My long-term goals as a translational bone marrow transplant physician and academic researcher are to translate novel aspects of immunology to improve treatments for patients with hematologic malignancies. My clinical hematology and oncology fellowship training at University of Minnesota provided time for post-doctoral training in the laboratory of Dr. Jeffrey Miller studying receptors in human NK cell biology. While working with Dr. Miller, we described the role of a metalloproteinase protein ADAM17 in regulating the expression of CD16 and CD62L, two key proteins which play an important role in the antibody dependent cell cytotoxicity (ADCC) and trafficking function of human NK cells. During my fellowship training at Washington University School of Medicine I worked in Dr. Todd Fehniger’s laboratory working on novel approaches to augment NK cell responses to leukemia and we described human cytokine induced memory-like (CIML) NK cells which exhibit enhanced anti-leukemia responses. I have extensive experience in concepts and techniques in the field of immunobiology, and specifically NK cell biology. As a translational physician my goal is to move forward new NK cell biology concepts into the clinic in pilot, phase 1, or phase 2 clinical studies. I am currently the PI on first-in-human phase 1 study using CIML NK cells for patients with rel/ref AML (Clinicaltrials.gov ID: NCT01898793) and the one which use CIML NK cells after haploidentical transplantation in active disease AML patients (Clinicaltrials.gov ID: NCT02782546). Based on the safety and preliminary promising results from our ongoing phase I CIML NK cell study, we also intend to expand the use of CIML NK cells to AML patients relapsed after allogeneic stem cell transplantation who have otherwise very limited treatment options.
I am also currently in charge of our haploidentical transplant program and am the PI on several early phase clinical trials using post transplant cyclophosphamide based haploidentical transplant as a platform for cellular therapies and novel agents targeting graft versus host disease causing alloreactive T cells.