Christopher Porter
Associate Professor
The goal of Christopher Porter's lab is to develop novel therapeutic strategies for leukemia through better understanding of molecular mechanisms of leukemogenesis and treatment resistance. We employ a wide variety of techniques, in vitro and in vivo, for discovery and validation of molecular vulnerabilities in cancer cells. For example, using a genome-scale shRNA screen, we identified WEE1 as a chemosensitizing target in acute myeloid leukemia (AML) cells. Subsequent studies funded by the NCI have validated this finding and supported the development of a clinical trials a WEE1 inhibitor in subjects with AML. More recently, we have discovered a novel function for the transcription factor ETV6 in regulating normal hematopoiesis and are testing whether and how Etv6 mutation promotes leukemogenesis using a new mouse model with a point mutation in Etv6. Another project in the lab is directed at understanding mechanisms of immune evasion during leukemogenesis, as well as enhancing immune cells’ response to leukemia cells.
720-232-9003
Office Location:
HSRB, Emory University
- Cancer Biology
The goal of the Porter lab is to develop novel therapeutic strategies for leukemia through better understanding of molecular mechanisms of leukemogenesis and treatment resistance. We employ a wide variety of techniques, in vitro and in vivo, for discovery and validation of molecular vulnerabilities in cancer cells. For example, using a genome-scale shRNA screen, we identified WEE1 as a chemosensitizing target in AML cells. Subsequent studies funded by the NCI have validated this finding and supported the development of a clinical trial testing a WEE1 inhibitor in children with relapsed/refractory AML. More recently, we have discovered a novel function for the transcription factor ETV6 in regulating normal B cell development, and will test whether and how Etv6 mutation promotes leukemogenesis using a new mouse model with a point mutation in Etv6. A third project in the lab is directed at understanding mechanisms of immune evasion during leukemogenesis.
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