Our lab studies the genetic and epigenetic drivers of leukemia. Our gene of interest, CHAF1B, is located within the Down syndrome critical region of chromosome 21. Children with Down syndrome are predisposed to leukemias, suggesting that elevated expression of genes on chromosome 21 is somehow involved in leukemia progression.
We are excited to make fundamental discoveries about the molecular drivers of leukemia and are always trying to understand how cells use the process of chromatin assembly to maintain their state. Defects in this process lead to cancer or tissue failure. We found that chromatin assembly is directly linked to transcriptional regulation in acute myeloid leukemia, and that leukemias are driven by CHAF1B and the chromatin assembly complex binding regions of DNA associated with stem cell differentiation genes, repressing their expression.
I am honored to be a Transition to Independence Award recipient from the National Cancer Institute (NCI) K99/R00 (2019). My work has been published in many well-respected journals, including Genes and Development, Clinical Cancer Research, Cancer Cell, Leukemia, Cell, Molecular Cell, Stem Cells and Biochimica et Biophysica Acta-Gene Regulatory Mechanisms. I have more than 11 years of research experience, and I began my work at Cincinnati Children’s in 2020.
Epigenetics; chromatin assembly; Acute Myeloid Leukemia; down syndrome; genetic drivers of leukemia and bone marrow failure
Assistant Professor, UC Department of Pediatrics
Experimental Hematology and Cancer Biology