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Current Medical Student Summer Research Fellows

·	Current Medical Student Research Fellows

Brian Hanak Institution: Massachusetts General - Harvard Transformed tumor cells, including glioblastoma cells, express NKG2D ligands (NKG2DL) as a means of inducing a natural killer (NK) cell mediated immune response. NKG2DL expression is up-regulated by the induction of the DNA damage pathway. This may be significant to the progression of glioblastoma, given that CD133-expressing glioblastoma stem cells robustly activate the DNA damage pathway in response to genotoxic stress. This robust DNA damage response in CD133+ stem cells appears to contribute to their radiation resistance. My project will explore the nature of NKG2DL expression and NK cell mediated cytotoxicity before and after treating glioblastoma stem cells (CD133+) with radiation and chemotherapeutic agents. If NKG2DL expression is maintained in glioblastoma stem cells and that translates into an increased susceptibility to NK cell mediated cytotoxicity following induction of the DNA damage response then it could lead to novel therapeutic approaches to glioblastoma.