Kate Hyde, PhD, is an associate professor in the UNMC Department of Biochemistry and Molecular Biology. Her laboratory's goal is to understand the mechanisms that regulate leukemia development, with the aim of developing new and improved treatments for hematological malignancies.

Dr. Hyde's lab focuses on a subtype of acute myeloid leukemia that is caused by an inversion of chromosome 16 (Inv(16)). This inversion generates a fusion gene between the transcription factor CBFB and the gene for smooth muscle myosin heavy chain, MYH11, to generate CBFB-MYH11, which encodes the transcription factor CBFβ-SMMHC. It is known that expression of the fusion protein is the initiating event in leukemogenesis, but the role of CBFβ-SMMHC during leukemia progression is not understood. Using unique mouse models, Dr. Hyde and her lab are addressing this fundamental question. By identifying CBFβ-SMMHC’s required binding partners and its downstream target genes, the team hopes to identify new treatment strategies for patients with Inv(16) AML.

The lab also uses mouse models, cell lines, and primary patient samples to address features common to many subtypes of AML. In collaboration with David Oupicky, PhD at the UNMC College of Pharmacy, we are testing the potential of polymeric CXCR4 inhibitors for the treatment of leukemia. In the course of our experiments, we uncovered a potentially new, previously unrecognized role for CXCR4 in leukemia cells. Consequently, this project will not only test a new treatment strategy but will also have implications for our understanding of basic leukemia biology.

Students interested in research opportunities should email Dr. Hyde.