The Brekken laboratory is located in the Hamon Center for Therapeutic Oncology Research and studies tumor - host interactions with a particular emphasis on extracellular matrix (ECM) and angiogenesis. The function of matricellular proteins and the biology of anti-cancer therapy are the central areas of focus for the lab. The lab studies how angiogenesis and ECM remodeling are key components of the tumor microenvironment. Current projects are focused on the function of matricellular proteins (e.g., SPARC and fibulin-5) as regulators of ECM remodeling and angiogenesis.
Another major area of study in the lab is the development and evaluation of novel therapy for cancer with a particular focus on anti-angiogenic strategies. Vascular endothelial growth factor (VEGF) is a primary stimulant of blood vessel growth in tumors and as such is a relevant target for anti-angiogenic intervention. Currently we are studying the mechanism of anti-VEGF therapy and how inhibition of VEGF activity affects the tumor microenvironment.
RESEARCH INTERESTS
Angiogenesis
Cancer Therapy
Extracellular Matrix
Metastasis
Tumor Microenvironment
RECENT PUBLICATIONS
Beck, AW., Luster, T., Miller, AF., Holloway, SE., Conner, CR., Thorpe, PE., Fleming, JB., and Brekken, RA., "A monoclonal anti-phosphatidylserine antibody in combination with gemcitabine strongly inhibits the growth and metastasis of orthotopic pancreatic tumors in mice." The International Journal of Cancer, 118:2639-2643, May 2006
Korpanty, G., Carbon, JG., Grayburn, PA., Fleming, JB., and Brekken, RA, "Monitoring response to anti-cancer therapy by targeting microbubbles to tumor vasculature" Clin Can Res, 13:323, January 2007
Dineen et al, "VEGFR2 mediates macrophage infiltration into orthotopic pancreatic tumors in mice" Cancer Reserch, 68:4340-4346, June 2008
Udugamasooriya et al, "A peptoid antibody surrogate that antagonizes VEGF receptor 2 activity" J. Am. Chem. Soc., 130:5744-5752, February 2008
Arnold et al, "Forced expression of MMP9 rescues the loss of angiogenesis and abrogates metastasis of pancreatic tumors triggered by the absence of host SPARC" Exp. Biol. Med., 233:860-873, June 2008
SIGNIFICANT PUBLICATIONS
Brekken, R.A., Huang, X., King, S.K., and Thorpe, P.E., "Vascular endothelial growth factor as a marker of tumor endothelium." Cancer Research, 58:1952 - 1959, 1998
Bergers, G., Brekken, R., Vu, T.H., Itoh, T., Tamaki, K., Tanazawa, K., Thorpe, P., Itohara, S., Werb, Z., and Hanahan, D., "Gelatinase B triggers the angiogenic switch during carcinogenesis." Nature Cell Biology, 2:737 - 744, 2000
Brekken, R.A., Overholser, J.P., Stastny, V.A., Waltenberger, J., Minna, J.D., and Thorpe, P.E., "Selective inhibition of VEGFR2 activity by a monoclonal anti - VEGF antibody blocks tumor growth in mice." Cancer Research, 60:5117 - 5124, 2000
Puolakkainen*, P., Brekken*, R. A., Muneer, S., and Sage, E. H., "Enhanced growth of pancreatic tumors in SPARC-null mice is associated with decreased deposition of extracellular matrix and reduced tumor cell apoptosis" Molecular Cancer Research, 2:215-224, May 2004
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