Floris Foijer

Floris Foijer obtained his PhD degree at the Netherlands Cancer Institute in Amsterdam in 2006. His PhD research in the lab of Prof. Hein te Riele focused on alternative mechanisms of cell cycle arrest in cells that are predisposed to cancer. For his postdoc, funded by the Dutch Cancer Society (KWF fellow), Foijer went to the lab of Prof. Peter Sorger at Harvard Medical School in Boston, USA, where he pursued the link between cancer and chromosome instability. In Prof. Sorger’s lab, he developed murine models for chromosomal instability in the skin and the mammary gland and developed an interest in high resolution intravital imaging. In 2008, the need for more sophisticated murine models for high resolution imaging led him to the lab of Prof. Allan Bradley, at the Wellcome Trust Sanger institute in Cambridge, UK, where he, funded by a EMBO long term fellowship, started engineering a murine model to track chromosomal instability in living animals over time.

In 2011, Floris Foijer moved to ERIBA to start his lab focusing on the in vivo consequences of chromosomal instability. Foijer has a long-standing interest into how chromosomal instability shapes cancer genomes and collaborates with many (inter)national groups to map the single cell genomic landscapes of primary cancers and cancer models taking advantage of a unique single cell whole genome sequencing platform available at ERIBA. Furthermore, his group studies the cell intrinsic and cell extrinsic responses to chromosomal instability in vitro and in vivo and exploits these findings to selectively target aneuploid cancer cells in mouse models. In 2016, Foijer established the ERIBA/UMCG iPSC/CRISPR facility that supports scientists with the generation and characterization of iPS cells, CRISPR genome editing and CRISPR genome-wide screens.

• Hong C, Schubert M, Tijhuis AE, Requesens M, Roorda M, van den Brink A, Andrade Ruiz L, Bakker PL, van der Sluis T, Pieters W, Chen M, Wardenaar R, van der Vegt B, Spierings DCJ, de Bruyn M, van Vugt MATM, and Foijer F.(2022) IL6 signalling as a targetable vulnerability in chromosomally instable cancers. Nature.
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• Gemble S, Wardenaar R, Keuper K, Srivastava N, Nano M, Macé A, Tijhuis AE, Bernhard SV, Spierings DCJ, Simon A, Goundiam O, Hochegger H, Piel M, Foijer F, Storchová Z, and Basto R.(2022) Genetic instability from a single S-phase after whole genome duplication. Nature.
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• Shoshani O, Bakker B, WangY , Kim DH, Maldonado M, Demarest MA, Artates J, Zhengyu O, Mark A, Wardenaar R, Sasik R, Spierings DCJ, Vitre B, Fisch K, Foijer F, and Cleveland DW.(2021) Transient genomic instability drives tumorigenesis through accelerated clonal evolution. Genes & Development.
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• Schukken KM, Zhu Y, Bakker PL, Koster MH, Harkema L, Youssef SA, de Bruin A, Foijer F.(2021) Acute systemic loss of Mad2 leads to intestinal atrophy in adult mice. Scientific Reports.  
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• Bolhaqueiro ACF, Ponsioen B, Bakker B, Spierings DCJ, Klaasen SJ, Papaspyropoulos  A, Dutta D, Hami N, Verlaan-Klink I, van Jaarsveld RH, Lansdorp PM, van de Wetering M, Clevers H, Foijer F, Snippert HJG and Kops GJPL.(2019) Ongoing chromosomal instability and karyotype evolution in human colorectal cancer. Nature Genetics.  
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• Bakker B, Taudt A, Belderbos ME, Porubsky D, Spierings DC, de Jong TV, Halsema N, Kazemier HG, Hoekstra-Wakker K, Bradley A, de Bont ES, van den Berg A, Guryev V, Lansdorp PM, Colomé-Tatché M, Foijer F. (2016) Single-cell sequencing reveals karyotype heterogeneity in murine and human malignancies. Genome Biology.
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• Foijer F, DiTommaso T, Donati G, Hautaviita K, Xie SZ, Heath E, Smyth I, Watt FM, Sorger PK, Bradley A. (2013) Spindle checkpoint deficiency is tolerated by murine epidermal cells but not hair follicle stem cells. PNAS.
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• van Harn T, Foijer F, van Vugt M, Banerjee R, Yang F, Oostra A, Joenje H, te Riele H. (2010) Loss of Rb proteins causes genomic instability in the absence of mitogenic signaling. Genes & development.
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• Foijer F, Wolthuis RM, Doodeman V, Medema RH, te Riele H. (2005) Mitogen requirement for cell cycle progression in the absence of pocket protein activity. Cancer cell.
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