Bastians, Holger, Prof. Dr.

Professor for Cellular Oncology


  • since 2019 Speaker of the DFG Research Unit 2800 (FOR2800) “Chromosome Instability: Cross-talk of DNA replication stress and mitotic dysfunction”
  • since 2013 Professor for Cellular Oncology, University Medical Center Göttingen (UMG)
  • 2011-2013 Heisenberg-Professor for Cellular Oncology, University Medical Center Göttingen (UMG)
  • Heisenberg fellow, Philipps-University Marburg, 2008 – 2011
  • Group leader, Institute for Molecular Biology and Tumor Research (IMT), Philipps-University Marburg, 2000 – 2010
  • Postdoctoral fellow with Prof. Joan Ruderman, Harvard Medical School, Boston, USA, 1996 - 1999
  • Dr. rer. nat., German Cancer Research Center (DKFZ), Heidelberg, 1996




Major Research Interests

A hallmark of human cancer is genome instability. A major form of genome instability is chromosomal instability (CIN), which is defined as the perpetual gain or loss of whole chromosomes leading to aneuploidy. Evolving aneuploidy results in massive changes in gene expression and drives adaptation and the aquirement of new tumor phenotypes including metastasis and therapy resistance, a process now known as tumor evolution. Since chromosome missegregation takes place during mitosis it is pivotal to identify the mitotic defects underlying CIN. In fact, our lab discovered that abnormal microtubule dynamics during mitosis acts as a major trigger for CIN in human cancer cells. Moreover, we identified several oncogenes and tumor suppressor genes including BRCA1 and p53/p73 as well as Wnt signaling as important regulators of CIN. Most recently, we surprisingly found that also defects during DNA replication, so-called replication stress, can contribute to mitotic dysfunction and CIN. These cross-talks between DNA replication and mitosis are subject of our newly established DFG-Research Unit (FOR2800), in which we collaborate with seven laboratories in Göttingen and in Germany to address this important question regarding the origin of genome instability (see: www.for2800.de). Current work in our lab focuses on the following research questions:

1. How do oncogenes and tumor suppressors (e.g. BRCA1) and other cancer-relevant signaling pathways (e.g. Wnt signaling) (de)regulate mitosis to trigger CIN?
2. What are the molecular mechanisms of mitotic chromosome missegregation in response to deregulated microtubule dynamics?
3. What are the cross-talk mechanisms between DNA replication stress and mitotic chromosome missegregation?



Homepage Department/Research Group
http://www.moloncol.med.uni-goettingen.de/de/content/researchgroups/101.html


Selected Recent Publications


  • Böhly N, Kistner M, Bastians H (2019) Mild replication stress causes aneuploidy by deregulating microtubule dynamics in mitosis. Cell Cycle Aug: 1-14

  • Ertych N, Stolz A, Valerius O, Braus GH, Bastians, H (2016) The CHK2-BRCA1 tumor suppressor axis restrains oncogenic AURORA-A to ensure proper mitotic microtubule assembly. Proceedings of the National Academy of Sciences USA, in press

  • Lüddecke S, Ertych N, Stenzinger A, Weichert W, Beissbarth T, Dyczkowski J, Gaedcke J, Valerius O, Braus GH, Kschischo M, Bastians H (2015) The putative oncogene CEP72 inhibits the mitotic function of BRCA1 and induces chromosomal instability. Oncogene, in press

  • Stolz A, Neufeld K, Ertych N Bastians H (2015). Wnt mediated protein stabilization ensures proper mitotic microtubule assembly and chromosomal stability. EMBO Reports: 16: 490-499

  • Ertych N, Stolz A, Stenzinger A, Weichert W, Kaulfuß S, Burfeind P, Aigner A, Wordeman L, Bastians H (2014) Increased microtubule assembly rates influence chromosomal instability in colorectal cancer cells. Nature Cell Biol 16: 779-91

  • Stolz A, Ertych N, Kienitz A, Vogel C, Schneider V, Fritz B, Jacob R, Dittmar G, Weichert W, Petersen I Bastians H (2010) The CHK2-BRCA1 tumor suppressor pathway ensures chromosomal stability in human somatic cells. Nature Cell Biol 12: 492-499

  • Kaestner P, Stolz A, Bastians H (2009) Determinants for the efficiency of anti-cancer drugs targeting either Aurora-A or Aurora-B kinases. Mol Cancer Ther 8: 2046-2056