PI Gerda Egger

Research Focus

Epigenetic mechanisms include DNA methylation, histone modification/ remodeling and the action of non-coding RNAs, which are intertwined processes essential for the inheritance of gene expression patterns that determine development, cellular identity or differentiation. Deregulation of the epigenetic machinery has been implicated in various pathological conditions including cancer, which has important implications for biomarker development and therapy using epigenetic drugs. 

We employed genome-scale epigenomic analyses to define targets of differential DNA methylation, chromatin modification or miRNA expression in different primary tumors and tumor cell lines to define epigenetic biomarkers and to discover epigenetic drivers of tumorigenesis (Saito, Egger et al., 2006; Gal-Yam, Egger et al, 2008; Hassler et al, 2016; Exner et al, 2015). Using xenograft models, we demonstrated the efficacy of DNMT inhibitors towards T- cell lymphoma (Hassler et al, 2012).

Main Objectives

Our main goal is to understand the causative function of key epigenetic proteins such as DNA methyltransferases or histone deacetylases for tumorigenesis. We want to identify the specific targets of these enzymes, in order to better understand the biological impact for diverse cancers. Furthermore, we aim to translate our findings into clinical settings to develop epigenetic biomarkers with potential use for diagnostic, prognostic or predictive purposes in liquid biopsies. 

Content Research

We use different preclinical models including tumor organoids and transgenic mouse models but also primary tumor specimen as our model systems. Molecular tools include genome-wide chromatin (ATAC-Seq, ChIP-Seq) and DNA methylation analyses (RRBS, Illumina arrays), as well as proteomics (phospho, acetylomics).