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To: tnsaf who wrote (1461)	2/3/2002 4:34:10 PM
From: tnsaf	Read Replies (2) \| Respond to of 7143

Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 2, 715-720, January 22, 2002 Reactive oxygen generated by Nox1 triggers the angiogenic switch Jack L. Arbiser,, John Petros, Robert Klafter§, Baskaran Govindajaran, Elizabeth R. McLaughlin, Lawrence F. Brown¶, Cynthia Cohen, Marsha Moses, Susan Kilroy, Rebecca S. Arnold, and J. David Lambeth, Departments of Dermatology, Urology, § Hematology/Oncology, and Pathology Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322; ¶ Department of Pathology, Beth Israel Deaconess Hospital, Boston, MA 02215; and ** Department of Surgical Research, Children's Hospital and Harvard Medical School, Boston, MA 02115 The reactive oxygen-generating enzyme Nox1 transforms NIH 3T3 cells, rendering them highly tumorigenic and, as shown herein, also increases tumorigenicity of DU-145 prostate epithelial cells. Although Nox1 modestly stimulates cell division in both fibroblasts and epithelial cells, an increased mitogenic rate alone did not account fully for the marked tumorigenicity. Herein, we show that Nox1 is a potent trigger of the angiogenic switch, increasing the vascularity of tumors and inducing molecular markers of angiogenesis. Vascular endothelial growth factor (VEGF) mRNA becomes markedly up-regulated by Nox1 both in cultured cells and in tumors, and VEGF receptors (VEGFR1 and VEGFR2) are highly induced in vascular cells in Nox1-expressing tumors. Matrix metalloproteinase activity, another marker of the angiogenic switch, also is induced by Nox1. Nox1 induction of VEGF is eliminated by coexpression of catalase, indicating that hydrogen peroxide signals part of the switch to the angiogenic phenotype. ------------------------------------------------------------ www.pnas.org/cgi/doi/10.1073/pnas.022630199

To: tnsaf who wrote (1461)	2/5/2002 1:54:17 AM
From: scaram(o)uche	Respond to of 7143

>> we propose that this allele originated as a rare mutational event that nevertheless increased to high frequency in human populations by positive selection. << Well..... I don't think the "novelty seeking" linkage has held up to extensive testing (not certain, however). But..... if there is a relation..... is it surprising that thrill seekers might breed a bit faster than their reflective brothers and sisters? ("hey, baby, I have a really big dopamine receptor!")