Prof. Dr. rer. nat. Christine Sers

Research Group Molecular Tumor Pathology
Institute of Pathology
Charité - Universitätsmedizin Berlin
Charitéplatz 1
10117 Berlin
Tel:+49 30 450 536 185

E-Mail: christine.sers(at)charite.de
https://pathologie-ccm.charite.de/en/research/research_groups/research_group_sers_molecular_tumor_pathology/

University Education

  • 1988 Diploma in genetics and immunology, Universität München
  • 1992 Ph.D., Institute of Immunology, Universität München
  • 2002 Habilitation

Professional Experience (selection)

  • 1991 Visiting scientist, Institute of Biochemistry, University Njimegen, Netherlands
  • 1992 Postdoctoral Scientist, Institute of Immunology; University Munich, Germany
  • 1993-1996 Postdoctoral Scientist, Institute of Pathology; University Zürich; Switzerland
  • 1996-1998 Postdoctoral Scientist, Institute of Pathology, Charité, Germany
  • 1998 Visiting scientist, Institute of Biochemistry, University Njimegen, Netherlands
  • Since 1998 Group leader Institute of Pathology, Charité, Germany
  • 2012 Professor for Tumor Systemsbiology, Charité, Germany

Research Fields

  • i) Cancer Research
  • ii) Signal Transduction
  • iii) Systems Biology

Scientific Scope

A main research focus is the analysis of genetic and epigenetic alterations in tumors with an impact in tumor progression and therapy response. An important question addressed here is to what extends such alterations can be potentially used as predictive diagnostic biomarkers. For this purpose, CS has founded the ColoNET consortium in 2008, a research group dedicated to the study of biomarkers in colorectal cancer using high-through put technology combined with mathematical modeling of signaling pathways emerging downstream of RAS and growth factor receptors. Within this project, cell culture and Xenograft models for colorectal cancer where established and characterized at multiple levels. The impact of distinct oncogenic alterations on pathway robustness was investigated and modeled, a model of the circadian clock and its alteration via oncogenic RAS was implemented and the epigenetic regulation and effects of EGFR ligands onto inhibitor response were investigated. The project will continue from 2013 on for another 3 years further investigating the quantitative and qualitative impact of the most important oncogenes and tumor suppressor genes deregulated in colorectal cancer. For this purpose, again a combination of experimental investigation and mathematical modeling will be used. Pathway wiring and activation will be analyzed in cell culture systems using conditional oncogenes or siRNAs, targeted interference and read-out measurement of pathway activation, growth or apoptosis induction. The data will be integrated into mathematical models and the model will be improved in an iterative process to be best able to predict cellular behavior (based on a given genetic/epigenetic background). A long-term goal is to use such models for predictions in terms of therapy response and to test predictions both in vitro and upon analysis of patient material and data.

Most important Awards, Grants or Scientific Achievements

  • 2007-2008 NGFN2 Infection and Inflammation Network SIPAGE
  • 2002005-2013 CRC SFB 618
  • 2009-2012 BMBF ColoNET
  • 2013-2015 BMBF eBIO Oncopath
  • 2012-2016 BMBF DKTK (Molecular Diagnostics of colorectal cancer)

Selected References

  • Fritsche-Guenther R, Witzel F, Sieber A, Herr R, Schmidt N, Braun S, Brummer T, Sers C, Blüthgen N. Strong negative feedback from Erk to Raf confers robustness to MAPK signalling. Mol Syst Biol. 2011 May 24;7:489
  • Stelniec-Klotz I, Legewie S, Tchernitsa O, Witzel F, Klinger B, Sers C, Herzel H, Blüthgen N, Schäfer R. Reverse engineering a hierarchical regulatory network downstream of oncogenic KRAS. Mol Syst Biol. 2012 Jul 31;8:601. doi: 10.1038/msb.2012.32
  • Nazarenko I, Jenny M, Keil J, Gieseler C, Weisshaupt K, Sehouli J, Legewie S, Herbst L, Weichert W, Darb-Esfahani S, Dietel M, Schäfer R, Ueberall F, Sers C. Atypical protein kinase C zeta exhibits a proapoptotic function in ovarian cancer. Mol Cancer Res. 2010 Jun;8(6):919-34.
  • Blüthgen N, Legewie S, Kielbasa SM, Schramme A, Tchernitsa O, Keil J, Solf A, Vingron M, Schäfer R, Herzel H, Sers C. A systems biological approach suggests that transcriptional feedback regulation by dual-specificity phosphatase 6 shapes extracellular signal-related kinase activity in RAS-transformed fibroblasts. FEBS J. 2009 Feb;276(4):1024-35
  • Sers C, Kuner R, Falk CS, Lund P, Sueltmann H, Braun M, Buness A, Ruschhaupt M, Conrad J, Mang-Fatehi S, Stelniec I, Krapfenbauer U, Poustka A, Schäfer R. Down-regulation of HLA Class I and NKG2D ligands through a concerted action of MAPK and DNA methyltransferases in colorectal cancer cells. Int J Cancer. 2009 Oct 1;125(7):1626-39
  • I. Nazarenko, R. Schäfer, C. Sers.The tumor suppressor H-REV107-1 induces apoptosis in ovarian carcinoma cells via negative regulation of PP2A. J.Cell Science, 120:1393-404 (2007)
  • Lund, K. Weißhaupt, T. Mikeska, D. Jammas, X. Chen, R.-J. Kuban, U. Ungethüm, U. Krapfenbauer, H. Herzel, R. Schäfer, J. Walter, C. Sers. Oncogenic HRAS suppresses Clusterin and MMP2 expression through epigenetic modification. Oncogene, 25:4890-903 (2006)
  • I. Nazarenko, G. Kristiansen, Y. Yongwei, C. Gieseler, K. Schlüns, R. Schäfer, I. Petersen and C. Sers Cytoplasmic versus nuclear localization of the H-REV107-1 proteins is of prognostic value in non-small cell lung cancer. Am Journal of Pathology, 169(4):1427-39 (2006)
  • O. I. Tchernitsa, C. Sers, J.Zuber, B. Hinzmann, M. Grips, M. Hellriegel, A. Rosenthal and R. Schäfer The transcriptional basis of KRAS-mediated cellular transformation in ovarian epithelial cells. Oncogene 23: 4536-4555 (2004)
  • J. Zuber, O. I. Tchernitsa, B. Hinzmann, A.-C. Schmitz, M. Grips, M. Hellriegel, C. Sers, A. Rosenthal & R. Schäfer A genome-wide survey of RAS transformation targets. Nat Genetics 24, 144-152 (2000)