When: November 25, 2015, 2:00 PM
Location: 3rd Floor Orchard View Room , Discovery Building
Contact: 608-316-4401, email@example.com
Investigating how Histone H3 mutations drive childhood cancers
The establishment of cell type-specific gene expression patterns helps define cell identity during differentiation and development. My research program is rooted in the idea that chromatin, the physiologically relevant form of eukaryotic genomes, contains an indexing system, sometimes referred to as a “histone or epigenetic code”, that represents a fundamental regulatory mechanism that operates outside of the DNA sequence itself. Covalent modifications to DNA and histones – the proteins that package our genome – are implicated in the epigenetic regulation of gene expression and the stable maintenance of cell type-specific gene expression patterns and cellular identity. A growing literature points to altered chromatin structure as a previously unsuspected driver of many human cancers. Very recently, a remarkably high frequency of pediatric gliomas and bone tumors were reported to harbor monoallelic, gain-of-function mutations in genes encoding histone H3. These high frequency mutant histones (collectively referred to as ‘oncohistones’) are suspected drivers of specific types of human cancer. I will discuss our recent work to characterize how oncohistones perturb cellular differentiation through inhibition of specific chromatin-modifying enzymes.
All SysBioM (Systems Biology in Madison) sponsored talks take place on Wednesdays at 2p.m. in the 3rd floor Orchard View room of the Discovery Building. Talks are open to the public. Access to the room is via the elevator behind Aldo’s Cafe in the Northeast corner of the building.