Partner 8
G. Høyer-Hansen - Niels Behrendt
FINSEN - Copenhagen (DK)
www.finsenlab.dk
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| Qualifications and capacity: |
Finsen Laboratory is a part of Copenhagen University Hospital and is the only clinic dedicated to
full-time cancer research.
The purpose of the laboratory is to perform basic research and bring
the scientific results to the clinic. Finsen Laboratory has a strong connection to the oncologists
and several MDs have completed their scientific education with a ph.d. at the laboratory with
clinical relevant research projects. Located in the new Copenhagen Biocenter the Finsen Laboratory
has state-of-the-art research equipment as well as many high-end facilities such as mass spectrometry,
BIAcore, cell culture facilities and animal facilities.
Finsen Laboratory emplyoes almost 50 people dedicated to
cancer research. Currently
the staff at the Finsen Laboratory consists of 23 scientific employees, 15 laboratory technicians,
1 research coordinator, 1 office assistant, 1 photographer and a varying number of master
students and student assistants.
Please visit the Finsen Laboratory website www.finsenlab.dk for more information about our research
and vacant positions.
Research leaders, Gunilla Høyer-Hansen (PhD) and Niels Behrendt (PhD, DSc),
are co-coordinating the work of the Proteolysis Group at the Finsen Laboratory in Copenhagen.
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Gunilla Høyer-Hansen (PhD) has made batteries of monoclonal antibodies
to several both human and murine components of the
protease systems and
designed quantitative
immunoassays used in prognostic/diagnostic studies. Her group has also made in vitro and in
vivo studies of the tumour biology of the urokinase receptor and is now doing therapeutic
experiments in mouse models with monoclonal antibodies.
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Niels Behrendt (PhD, DSc) has special experience in protein chemical
and functional analysis of membrane proteins and enzymatic studies of proteolytic cascade
systems and was instrumental for the cloning of uPAR. He discovered uPARAP, a receptor
involved in collagen internalization and has functionally characterized this molecule
and generated mice deficient in uPARAP.
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Most relevant publications:
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Two Distinct Expession Patterns of Urokinase, Urokinase Receptor and Plasminogen Activator Inhibitor-1 in Colon Cancer Liver Metastases.
Illemann, M., Bird, N., Majeed, A., Lærum, O.D., Lund, L.R., Danø, K. and Nielsen, B.S.
International Journal of Cancer. 2008, 124: 1860-1870.
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Spontaneous metastasis in matrix metalloproteinase 3-deficient mice.
Juncker-Jensen, A., Rømer, J., Pennington, C.J., Lund, L.R., and Almholt, K.
Mol. Carcinogenesis. 2009, 48: 618–625.
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Antibody-mediated targeting of the uPA proteolytic function neutralizes fibrinolysis in vivo.
Lund, I.K., Jögi, A., Rønø, B., Rasch, M.G., Lund, L.R., Almholt, K., Gårdsvoll, H., Behrendt, N., Rømer, J.R., Høyer-Hansen, G.
J Biol Chem. 2008 Sep 17
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Metastasis is strongly reduced by the matrix metalloproteinase inhibitor Galardin in the MMTV-PymT transgenic breast cancer model.
Almholt K, Junker-Jensen A, Learum OD, Danø K, Lund LR, Rømer J.
Mol Cancer Ther. 2008 Sep;7(9):2758-67.
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Matrix metalloproteinase 13 is induced in fibroblasts in polyomavirus middle T antigen-driven mammary carcinoma without influencing tumor progression.
Nielsen BS, Egeblad M, Rank F, Askautrud HA, Pennington CJ, Pedersen TX, Christensen IJ, Edwards DR, Werb Z, Lund LR
PLoS ONE. 2008 Aug 13
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Imaging of urokinase-type plasminogen activator receptor expression using a 64Cu-labeled linear peptide antagonist by microPET.
Li ZB, Niu G, Wang H, He L, Yang L, Ploug M, Chen X
Clin Cancer Res. 2008 Aug 1;14(15):4758-66.
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Dimerization of endogenous MT1-MMP is a regulatory step in the activation of the 72-kDa gelatinase MMP-2 on fibroblasts and fibrosarcoma cells.
S. Ingvarsen, D. H. Madsen, T. Hillig, L. R. Lund, K. Holmbeck, N. Behrendt, L. H. Engelholm.
Biol. Chem., Vol. 389, pp. 943–953, July 2008.
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Cleaved forms of the urokinase plasminogen activator receptor in plasma enhance discrimination of benign from malignant disease and predict survival in patients with ovarian cancer.
Henic, E., Borgfeldt, C., Christensen, I.J., Casslén, B., Høyer-Hansen, G.
Clin Cancer Res. 2008 Sep 15;14(18):5785-93.
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Systemic administration of anti-uPAR monoclonal antibodies induces hepatic fibrin deposition in tPA-deficient mice.
Jögi, A., Pass, J., Høyer-Hansen, G, Lund, L.R., Nielsen B.S., Danø, K., Rømer, J.
J Thromb Haem. 2007; 5:1936-1944.
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Extracellular collagenases and the endocytic receptor, urokinase plasminogen activator receptor-associated protein/Endo180, cooperate in fibroblast-mediated collagen degradation.
Madsen, D.H., Engelholm, L.H., Ingvarsen, S., Hilling, T., Wagenaar-Miller, R.A., Kjøller, L., Gårdsvoll, H., Høyer-Hansen, G., Holmbeck, K., Bugge, T.H., Behrendt N.
J Biol Chem. 2007; 282:27037-45.
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Murine monoclonal antibodies against murine uPA receptor produced in gene-deficient mice: Inhibitory effects on receptor-mediated uPA activity in vitro and in vivo.
Pass J, Jögi A, Lund IK, Rønø B, Rasch MG, Gårdsvoll H, Lund LR, Ploug M, Rømer J, Danø K and Høyer-Hansen G
Thromb Haemost. 2007 Jun;97(6):1013-22.
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Plasminogen activation independent of uPA and tPA maintains wound healing in gene-deficient mice.
Lund LR, Green KA, Stoop A, Almholt K, Lilla J, Nielsen BS, Christensen IJ, Craik CS, Werb Z, Danø K and Rømer J
EMBO J, 25: 2686-97, 2006.
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Reduced metastasis of transgenic mammary cancer in urokinase-deficient mice.
Almholt K, Lund LR, Rygaard J, Nielsen BS, Danø K, Rømer J and Johnsen M
Int J Cancer, 113: 525-32, 2005.
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