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Terhi Karpanen

Researcher at Ludwig Institute for Cancer Research

Publications -  47
Citations -  9405

Terhi Karpanen is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Lymphatic system & Vascular endothelial growth factor. The author has an hindex of 33, co-authored 47 publications receiving 8899 citations. Previous affiliations of Terhi Karpanen include University of Helsinki & Helsinki University Central Hospital.

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Isolated lymphatic endothelial cells transduce growth, survival and migratory signals via the VEGF‐C/D receptor VEGFR‐3

TL;DR: It is shown that VEGFR‐3 stimulation alone protects the lymphatic endothelial cells from serum deprivation‐induced apoptosis and induces their growth and migration, and defines the critical role of VEGF‐C/VEG FR‐3 signalling in the growth and survival of lymphatichelial cells.
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Inhibition of lymphangiogenesis with resulting lymphedema in transgenic mice expressing soluble VEGF receptor-3.

TL;DR: It is shown that a soluble form of VEGFR-3 is a potent inhibitor of Vascular endothelial growth factor (VEGF)-C and VEGF-D signaling, and when expressed in the skin of transgenic mice, it inhibits fetal lymphangiogenesis and induces a regression of already formed lymphatic vessels, though the blood vasculature remains normal.
Journal Article

Vascular Endothelial Growth Factor C Promotes Tumor Lymphangiogenesis and Intralymphatic Tumor Growth

TL;DR: It is suggested 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.
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Vascular Endothelial Growth Factor Ligands and Receptors That Regulate Human Cytotrophoblast Survival Are Dysregulated in Severe Preeclampsia and Hemolysis, Elevated Liver Enzymes, and Low Platelets Syndrome

TL;DR: VEGF family members regulate cytotrophoblast survival and that expression of a subset of family members is dysregulated in severe forms of preeclampsia, which is shown to be key regulators of conventional vasculogenesis and angiogenesis.