Göttinger Graduiertenschule für Neurowissenschaften, Biophysik und Molekulare Biowissenschaften

Bastians, Holger, Prof. Dr.

Professor of Cellular Oncology


  • since 2013 Professor of Cellular Oncology, University Medical Center Göttingen (UMG)
  • 2011-2013 Heisenberg-Professor of 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

Mitosis represents the key event during the eukaryotic cell cycle during which the DNA is equally distributed onto the two daughter cells. Defects in mitotic signaling pathways are often detected in human cancer and are directly associated with the missegregation of sister chromatids resulting in chromosomal instability (CIN) and aneuploidy. In fact, this is directly linked to tumorigenesis and represents a major characteristic of human cancer. However, the molecular mechanisms underlying CIN and the genetic lesions causing aneuploidy in human cancer are largely unknown.
In addition to its fundamental role for the maintenance of chromosomal stability, mitosis represents an important target for anti-cancer therapy and many anti-mitotic drugs including taxanes and Vinca alkaloids are frequently used in the clinic to treat various malignancies. However, it is still unclear how the interference with the mitotic progression is linked to tumor cell death, the desired outcome of therapy. A knowledge of this cross-talk is required for the development of future therapy concepts.

Based on these key points of cancer research our lab is focusing on the following main questions:

1. What are the molecular mechanisms of chromosome segregation during mitosis and what are genetic lesions in human cancer responsible for chromosomal instability?
2. What are the molecular mechanisms of mitosis associated cell death after chemotherapeutic treatment and waht are the routes of chemotherapy resistance in human cancer?
3. Based on our investigations of mitotic signaling pathways we are aiming to identify novel mitotic drug targets in order to improve current therapies and to develop novel therapeutic concepts.


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


Selected Recent Publications


  • 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