My research is focused on characterizing aberrant signaling pathways in hematological cancer in order to identify potential targets for much need therapeutic strategies. While past focus in the lab has been on acute myeloid leukemia, currently we are interested in understanding the significance of the JAK2-V617F mutation in a family of blood diseases termed myeloproliferative neoplasms (MPNs). While patients with MPNs have an increased risk of potentially deadly coronary and blood clotting complications, MPNs also transform into acute myeloid leukemia, which is generally incurable. JAK2 is a tyrosine kinase and the V617F mutation leads to constitutive kinase activity. This mutation is prevalent in MPNs and its expression in mouse models induces an MPN-like phenotype. JAK2 inhibitors are under development, with one recently being approved for clinical use. However, to date these inhibitors have not had a significant effect at eliminating diseased cells from patients and thus do not induce remission. Therefore, there remains a need for alternative strategies to target MPN cells. It is possible that combination treatments of JAK2 inhibitors with other small molecule targeted therapies or chemotherapies will provide benefit to MPN patients. Our research is focused on understanding JAK2-V617F activation and signaling in MPNs, and identifying possible alternative therapeutic targets in MPN cells. To this end, we utilize molecular biological, cell biological, biochemical, and proteomic approaches to further our understanding of aberrant JAK2 signaling in MPNs.