KMT2A is a prerequisite of malignant transformation during IDH-mutant gliomagenesis
Disrupting KMT2A-mediated H3K4me3 reshapes the epigenome and attenuates LGG-relevant programs and phenotypes in vitro, supporting a strong role in tumor initiation. In vivo, the TS603 survival result highlights context-dependent maintenance and motivates cautious, microenvironment-aware therapeutic exploration of the KMT2A axis and downstream targets such as SCD.
Authors
- Marilin Koch (ORCID: https://orcid.org/0000-0002-8335-3543)
- Şevin Turcan (ORCID: https://orcid.org/0000-0002-0885-5607)
- Michael S. Hoetker (ORCID: https://orcid.org/0000-0001-8784-8263)
- Julián Taranda (ORCID: https://orcid.org/0000-0002-2948-2133)
- Claudia Schmidt (ORCID: https://orcid.org/0000-0001-8532-2604)
- Minh Deo
- Adrianna Podolak
Institutions
- German Cancer Research Center (DE)
- Heidelberg University (DE)
- University Hospital Heidelberg (DE)
- National Center for Tumor Diseases (DE)
Publication Details
- Journal
- Neuro-Oncology
- Published
- 2026-01-13
- DOI
- https://doi.org/10.1093/neuonc/noag006
- Primary Topic
- Glioma Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00