Prof. Kari Alitalo Molecular/Cancer Biology Laboratory, University of Helsinki, Finland

Prof. Kari Alitalo is a tenured Research Professor of the Finnish Academy of Sciences and the Director of the Molecular/Cancer Biology Program and Centre of Excellence in the Biomedicum Helsinki. During his postdoctoral period in 1982-1983 Dr. Alitalo worked with Dr. J. Michael Bishop his collaborator, Dr. Harold E. Varmus... read morein San Francisco, where he made important contributions to the characterization of the Myc oncogene and -protein. He was furthermore among the first to discover (Myc) oncogene amplification in chromosomal abnormalities of tumor cells. He has also discovered several novel receptor tyrosine kinases, particularly in endothelial cells. He has shown that some of these receptors and their ligands play important roles in tumor angiogenesis. Among the original findings are the cloning and characterization of fibroblast growth factor receptor-4, the C-terminal Src tyrosine kinase and the first endothelial specific receptor tyrosine kinase, Tie, as well as VEGFR-3 and the cloning and characterization of VEGF-B in collaboration with Dr. Ulf Eriksson and determination of VEGFR-1 and NP-1 as its receptors. A significant achievement by Dr. Alitalo was the isolation, cloning and characterization of the first lymphangiogenic growth factor VEGF-C and isolation of lymphatic endothelial cells, opening up the lymphatic vascular system to molecular analysis after over a hundred years of descriptive pathology. He has also been central in the characterization of VEGF-B, VEGF-C and VEGF-D receptors and signal transduction pathways and the function of VEGFR-3, showing that this receptor is required for angiogenesis and later in lymphangiogenesis in embryos. He has invented molecular therapies for lymphedema that are now entering clinical trials. He has furthermore demonstrated that VEGF-C is overexpressed in tumors and its receptor VEGFR-3 is upregulated in angiogenic tumor vasculature. His studies led to the demonstration of VEGF-C associated tumor lymphangiogenesis, intralymphatic tumor growth and tumor metastasis and their inhibition by blocking the VEGFR-3 signal transduction pathway.