Randi Gussgard Syljuåsen

  • Scientist, Group Leader Ph.D
  • +47 22 78 14 68

Mobile phone: +47 474 48 822
Fax: +47 22 78 14 95

1996: Ph.D., University of California, Los Angeles (UCLA). 
1991: Sivilingeniør (M.Sc), The Norwegian Institute of Technology (NTNU). 

2012: - Group Leader, Dept Radiation Biology, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
2007-2012: Project group leader, Dept Radiation Biology, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
2007 (6 months): Guest researcher, BRIC Biocenter, Copenhagen University, Denmark.
1999-2006: Postdoc, Dept Cell Cycle and Cancer, The Danish Cancer Society, Copenhagen, Denmark.
1997-1998: Postdoc, Laboratory of Radiobiology, Harvard School of Public Health, Boston, USA.
1996-1997: Postdoc, Dept Radiation Oncology, UCLA, USA.

Selected publications:

H.B. Landsverk, L.E. Sandquist, S.C. Sridhara, G.E. Rødland, J.C. Sabino, S.F. de Almeida, B. Grallert, L. Trinkle-Mulcahy, R.G.Syljuåsen. Regulation of ATR activity via the RNA polymerase II associated factors CDC73 and PNUTS-PP1. Nucleic Acids Research, 47 (4), 1797-1813, 2019.

Hauge, C. Naucke, G. Hasvold, M. Joel, G.E. Rødland, P. Juzenas, T. Stokke, R.G. Syljuåsen. Combined inhibition of Wee1 and Chk1 gives synergistic DNA damage in S-phase due to distinct regulation of CDK activity and CDC45 loading. Oncotarget, 8(7), 10966-10979, 2017.

T.W. Håland, E.Boye, T.Stokke, B.Grallert, R.G. Syljuåsen. Simultaneous measurement of passage through the restriction point and MCM loading in single cells. Nucleic Acids Research, 43 (22), e150, 2015.

Lund-Andersen, S. Patzke, V. Nähse-Kumpf, R.G. Syljuåsen. Plk1-inhibition can cause radiosensitization or radioresistance dependent on the treatment schedule. Radiation Therapy and Oncology, 110, p.355-361, 2014.

Hasvold, V. Nähse-Kumpf, K. Tkacz-Stachowska, E. Rofstad, R.G. Syljuåsen. The efficacy of CHK1-inhibitors is not altered by hypoxia, but is enhanced after reoxygenation. Molecular Cancer Therapeutics, 12, 705-716, 2013.

H.Beck,V. Nähse-Kumpf, M.S Yoo Larsen, S. Patzke, C. Holmberg, O. Nielsen, R.G. Syljuåsen*, C.S. Sørensen*. CDK suppression by WEE1 kinase protects the genome through control of replication initiation and nucleotide consumption. Mol. Cell. Biol., 32, 4226-4236, 2012. *shared corresponding authorship

C.S. Sørensen, R.G. Syljuåsen. Safeguarding genome integrity: The checkpoint kinases ATR, CHK1 and WEE1 restrain CDK activity during normal DNA replication. Nucleic Acids Research, 40, 477-486, 2012.

Menzel, V. Nähse-Kumpf, A. Nedergaard Kousholt, D. Kjærsgaard Klein, C. Lund-Andersen, M. Lees, J. Vilstrup Johansen, R.G. Syljuåsen*, C. S. Sørensen*. A genetic screen identifies BRCA2 and PALB2 as key regulators of G2 checkpoint maintenance. EMBO Reports, 12, 705-712,2011. *shared corresponding authorship

H.B. Landsverk, F. Mora-Bermudez, O.J.B. Landsverk, G. Hasvold, S. Naderi, O. Bakke, J. Ellenberg, P. Collas, R.G. Syljuåsen*, T. Küntziger*. The protein phosphatase 1 regulator PNUTS is a new component of the DNA damage response. EMBO Reports, 11,868-75, 2010. *shared corresponding authorship

R.G. Syljuåsen, S. Jensen, J. Bartek and J. Lukas. Adaptation to the ionizing radiation-induced G2 checkpoint occurs in human cells and depends on Chk1 and Plk1 kinases. Cancer Research, 66, p. 10253-10257, 2006. 

R.G. Syljuåsen, C.S. Sørensen, L.T. Hansen, K.Fugger, C. Lundin, F. Johansson, T. Helleday, M. Sehested, J. Lukas, and J. Bartek. Inhibition of human Chk1 causes increased initiation of DNA replication, phosphorylation of ATR targets, and DNA breakage. Mol. Cell. Biol., 25, p.3553-3562, 2005.

R.G. Syljuåsen, C.S. Sørensen, J. Nylandsted, C. Lukas, J. Lukas, J. Bartek. Inhibition of Chk1 by CEP-3891 accelerates mitotic nuclear fragmentation in response to ionizing Radiation. Cancer Research, 64 (24), 9035-40, 2004.

C.S. Sørensen*, R.G. Syljuåsen*, J. Falck, T. Schroeder, L. Rönnstrand, K.K. Khanna, B.B. Zhou, J. Bartek, and J. Lukas. Chk1 regulates the S phase checkpoint by coupling the physiological turnover and ionizing radiation-induced accelerated proteolysis of Cdc25A. Cancer Cell, 3, p. 247-258, 2003.*shared 1st-authorship

R.G. Syljuåsen, B. Krolewski and J. B. Little. Loss of normal G1 checkpoint control is an early step in carcinogenesis, independent of p53-status. Cancer Research, 59, p.1008-1014, 1999.

R.G. Syljuåsen, A. Belldegrun, C-L. Tso, H.R. Withers and W.H. McBride: Sensitization of renal carcinoma to radiation using alpha interferon (IFNA) gene transfection. Radiation Research, 148, p.443-448, 1997.

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