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Kari Alitalo

Researcher at University of Helsinki

Publications -  844
Citations -  122462

Kari Alitalo is an academic researcher from University of Helsinki. The author has contributed to research in topics: Angiogenesis & Vascular endothelial growth factor C. The author has an hindex of 174, co-authored 817 publications receiving 114231 citations. Previous affiliations of Kari Alitalo include Mount Sinai Hospital, Toronto & Cornell University.

Papers
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Journal ArticleDOI

Expression and prognostic value of transcription factor PROX1 in colorectal cancer.

TL;DR: The results strengthen the previous preclinical observations that PROX1 has a role in tumour progression in CRC and associated with a poor grade of tumour differentiation, and, in colon cancer patients, also with less favourable patient outcome.
Patent

FIt4 ligand and methods of use

TL;DR: In this paper, ligands for the receptor tyrosine kinase, Flt4, were provided along with cDNAs and vectors encoding the ligand, pharmaceutical compositions and diagnostic reagents.
Journal ArticleDOI

Early Lymph Vessel Development From Embryonic Stem Cells

TL;DR: The present model closely mimics the early steps of lymph vessel development in mouse embryos, and different subpopulations of lymphatic endothelial cells were identified on the basis of differential expression of several lymphatic and blood vessel markers, indicating vascular heterogeneity.
Journal ArticleDOI

The N-myc proto-oncogene and IGF-II growth factor mRNAs are expressed by distinct cells in human fetal kidney and brain.

TL;DR: The fetal expression patterns of the N- myc and IGF-II mRNAs are reflected by the types of tumors known to express the corresponding genes during postnatal life such as Wilms' tumor, however, the apparent coexpression of the IGF- II and N-myc genes in immature kidneys occurs largely in distinct cell types.
Patent

Vascular endothelial growth factor C (VEGF-C) ΔCys156 protein and gene, and uses thereof

TL;DR: In this article, purified and isolated VEGF-C cysteine deletion variants that bind to Flt4 receptor tyrosine kinase (VEGFR-3) but demonstrate reduced binding (relative to VEGFs-C) to kdr receptor tyrolyine Kinase (VGFR) were presented.