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Vascular endothelial growth factor C promotes tumor lymphangiogenesis and intralymphatic tumor growth.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Karpanen, Terhi Egeblad, Mikala Karkkainen, Marika J. Kubo, Hitomi Ylä-Herttuala, Seppo Jäättelä, Marja Alitalo, Kari |
| Copyright Year | 2001 |
| Abstract | Many solid tumors produce vascular endothelial growth factor C (VEGF-C), and its receptor, VEGFR-3, is expressed in tumor blood vessels. To study the role of VEGF-C in tumorigenesis, we implanted MCF-7 human breast carcinoma cells overexpressing recombinant VEGF-C orthotopically into severe combined immunodeficient mice. VEGF-C increased tumor growth, but unlike VEGF, it had little effect on tumor angiogenesis. Instead, VEGF-C strongly promoted the growth of tumor-associated lymphatic vessels, which in the tumor periphery were commonly infiltrated with the tumor cells. These effects of VEGF-C were inhibited by a soluble VEGFR-3 fusion protein. Our data suggest 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. |
| File Format | PDF HTM / HTML |
| PubMed reference number | 11280723 |
| Journal | Medline |
| Volume Number | 61 |
| Issue Number | 5 |
| Alternate Webpage(s) | http://cancerres.aacrjournals.org/content/canres/61/5/1786.full.pdf |
| Alternate Webpage(s) | http://cancerres.aacrjournals.org/content/61/5/1786.full.pdf |
| Journal | Cancer research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
