A PhD student position is available in the Laboratory of Cellular Oncology at the University Medical Center in Göttingen, Germany.
Our lab is interested in the molecular mechanisms that underly the chromosomal instability (CIN) phenotype and the induction of aneuploidy in human cancer.
Most recently, we identified the Chk2-Brca1 tumor suppressor pathway as a pathway that regulates the proper mitotic spindle assembly and thereby, can contribute to CIN. Remarkably, this pathway is most frequently impaired in human lung and colorectal cancer and might directly contribute to CIN particularly in these tumor entities.
However, the molecular mechanisms of how the tumor suppressors Chk2 and Brca1 contribute to spindle assembly and proper chromosome segregation during mitosis are still elusive and will be within the focus of our future work.
In addition, we are also interested in investigating how genes that contribute to CIN can influence the response to chemotherapeutic treatment and how the CIN phenotype can be exploited for the development of novel therapeutic concepts.
For further information on the topic see:
Stolz et al., (2010). The CHK2-BRCA1 tumor suppressor pathway ensures chromosomal stability in human somatic cells. Nature Cell Biology 12: 492 – 499.
Stolz, A., Ertych, N. and Bastians, H. (2011). The tumor suppressor CHK2: regulator of DNA damage response and mediator of chromosomal stability. Clinical Cancer Research, 17; 401 – 405.
Kaestner, P. and Bastians, H. (2010). Mitotic drug targets. J. Cell. Biochem., 111: 258 – 265.
Kaestner, P., Aigner, A. and Bastians, H. (2011). Therapeutic targeting of the spindle checkpoint through nanoparticle-mediated siRNA delivery inhibits tumor growth in vivo. Cancer Letters, 304: 128 – 136.
The Georg-August University is one of the german university, which was elected as a university of excellence and the research area of oncology is further expanding as part of the Göttingen Comprehensive Cancer Center.
The selected candidate will be given the chance to apply to the Göttingen Graduate School in Neurosciences and Molecular Biosciences (GGNB; www.uni-goettingen.de/en/sh/56640.html), which is one of the leading graduate schools funded by the German Excellence Initiative.
Work in our laboratory is supported by the Heisenberg excellence program and is part of two reaserch consortia in Göttingen (DFG-FOR942 and DFG-KFO179). Further information on this can be found at: www.for942.med.uni-goettingen.de/ and www.kfo179.de/index.php?id=4&L=1
We provide brandnew lab space with state-of-the-art equipment. Methods frequently used in our lab include cell biological, biochemical and molecular biological methods including human tissue culture, transfection, infection, siRNA methodologies, FACS and various microscopy techniques including life-cell imaging.
Highly motivated and career-oriented candidates with a strong interest (and preferentially strong experience) in mitosis research and in questions investigating the molecular mechanismsm of chromosomal instability and therapy response in human cancer are invited to submit their CV including a brief description of their research experience and interests and the names of two references preferentially via email to:
Holger Bastians, Ph.D
Professor for Cellular Oncology
University Medical Center Göttingen
Grisebachstrasse 8
D-37077 Göttingen
Email: holger.bastians@uni-goettingen.de
Anfangsdatum: 1. Oktober 2011
geschätzte Dauer: ca. 3 - 4 Jahre
Veröffentlichungen:
Stolz et al., (2010). The CHK2-BRCA1 tumor suppressor pathway ensures chromosomal stability in human somatic cells. Nature Cell Biology 12: 492 – 499.
Stolz, A., Ertych, N. and Bastians, H. (2011). The tumor suppressor CHK2: regulator of DNA damage response and mediator of chromosomal stability. Clinical Cancer Research, 17; 401 – 405.
Kaestner, P. and Bastians, H. (2010). Mitotic drug targets. J. Cell. Biochem., 111: 258 – 265.
Kaestner, P., Aigner, A. and Bastians, H. (2011). Therapeutic targeting of the spindle checkpoint through nanoparticle-mediated siRNA delivery inhibits tumor growth in vivo. Cancer Letters, 304: 128 – 136.