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DMBA-induced mammary tumor progression depends on VEGF-dependent angiogenesis.

Women's Health Weekly

| October 07, 2004 | COPYRIGHT 2004 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2004 OCT 7 - (NewsRx.com & NewsRx.net) -- DMBA-induced mammary tumor progression depends on VEGF-dependent angiogenesis.

According to a study from the United States, "preinvasive mammary pathologies in humans and rat chemical carcinogenesis model systems have an increased microvascular density relative to normal tissue. This suggests the possibility of preventing invasive breast cancer by inhibiting angiogenesis. Vascular endothelial cell growth factor (VEGF) is a potent angiogenic growth factor, commonly involved in tumor-induced angiogenesis."

"Here, we show that both VEGF and VEGF receptor 2 (VEGFR2)expression increase with histological progression to invasive disease in the rat 7,12-dimethylbenz[a]anthracene (DMBA) model. Other VEGF receptors, VEGFRI, neuropilin 1 and neuropilin 2, are constitutively expressed throughout progression," said S.C. Heffelfinger and colleagues, University of Cincinnati, Department of Pathology.

"To examine whether VEGF signaling is functionally relevant to tumor-induced endothelial tubule formation in vitro and for tumor formation in vivo, we utilized the VEGFR2 inhibitor, ZD6474. In vitro endothelial cell tubulogenesis induced by isolated mammary organoids or carcinoma in situ from DMBA-treated rats is inhibited by ZD6474 in a ...

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