Harvard-MIT Division of Health Sciences and Technology
Massachusetts Institute of Technology (Cambridge, MA)
Harvard Medical School (Boston, MA)
Many cancers are continuously dependent on heterotypic interactions for their proliferation and metastasis. Angiogenesis has been shown to be crucial for tumor growth beyond a certain (microscopic) size. There are currently two canonical mechanisms for cancers' angiogenesis dependence: (1) angiogenesis as a perfusion source for tumors (Folkman et al), and (2) angiogenesis as a means of elevating intratumoral pressure and thereby facilitating metastasis and impeding physiologic humoral control of tumors (Jain et al). I am investigating the hypothesis that, in addition to the above two mechanisms, angiogenesis is also important because it delivers a source of potent regulatory cells, endothelial cells, to tumors. I am using tissue-engineered endothelial implants, which our lab has shown to be powerful regulatory constructs, to decouple the paracrine regulatory capabilities of endothelial cells from their vascular/perfusing functions.
2003 Summer Intern, Dow Chemical Chemistry and Catalysis R&D
2005-present NIH MSTP fellowship


The Adobe Flash Player plugin (version 8) is required to view the genealogy tree.
Download the plugin here.