TY  - JOUR
A1  - Blaheta, Roman A.
A1  - Powerski, Maciej Janusz
A1  - Hudak, Lukasz
A1  - Jüngel, Eva
A1  - Jonas, Dietger
A1  - Knethen, Andreas von
A1  - Doerr, Hans Wilhelm
A1  - Cinatl, Jindrich
T1  - Tumor-endothelium cross talk blocks recruitment of neutrophils to endothelial cells: a novel mechanism of endothelial cell anergy
T2  - Neoplasia
N2  - The mode of the antitumoral activity of multimutated oncolytic herpes simplex virus type 1 G207 has not been fully elucidated yet. Because the antitumoral activity of many drugs involves the inhibition of tumor blood vessel formation, we determined if G207 had an influence on angiogenesis. Monolayers of human umbilical vein endothelial cells and human dermal microvascular endothelial cells, but not human dermal fibroblasts, bronchial epithelial cells, and retinal glial cells, were highly sensitive to the replicative and cytotoxic effects of G207. Moreover, G207 infection caused the destruction of endothelial cell tubes in vitro. In the in vivo Matrigel plug assay in mice, G207 suppressed the formation of perfused vessels. Intratumoral treatment of established human rhabdomyosarcoma xenografts with G207 led to the destruction of tumor vessels and tumor regression. Ultrastructural investigations revealed the presence of viral particles in both tumor and endothelial cells of G207-treated xenografts, but not in adjacent normal tissues. These findings show that G207 may suppress tumor growth, in part, due to inhibition of angiogenesis.
Y1  - 2014
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/75946
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-759460
SN  - 1476-5586
VL  - 11
IS  - 10
SP  - 1054
EP  - 1063
PB  - Elsevier
CY  - Amsterdam
ER  -