Matthias Dobbelstein


Prof. Dr. med. Matthias Dobbelstein
Work address: University of Göttingen
University Medical Center (UMG)
Göttingen Center for Molecular Biosciences
Institute of Molecular Oncology
Justus-von-Liebig-Weg 11
37077 Göttingen
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Current position: Professor for Molecular Oncology, Director,
Principal Investigator
FOR 2800 Project

Centrosome integrity as a determinant of replication stress and mitotic dysfunction
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Academic education
1989-1991 M.D. thesis studies, Ludwig-Maximilians-University, Munich, Germany
1986-1992 Undergraduate studies in Medicine, Ludwig-Maximilians-University, Munich, Germany
Scientific Degrees
2002 Habilitation; Phillips-University Marburg, Germany
1994 Dr. med.; Ludwig-Maximilians-University, Munich, Germany
1992 Final Medical Examination, Ludwig-Maximilians-University, Munich, Germany
Scientific career
Since 2005 Professor of Molecular Oncology, Director, Institute of Molecular Oncology, University Medical Center Göttingen, Germany
2004-2005 Professor of Molecular Oncology, Medical Biotechnology Center, University of Southern Denmark, Odense, Denmark
1997-2004 Group leader, Institute of Virology, Phillips-University Marburg, Germany
1993-1996 Postdoctoral fellow with Prof. Dr. T. Shenk, Department of Molecular Biology, Princeton University, NJ, USA
Additional information
2007 Award „Lecturer of the Year”, Molecular Medicine Master program Göttingen
1999 Postdoctoral Award, Robert Koch Foundation
1998 Research Award, Hessian Cancer Society (Hessische Krebsgesellschaft)
1993-1996 Scholarship Infectious Biology (AIDS scholarship), German Cancer Research Center (DKFZ)
1986-1992 Stipendium nach dem Bayerischen Begabtenförderungsgesetz
1986-1992 Scholarship, German Academic Scholarship Foundation (Studienstiftung des deutschen Volkes)

Welcome to the homepage of the DFG-funded Research Unit 2800 (FOR2800): Chromosome Instability: „Cross-talk of DNA replication stress and mitotic dysfunction”

The Research Unit 2800 involves the collaborative work from seven laboratories in Göttingen, Kaiserslautern, Duisburg-Essen, Mainz and Koblenz. We have now started our second funding period and we continue to address the scientific question regarding the origin of chromosome instability (CIN), which causes structural as well as numerical chromosome aberrations.

Petra Beli
Holger Bastians
Maik Kschischo
Markus      Räschle
Zuzana Storchová
Dominik Boos
Bernd Wollnik
DNA replication stress DNA replication stress DNA damage signaling
genome instability
mitosis aneuploidy

It is well established that CIN and increased levels of chromosome aberrations are closely associated with many human diseases including cancer, neurodegenerative diseases and age-related syndromes and can act as key drivers for disease development and progression. An important cellular condition that causes structural chromosome instability (S-CIN) and leading to structural chromosome aberrations is “replication stress”, which is characterized by a slowed-down or aberrant progression of replication forks during DNA replication in S phase of the cell cycle. On the other hand, errors during mitosis that result in chromosome missegregation are well-known causes of whole chromosome instability (W-CIN) leading to the induction and evolvement of aneuploidy. Since S-CIN and W-CIN are often, if not always, detected concomitantly in various CIN-associated diseases including cancer, the two forms of chromosomal instability might be mechanistically interlinked. In fact, recent evidence indicate that replication stress can promote mitotic chromosome missegregation and aneuploidy. Vice versa, whole chromosome aneuploidy can also contribute to replication stress, thereby establishing a vicious cycle between DNA replication stress and mitotic dysfunction.

The FOR 2800 combines complementary scientific expertise on replication stress, mitotic chromosome segregation, genome instability and aneuploidy to elucidate the mechanistic links between DNA replication stress in S-phase and perturbed chromosome segregation during mitosis and vice versa. The central goal of the research unit 2800 is to define and characterize the molecular mechanisms linking structural and numerical chromosome instability, which are key drivers of human diseases and aging processes.