-environment and associating with RNA or viral partners. We also summarize different strategies to directly inhibit PRC2-EZH2 or to intervene EZH2 upstream signaling. © 2019 The Author(s).
dc.publisherBioMed Central Ltd.
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2019
dc.subjectB cell
dc.subjectEBV
dc.subjectEZH2
dc.subjectEZH2 inhibitor
dc.subjectLymphoid malignancies
dc.subjectLymphoma
dc.subjectT cell
dc.typeReview
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentMEDICINE
dc.description.doi10.1186/s13045-019-0814-6
dc.description.sourcetitleJournal of Hematology and Oncology
dc.description.volume12
dc.description.issue1
dc.description.page118
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