Current Research Projects

Developing an Organ-On-Chip Model of the Bone Marrow to Study AML

AML is the most aggressive type of adult leukemia that results in less than 30%  5-year survival rates. Historically, most AML studies focus on discovering the intrinsic mutations that generate AML cells; however, less is known about the role of the BMME in progressing the disease. The project is taking an innovative approach to explore the role of CCL3-mediated BMME dysregulation during AML using an in vitro model of the BMME-on-a-chip.

Targeting CCL3 Signaling as a Therapeutic Strategy for AML

Previous work by our lab and others has shown that CCL3 is upregulated in AML, and that CCL3 overexpression in murine models of AML result in a loss of osteoblastic cells, a lack of osteoblastic differentiation, and the aberrant expansion of mesenchymal stem cells. The mechanisms governing these phenomena, however, remain incompletely explored. Previous work has also shown that malignant cells lacking CCL3 are unable to maintain a leukemia stem cell population, and that inhibiting CCL3 via CCR5 antagonism reduces leukemic burden in mice.  As such, the lab is interested in the characterization of CCL3 mediated BMME dysfunction with the goal of targeting CCL3 signaling as a therapeutic strategy for AML.

Characterizing T Cell Functions in Acute Myeloid Leukemia (AML) Bone Marrow Microenvironment (BMME)

T cells are severely suppressed in the AML BMME, rendering them unable to target leukemic cells. In our lab, we aim to characterize the phenotype of T cells and study how T cells interact with other components of the BMME (leukemic cells, innate immune cells, stromal cells…etc.) in order to maintain their immunosuppression phenotypes, with the long-term goal of finding the key to reinvigorate the functionality of T cells to kill leukemic cells.