Skip to main content
. Author manuscript; available in PMC: 2009 Dec 25.
Published in final edited form as: Nature. 2009 May 20;459(7250):1126–1130. doi: 10.1038/nature08062

Figure 1. Dscr1 expression is upregulated in Down syndrome tissues and tumor angiogenesis is suppressed in Down syndrome models.

Figure 1

(a) Increased DSCR1 expression in human fetal Down syndrome (DS) tissues versus age-matched control (ctrl) tissues relative to β-actin. (b) Tumor growth is suppressed in the Ts65Dn Down syndrome mouse model. Values are mean ± s.e.m. n=10–12, *p<0.03; **p <0.01. (c) Microvessel density (MVD) per high-powered field (hpf) of tumors is quantified by anti-CD31 immunofluorescence. Bar, 20 µM. Values are mean ± s.e.m. *p <0.02; **p<0.01. (d) Angiogenesis in tumors from induced pluripotent stem cells (iPS) isolated from Down syndrome or cytogenetically normal cells was quantified by human specific anti-CD31 immunofluorescence. Arrows, hCD31-positive vessels. Values are mean ± s.e.m. n=3–6, **p<0.01.