prof. dr. M.A.T.M. (Marcel) 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 Full Professor of Molecular Oncology. From 2018-2023, he was director of the Cancer Research Center Groningen. From 2022, he is a board member of the Comprehensive Cancer Center of the UMCG.

Selected Publications

Stok C. et al. FIRRM/C1orf112 is synthetic lethal with PICH and mediates RAD51 dynamics. Cell Rep. 2023 Jul 25;42(7):112668.

Heijink A.M. et al. Sister chromatid exchanges induced by perturbed replication can form independently of BRCA1, BRCA2 and RAD51. Nat Commun. 2022 Nov 7;13(1):6722.

Chen M. et al. Genomic instability, inflammatory signaling and response to cancer immunotherapy. Biochim Biophys Acta Rev Cancer. (2022) 1877(1):188661.

Zimmerli D. et al. MYC promotes immune-suppression in triple-negative breast cancer via inhibition of interferon signaling. Nat Commun. 2022 Nov 2;13(1):6579.

Hong C. et al. cGAS-STING drives the IL-6-dependent survival of chromosomally instable cancers. Nature. 2022 Jul;607(7918):366-373.

Heijink A.M. et al., BRCA2 deficiency instigates cGAS-mediated inflammatory signaling and confers sensitivity to Tumor Necrosis Factor-alpha-mediated cytotoxicity. Nature Communications (2019) 10(1):100

Heijink A.M. et al., Modeling of Cisplatin-Induced Signaling Dynamics in Triple-Negative Breast Cancer Cells Reveals Mediators of Sensitivity. Cell Rep. (2019) ;28(9):2345-2357.

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

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.