Mammalian Target of Rapamycin (mTOR) is Activated in Cutaneous Vascular Malformations <i>in Vivo</i>

Abstract

Endothelial expression of Akt is responsible for tumor responsiveness to rapamycin. We demonstrate that expression of phosphorylated S6 is elevated in specimens. Our findings provide a rationale for clinical trials of rapamycin on Sturge-Weber or Klippel-Trenaunay-Weber patients.