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Evan Group - Roderik Kortlever

Roderik Kortlever

Position: Research Associate

Joined the lab: May 2008

Background: After studying Biochemistry at the Rotterdam University of Applied Sciences and at the University of Leiden in 2000 I joined the lab of Professor René Bernards at the Netherlands Cancer Institute (NKI) in Amsterdam as a research technician. In 2002 I decided to move on for my doctorate in the same lab, where I focused on the role of tumour suppressor p53 in replicative senescence. This spearheaded a now widely accredited realisation that senescence is regulated through secreted factors and, at least in part, a cell non-autonomous process. In 2008 I moved to the Evan lab to utilise unique mouse tumour models to uncover how cancer is dependent on and regulated by oncogenes.

Current Projects: Using multiple unique models of switchable genetics I am ascertaining if and how various types of breast cancer are critically dependent on Myc and how this can guide therapeutic targeting. Further, also using switchable mouse models of non-small cell lung cancer that were generated in the lab, I have uncovered that deregulated Myc directly and critically controls immune evasion of tumours by manipulation of immune cell behaviour and activity. Potential implications for therapy and whether this may be a common prerequisite for tumour growth is of current concern.

Publications:

    • Kortlever RM, Sodir NM, Wilson CH, Burkhart DL, Pellegrinet L, Brown Swigart L, Littlewood TD, EvanGI. Myc cooperates with Ras by programming inflammation and immune suppression, Cell 2017 Nov; 171 (6):1301-1315.
    • von Eyss B, Jaenicke LA, Kortlever RM, Royla N, Wiese KE, Letschert S, McDuffus L-A, Sauer M, Rosenwald A, I. Evan GI, Kempa S, Eilers M, A MYC-driven change in mitochondrial dynamics limits YAP/TAZ function in mammary epithelial cells and breast cancer, Cancer Cell 2015 Dec 14;28(6):743-57.
    • Soucek L, Buggy JJ, Kortlever R, Adimoolam S, Monclús HA, Allende MT, Swigart LB, Evan GI. Modeling pharmacological inhibition of mast cell degranulation as a therapy for insulinoma. Neoplasia 2011 Nov; 13 (11):1093-100.
    • Junttila MR, Karnezis AN, Garcia D, Madriles F, Kortlever RM, Rostker F, Brown Swigart L, Pham DM, Seo Y, Evan GI, Martins CP. Selective activation of p53-mediated suppression in high-grade tumors. Nature 2010 Nov 25; 468 (7323):567-71.
    • Kortlever RM, Brummelkamp TR, van Meeteren LA, Moolenaar WH, Bernards R.  Suppression of the p53-dependent replicative senescence response by lysophosphatidic acid signaling. Mol Cancer Res. 2008 Sep; 6 (9):1452-60.
    • Kortlever RM, Nijwening JH, Bernards R. Transforming growth factor-ß requires its target plasminogen activator inhibitor-1 for cytostatic activity. J Biol Chem. 2008 Sep 5; 283 (36):24308-13.
    • Kortlever RM and Bernards, R. Senescence, wound healing, and cancer: the PAI-1 connection. Cell Cycle 2006 Dec 5 (23):2697-703.
    • Kortlever RM, Higgins PJ, Bernards R. Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence. Nat Cell Biol. 2006 Aug; 8 (8):877-84.
    • Brummelkamp TR, Kortlever RM, Lingbeek M, Trettel F, MacDonald ME, van Lohuizen M, Bernards R. TBX-3, the gene mutated in Ulnar-Mammary Syndrome, is a negative regulator of p19ARF and inhibits senescence. J Biol Chem. 2002 Feb 22; 277 (8):6567-72.
    • Deiman BA, Kortlever RM, Pleij CW. The role of the pseudoknot at the 3' end of turnip yellow mosaic virus RNA in minus-strand synthesis by the viral RNA-dependent RNA polymerase. Virology 1997 Aug; 71 (8):5990-6.