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Vascular Endothelial Growth Factor C–Induced Lymphangiogenesis DecreasesTumor Interstitial Fluid Pressure and Tumor Growth1

Identifieur interne : 002F98 ( Main/Curation ); précédent : 002F97; suivant : 002F99

Vascular Endothelial Growth Factor C–Induced Lymphangiogenesis DecreasesTumor Interstitial Fluid Pressure and Tumor Growth1

Auteurs : Matthias Hofmann [Allemagne] ; Ralph Pflanzer [Allemagne] ; Nadja Nicole Zoller [Allemagne] ; August Bernd [Allemagne] ; Roland Kaufmann [Allemagne] ; Diamant Thaci [Allemagne] ; Jurgen Bereiter-Hahn [Allemagne] ; Satoshi Hirohata [Japon] ; Stefan Kippenberger [Allemagne]

Source :

RBID : PMC:3730014

Abstract

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.


Url:
PubMed: 23908682
PubMed Central: 3730014

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PMC:3730014

Le document en format XML

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<p>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
<italic>in vivo</italic>
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