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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.

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Journal ArticleDOI

PROX1 is involved in progression of rectal neuroendocrine tumors, NETs

TL;DR: Results indicate that immunohistochemical detection of PROX1 correlates with a more malignant phenotype in rectal NETs and may be involved in progression of rectalNETs as a part of the Wnt pathway.
Book ChapterDOI

The TIE Receptor Family

TL;DR: Preclinical results demonstrate that genetic TIE1 deletion in mice inhibits the vascularization and growth of tumor isografts and protects from atherosclerosis, with little effect on normal vascular homeostasis in adult mice.
Journal ArticleDOI

Complex intrachromosomal rearrangement in the process of amplification of the L-myc gene in small-cell lung cancer

TL;DR: Long-range analysis using pulsed-field gel electrophoresis revealed that the amplified L-myc locus is involved in highly complex intrachromosomal rearrangements with jal and/or rlf, and suggests that the simultaneous presence of rearrangement both in rlf intron 1 and in regions immediately upstream of L- myc may be necessary for the expression of rlf-L-myC chimeric transcripts.
Journal Article

Expression of a rlf/L-myc minigene inhibits differentiation of embryonic stem cells and embroid body formation.

TL;DR: expression of a rlf/L-myc fusion may be of critical importance in tumorigenesis by blocking differentiation and thereby allowing continued proliferation of cells and the acquisition of further mutations leading to a fully malignant tumor.
Patent

Modified VEGF-A with improved angiogenic properties

TL;DR: In this article, the authors present methods and compositions for making and using chimeric polypeptides that comprise a VEGFR-2 ligand, and the chimeric molecules of the present invention retain VEG FR-2 binding activity and an enhanced angiogenic activity as compared to native VEGF-A.