%0 Journal Article %1 Karpanen.2001 %A Karpanen, T. %A Egeblad, M. %A Karkkainen, M. J. %A Kubo, H. %A Yla-Herttuala, S. %A Jaattela, M. %A Alitalo, K. %D 2001 %J Cancer Res. %K & Animals Blood Breast C Carcinoma Cell Division Endothelial Factor Factors Female Fusion Growth Heterologous Human Humans Immunoglobulins Kinase Kinases Laboratories Lymphangiogenesis Lymphatic Mice Neoplasm Neoplasms Neovascularization Pathologic Protein-Tyrosine Proteins Receptor Receptor-3 Receptors Recombinant Research Scid System Transfection Transplantation Vascular Vessels antagonists biosynthesis blood cells genetics inhibitors metabolism pathology physiology physiopathology protein supply %N 5 %P 1786-1790 %T Vascular endothelial growth factor C promotes tumor lymphangiogenesis and intralymphatic tumor growth %U PM:11280723 %V 61 %X Many solid tumors produce vascular endothelial growth factor C (VEGF-C), and its receptor, VEGFR-3, is expressed in tumor blood vessels. To study the role of VEGF-C in tumorigenesis, we implanted MCF-7 human breast carcinoma cells overexpressing recombinant VEGF-C orthotopically into severe combined immunodeficient mice. VEGF-C increased tumor growth, but unlike VEGF, it had little effect on tumor angiogenesis. Instead, VEGF-C strongly promoted the growth of tumor-associated lymphatic vessels, which in the tumor periphery were commonly infiltrated with the tumor cells. These effects of VEGF-C were inhibited by a soluble VEGFR-3 fusion protein. Our data suggest that VEGF-C facilitates tumor metastasis via the lymphatic vessels and that tumor spread can be inhibited by blocking the interaction between VEGF-C and its receptor

@article{Karpanen.2001, abstract = {Many solid tumors produce vascular endothelial growth factor C (VEGF-C), and its receptor, VEGFR-3, is expressed in tumor blood vessels. To study the role of VEGF-C in tumorigenesis, we implanted MCF-7 human breast carcinoma cells overexpressing recombinant VEGF-C orthotopically into severe combined immunodeficient mice. VEGF-C increased tumor growth, but unlike VEGF, it had little effect on tumor angiogenesis. Instead, VEGF-C strongly promoted the growth of tumor-associated lymphatic vessels, which in the tumor periphery were commonly infiltrated with the tumor cells. These effects of VEGF-C were inhibited by a soluble VEGFR-3 fusion protein. Our data suggest that VEGF-C facilitates tumor metastasis via the lymphatic vessels and that tumor spread can be inhibited by blocking the interaction between VEGF-C and its receptor}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Karpanen, T. and Egeblad, M. and Karkkainen, M. J. and Kubo, H. and Yla-Herttuala, S. and Jaattela, M. and Alitalo, K.}, biburl = {https://www.bibsonomy.org/bibtex/2867f7e0e3c2f4081da601dcd3859cbe1/kanefendt}, interhash = {582473aeb89be305f8cc5f0524e619cf}, intrahash = {867f7e0e3c2f4081da601dcd3859cbe1}, journal = {Cancer Res.}, keywords = {& Animals Blood Breast C Carcinoma Cell Division Endothelial Factor Factors Female Fusion Growth Heterologous Human Humans Immunoglobulins Kinase Kinases Laboratories Lymphangiogenesis Lymphatic Mice Neoplasm Neoplasms Neovascularization Pathologic Protein-Tyrosine Proteins Receptor Receptor-3 Receptors Recombinant Research Scid System Transfection Transplantation Vascular Vessels antagonists biosynthesis blood cells genetics inhibitors metabolism pathology physiology physiopathology protein supply}, number = 5, pages = {1786-1790}, timestamp = {2010-02-05T11:28:41.000+0100}, title = {Vascular endothelial growth factor C promotes tumor lymphangiogenesis and intralymphatic tumor growth}, url = {PM:11280723}, volume = 61, year = 2001 }