Pharmacologic and Oncohistone Inhibition of SETD2 Converge on Genomic Instability
Pharmacologic inhibition and oncohistone-mediated sequestration of SETD2 converge on the induction of mitotic defects, underscoring SETD2's essential role in maintaining genomic stability. Identification of loss of genomic stability as a canonical feature of SETD2 inactivation points to a potential therapeutic liability associated with targeting SETD2 in cancers where it is overexpressed and reveals a mechanism that could contribute to the progression of cancers expressing oncohistone mutations.
Authors
- Edward W. Pietryk (ORCID: https://orcid.org/0000-0003-1563-0219)
- Ashley Boice
- Cristian Coarfa (ORCID: https://orcid.org/0000-0002-4183-4939)
- Frank M. Mason (ORCID: https://orcid.org/0000-0003-1338-494X)
- Ian J. Frew (ORCID: https://orcid.org/0000-0003-2735-5509)
- Durga Nand Tripathi
- Rajkishor Nishad
- Ruhee Dere
- H. Josh Jang
- Seth A. Nelson
- W. Kimryn Rathmell
- Alyssa T. Paparella
- Cheryl Lyn Walker
- In Young Park
Institutions
- Van Andel Institute (US)
- University of Freiburg (DE)
- Baylor College of Medicine (US)
- The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (US)
- University Medical Center Freiburg (DE)
- Vanderbilt University Medical Center (US)
Publication Details
- Journal
- Cancers
- Published
- 2026-03-03
- DOI
- https://doi.org/10.3390/cancers18050819
- Primary Topic
- Epigenetics and DNA Methylation
- Type
- article
- Field-Weighted Citation Impact
- 0.00