Christopher C Porter
|Title||Assoc Professor Adjoint|
|Institution||University of Colorado Denver - Anschutz Medical Campus|
|1995||Peacock Family Award for Outstanding Performance in Gross Anatomy, Medical College of Georgia|
|1998||Alpha Omega Alpha Honor Medical Society, Medical College of Georgia|
|2003 - 2004||Ruth L. Kirschstein National Research Service Award, University of Colorado School of Medicine|
|2004||W.M. Thorkildson Research Fellowship, University of Colorado School of Medicine|
|2005 - 2006||Brent Eley/Brian Hicks Research Award, Brent Eley Foundation|
|2008 - 2009||Paul Calabresi Clinical Scholars Award, University of Colorado Cancer Center|
|2011||Scholars Award, Hyundai Hope on Wheels Foundation|
|2013||Acute Lymphoblastic Leukemia Young Investigator Award, CureSearch|
Dr. Porter is a Pediatric Hematologist-Oncologist with extensive training in basic, translational, and clinical sciences. After clinical training in pediatrics and pediatric hematology-oncology, he joined the laboratory of James DeGregori, Ph.D. for training in Biochemistry & Molecular Genetics. After fellowship, he was awarded the Paul Calabresi Clinical/Translational Scholars Award, which provided mentorship and training in Experimental Therapeutics with Lia Gore, M.D. He now runs a lab with the goal of improving the care of patients with leukemia. His lab now consists of 6 others focused on identifying and validating novel strategies for treating leukemia through functional genomic screening with RNA-interference libraries and translational murine models of disease. The clinical implications of these projects are emphasized, with the concrete goal of translating laboratory findings into clinical trials. In addition to directing the lab, he is the Study Chair/PI of an investigator initiated, NCI supported trial (NCT01456988) which translates preclinical data from similar functional genomics studies by "re-purposing" cyclosporine to inhibit WNT/calcineurin/NFAT signaling to sensitize BCR-ABL1+ leukemia cells to tyrosine kinase inhibition.
Several members of the lab are currently working on further validation of one particular molecule, WEE1 that, when inhibited, sensitizes acute myeloid leukemia cells to cytarbaine. WEE1 is a cell cycle checkpoint protein kinase that is activated to stall cell cycle progression in the context of DNA damage. Using shRNA and a small molecule inhibitor in clinical development, the lab has demonstrated that inhbition of WEE1 is synergistic with cytarabine in inhibiting AML cell proliferation by inhibiting the S-phase checkpoint and inducing apoptosis. These data are being confirmed in mouse models of leukemia including primary patient xenografts. Clinical trials testing the combination of cytarabine and WEE1 inhibition are being planned.
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