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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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The cellular response to induction of the p21 c-Ha-ras oncoprotein includes stimulation of jun gene expression.

TL;DR: It is demonstrated that the expression of ornithine decarboxylase (ODC) mRNA is enhanced approximately 4‐6 h after the induction of the p21c‐ Ha‐ras oncoprotein, while constitutively elevated ODC was characteristic for stably c‐Ha‐ras‐transformed cells.
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Expression of growth factors and growth factor receptors in capillary hemangioblastoma.

TL;DR: It is concluded that capillary hemangioblastomas express a variety of growth factor receptors and ligands, potentially involved in both autocrine and paracrine loops.
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Is Angiopoietin-2 Necessary for the Initiation of Tumor Angiogenesis?

TL;DR: The novel finding that the angiopoietin-2 (Ang-2) signaling molecule is up-regulated in a spotlike fashion in the endothelium of growing blood vessels in glioblastoma is reported, showing that complex orchestration is required in order for angiogenesis to proceed.
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Viral oncogene-induced DNA damage response is activated in Kaposi sarcoma tumorigenesis

TL;DR: It is found that antiproliferative checkpoints are activated upon KSHV infection of ECs, and in early-stage but not late-stage lesions of clinical Kaposi sarcoma specimens, some of the first results suggesting that DNA damage checkpoint response also functions as an anticancer barrier in virally induced cancers.
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Avian vegf-c : cloning, embryonic expression pattern and stimulation of the differentiation of vegfr2-expressing endothelial cell precursors

TL;DR: VEGF-C appears to act during two different developmental phases, one early in posterior mesodermal V EGFR2-positive endothelial cell precursors which are negative for VEGFR3 and one later in regions rich in lymphatic vessels at a time when endothelial cells express both VEG FR2 and VEGfr3.