Research
Our research focuses on the role certain pathways and mutations, namely the JAK2V617F mutation in the JAK/STAT signaling pathway, alongside other co-mutations, play in the role of disease progression in myeloproliferative neoplasms (MPNs). Previous work by Dunbar et al. has reported that the JAK2V617F mutation plays an essential role in MPN disease, particularly as JAK2V617F deletion has shown to abrogate MPN features, inducing depletion of mutant-specific hematopoietic stem-progenitor cells and suggesting improved JAK2V617F targeting offers greater therapeutic efficiency.
Our major ongoing research projects include the following:
- Pre-clinical testing of novel small molecule inhibitors, including “second-generation” JAK2 inhibitors, to compare efficacy against current standard of care agents
- Using novel genetically engineered murine models of MPN to study how different DNA mutations cooperate with one another to promote disease progression and resistance to current inhibitor agents
- Using novel spatial approaches, including proteomics, along with deep learning methods to investigate how MPN cells localize with one another and surrounding cells in the bone marrow microenvironment
- Collaborating with outside investigators to use novel single-cell multi-modal sequencing methods to uncover how MPNs transform into more aggressive acute leukemias
- Investigating novel drugs and drug combinations using various MPN model systems