Rene H. Medema started his career in 1989 in the lab of Hans Bos in Leiden as a PhD student working on signal transduction by p21ras. After his PhD he moved to the laboratory of Prof. Dr. R.A. Weinberg (Whitehead Institute, Cambridge, MA) for his postdoctoral training, working on cell cycle control. As an independent group leader he continued to study cell cycle control, first at the University Medical Center Utrecht (1995-2000) and subsequently at the Netherlands Cancer Institute (2001-2005). In 2005 he moved back to Utrecht to become professor in Experimental Oncology. In 2012, he was appointed director of research at the Netherlands Cancer Institute.
His group has made several key contributions to the general understanding of control of the cell cycle by Forkhead transcription factors, FoxO and FoxM1. In addition, work from his group has provided more insight on the role of motor proteins in spindle assembly and the consequences of chromosome missegregation on the genomic stability and viability of a tumor cell. His group was the first to show that recovery from a DNA damage-induced arrest is controlled by Polo-like kinase-1 in 2004, and his lab has since provided several major contributions to our understanding of the recovery process.
- 2013: Appointed member of the European Academy of Cancer Sciences
- 2013: Appointed member of the KNAW (Royal Netherlands Academy of Arts and Sciences)
- 2012: Elected member of the Academia Europea
- 2009: EMBO membership
- 2004: VICI Laureate
- Janssen, A., van der Burg, M., Szuhai, K., Kops, G. J., & Medema, R. H. (2011). Chromosome segregation errors as a cause of DNA damage and structural chromosome aberrations. Science, 333(6051), 1895-1898.
- Krenning, L., Feringa, F. M., Shaltiel, I. A., van den Berg, J., & Medema, R. H. (2014). Transient activation of p53 in G2 phase is sufficient to induce senescence. Molecular cell, 55(1), 59-72.
- Macůrek, L., Lindqvist, A., Lim, D., Lampson, M. A., Klompmaker, R., Freire, R., ... & Medema, R. H. (2008). Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery. Nature, 455(7209), 119.
- Smits, V. A., Klompmaker, R., Arnaud, L., Rijksen, G., Nigg, E. A., & Medema, R. H. (2000). Polo-like kinase-1 is a target of the DNA damage checkpoint. Nature cell biology, 2(9), 672.
- Van Vugt, M. A., Brás, A., & Medema, R. H. (2004). Polo-like kinase-1 controls recovery from a G2 DNA damage-induced arrest in mammalian cells. Molecular cell, 15(5), 799-811.