| Autor: |
Hofmann M; Department of Dermatology, Venereology and Allergology, Goethe University, Frankfurt/Main, Germany., Pflanzer R, Zoller NN, Bernd A, Kaufmann R, Thaci D, Bereiter-Hahn J, Hirohata S, Kippenberger S |
| Jazyk: |
angličtina |
| Zdroj: |
Translational oncology [Transl Oncol] 2013 Aug 01; Vol. 6 (4), pp. 398-404. Date of Electronic Publication: 2013 Aug 01 (Print Publication: 2013). |
| DOI: |
10.1593/tlo.13274 |
| Abstrakt: |
Characteristically, most solid tumors exhibit an increased tumor interstitial fluid pressure (TIFP) that directly contributes to the lowered uptake of macromolecular therapeutics into the tumor interstitium. Abnormalities in the tumor-associated lymph vessels are a central brick in the development and prolonged sustaining of an increased TIFP. In the current study, vascular endothelial growth factor C (VEGF-C) was used to enhance tumor-associated lymphangiogenesis as a new mechanism to actively reduce the TIFP by increased lymphatic drainage of the tumor tissue. Human A431 epidermoid vulva carcinoma cells were inoculated in NMRI nu/nu mice to generate a xenograft mouse model. Seven days after tumor cell injection, VEGF-C was peritumorally injected to induce lymphangiogenesis. Tumor growth and TIFP was lowered significantly over time in VEGF-C-treated tumors in comparison to control or VEGF-A-treated animals. These data demonstrate for the first time that actively induced lymphangiogenesis can lower the TIFP in a xenograft tumor model and apparently reduce tumor growth. This model represents a novel approach to modulate biomechanical properties of the tumor interstitium enabling a lowering of TIFP in vivo. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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