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Detail

Gerda Egger
Assoc.Prof. Dr. Gerda Egger

Department of Pathology
Position: Associate Professor

T +43 1 40400 63890
gerda.egger@meduniwien.ac.at

Keywords

Chromatin; DNA Methylation; Epigenomics; Molecular Diagnostic Techniques

Research group(s)

  • Epigenetics

Research interests

The main research focus of the lab lies in the field of cancer epigenetics. Using genetic modified mouse models and epigenomic analyses the goal is to understand how epigenetic aberrations such as DNA methylation are generated and how they impact on tumorigenesis. Furthermore, we study the effect of inhibition of epigenetic pathways on tumor development and progression. We use genome-wide epigenomic analyses to develop epigenetic biomarkers for tumor diagnostics. In close collaboration with pathologists and clinicians we aim to establish epigenetic biomarkers for minimal-invasive tumor classification and diagnosis from circulating free tumor DNA (cfDNA) isolated from body fluids (e.g. plasma, urine) of cancer patients. 

Techniques, methods & infrastructure

Next to standard molecular biology methods we employ transgenic mouse models inlcuding tumor models and knockout mice for epigenetic modifyiers. We use genome-wide and locus specific DNA methylation analyses, Chromatin Immunoprecipitation and chromatin accessibility assays. Furthermore, techniques to analyse limited amounts of material including circulating free tumor DNA or microdissected tissues are established in the lab.

Grants

  • ALKATRAS - ALK Activation as a target of TRAanslational Science: Break free from cancer (participant) (2015)
    Source of Funding: EU, H2020-MSCA-ITN-2015
    Principal Investigator
  • Identification of novel nuclear targets of the oncogenic tyrosine kinase NPM-ALK (2015)
    Source of Funding: Herzfelder'sche Familienstiftung,
    Principal Investigator
  • The function of DNMT1 for NPM-ALK driven Lymphomagenesis (2014)
    Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
    Principal Investigator
  • Epigenetisches Profiling von prämalignen und malignen Stadien des Cholangiokarzinoms (2013)
    Source of Funding: OeNB (Oesterreichische Nationalbank), Anniversary Fund
    Principal Investigator
  • Die Rolle epigenetischer Biomarker für das Prostatakarzinom vor und nach Hormontherapie (2008)
    Source of Funding: OeNB (Oesterreichische Nationalbank), Anniversary Fund
    Principal Investigator
  • Epigenetic marker - Evaluation of epigeneitc biomarkers in prostate cancer patients before and after hormone ablation therapy (fellow) (2008)
    Source of Funding: EU, FP7-PEOPLE-IRG-2008
    Principal Investigator
  • Epigenetics in NPM-ALK Positive Lymphomas (2008)
    Source of Funding: FWF (Austrian Science Fund), Elise Richter Programme
    Principal Investigator

Selected publications

  1. Exner, R. et al., 2015. Potential of DNA methylation in rectal cancer as diagnostic and prognostic biomarkers. British Journal of Cancer, 113(7), pp.1035-1045. Available at: http://dx.doi.org/10.1038/bjc.2015.303.
  2. Hassler, M.R. et al., 2012. Antineoplastic activity of the DNA methyltransferase inhibitor 5-aza-2�-deoxycytidine in anaplastic large cell lymphoma. Biochimie, 94(11), pp.2297-2307. Available at: http://dx.doi.org/10.1016/j.biochi.2012.05.029.
  3. Gal-Yam, E.N. et al., 2008. Frequent switching of Polycomb repressive marks and DNA hypermethylation in the PC3 prostate cancer cell line. Proceedings of the National Academy of Sciences, 105(35), pp.12979-12984. Available at: http://dx.doi.org/10.1073/pnas.0806437105.
  4. Egger, G. et al., 2006. Identification of DNMT1 (DNA methyltransferase 1) hypomorphs in somatic knockouts suggests an essential role for DNMT1 in cell survival. Proceedings of the National Academy of Sciences, 103(38), pp.14080-14085. Available at: http://dx.doi.org/10.1073/pnas.0604602103.
  5. Saito, Y. et al., 2006. Specific activation of microRNA-127 with downregulation of the proto-oncogene BCL6 by chromatin-modifying drugs in human cancer cells. Cancer Cell, 9(6), pp.435-443. Available at: http://dx.doi.org/10.1016/j.ccr.2006.04.020.