The Richard J. Jones Lab studies normal and cancerous stem cells in order to make clinical improvements in areas such as blood and marrow transplantation (BMT). We discovered one of the most common stem-cell markers, Aldefluor, which identifies cells based on their expression of aldehyde dehydrogenase 1 (ALDH1), and have used this marker to detect and characterize normal stem cells and cancer stem cells from many hematologic malignancies. We also developed post-transplant cyclophosphamide and effective related haploidentical BMT.

The Linda Smith-Resar Lab primarily investigates hematologic malignancy and molecular mechanisms that lead to cancer as well as sickle cell anemia. Recent studies suggest that education is an important and effective component of a patient blood management program and that computerized provider order entry algorithms may serve to maintain compliance with evidence-based transfusion guidelines. Another recent study indicated that colonic epithelial cells undergo metabolic reprogramming during their evolution to colorectal cancer, and the distinct metabolites could serve as diagnostic tools or potential targets in therapy or primary prevention.

Our broad research goals are to identify and validate novel molecular therapeutic targets in hematopoietic malignancies. We are interested in the identification and pre-clinical development of novel targeted therapies, and, in particular, the “translational” step of this research by using correlative studies to incorporate these novel therapies into existing treatments. Our research is of particular interest to those who wish to be involved in directly translating the results of laboratory bench work into meaningful benefits for patients. Currently, we are actively involved in the pre-clinical and clinical development of small molecule kinase inhibitors targeting the FLT3 signaling pathway in acute myeloid leukemia. We are interested in 3 compounds in particular- AC220, a FLT3/KIT inhibitor; crenolanib,a selective FLT3 inhibitor with activity against resistant point mutations; and PLX3397, another inhibitor of KIT and FLT3. The active projects in the lab include: 1) Characterization of cytotoxic responses of different hematologic malignancies to FLT3 and KIT kinase inhibition; 2) Examination of the interaction of bone marrow stroma and stroma-derived cytokines on the efficacy of these inhibitors; 3) Examination of the differential effect of FLT3 inhibition versus combined FLT3/KIT inhibition on acute myeloid leukemia and bone marrow progenitor cells; and 4) Correlative laboratory studies using blood and marrow samples from patients treated with FLT3 inhibitors, with the aim of developing predictive models for clinical response.