prof. dr. M.A.T.M. van Vugt
Marcel van Vugt ('s-Hertogenbosch, 1977) studied Medical Biology at the Faculty of Medicine of the University of Utrecht. Subsequently, PhD thesis work was done under supervision of Prof. Rene Medema at the Netherlands Cancer Institute in Amsterdam (Thesis: Cell Cycle regulation by Polo-like kinase-1, 2005). Post-doctoral research was performed at the Massachusetts Institute of Technology (MIT, Cambridge, USA) in the research group of Prof. Michael Yaffe, focused on cell cycle regulation and DNA damage signaling. Since 2009, Marcel van Vugt heads an independent research group at the University Medical Center Groningen. His research focuses on how normal cells and cancer cells deal with DNA damage, and how this knowledge can be used to improve cancer therapy. Since April 2018, Marcel is appointed ull Professor of Molecular Oncology, and since November 2018 he is director of the Cancer Research Center Groningen.
Heijink et al., BRCA2 deficiency instigates cGAS-mediated inflammatory signaling and confers sensitivity to Tumor Necrosis Factor-alpha-mediated cytotoxicity. Nature Communications (2018) in press
de Boer R. et al., Quantitative proteomics analysis identifies MUC1 as an effect sensor of EGFR inhibition. Oncogene. (2018) Oct 10, epub ahead of print.
van Gijn S. et al., TPX2/Aurora kinase A signaling as a potential therapeutic target in genomically unstable cancer cells. Oncogene. (2018) Sep 3, epub ahead of print.
Gogola E. et al., Selective Loss of PARG Restores PARylation and Counteracts PARP Inhibitor-Mediated Synthetic Lethality. Cancer Cell. (2018) Jun 11;33(6):1078-1093
Zomerman W.W. et al., Identification of Two Protein-Signaling States Delineating Transcriptionally Heterogeneous Human Medulloblastoma. Cell Reports. (2018) Mar 20;22(12):3206-3216.
Schoonen P.M., et al, Progression through mitosis promotes PARP inhibitor-induced cytotoxicity in homologous recombination-deficient cancer cells. Nature Communications. ( 2017) Jul 17;8:15981.
Heijink A.M., et al. A haploid genetic screen identifies the G1/S regulatory machinery as a determinant of Wee1 inhibitor sensitivity. Proc. Natl. Acad. Sci. U.S.A. (2015) Dec 8;112(49):15160-5
Hengeveld R.C., et al. Rif1 Is Required for Resolution of Ultrafine DNA Bridges in Anaphase to Ensure Genomic Stability. Dev Cell. (2015) Aug 24;34(4):466-74.
Fehrmann, R.S.N., et al. Gene expression analysis identifies global gene dosage sensitivity in cancer. Nature Genetics (2015) Feb;47(2):115-25
Lafranchi, L. et al. APC/CCdh1 controls CtIP stability during the cell cycle and in response to DNA damage. EMBO J. (2014) Dec 1;33(23):2860-79
Krajewska, M. et al. ATR inhibition preferentially targets homologous recombination-deficient tumor cells. Oncogene. (2015) 34(26):3474-81
Krajewska, M. et al. Forced activation of Cdk1 via Wee1 inhibition impairs homologous recombination. Oncogene (2013) Jun 13;32(24):3001-8
van Vugt, M.A. et al. A mitotic phosphorylation feedback network connects Cdk1, Plk1, 53BP1 and Chk2 to inactivate the G2/M DNA damage checkpoint. PLoS Biology (2010) 8, e1000287
Linding, R. et al. Systematic discovery of in vivo phosphorylation networks. Cell (2007) 129(7):1415-26
Wilker, E. et al. 14-3-3sigma controls mitotic translation to facilitate cytokinesis. Nature (2007) 446:329-32.
van Vugt, M.A. et al. Polo-like kinase-1 controls recovery from a G2 DNA damage-induced arrest in mammalian cells. Molecular Cell (2004) 15:799-811.
|Last modified:||22 December 2018 11.35 a.m.|