Dissecting and Targeting Epigenetic and Transcriptional Dependencies in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) is an aggressive blood cancer that remains very difficult to treat. Many leukemia cells rely on changes in epigenetic regulation, which are chemical marks and molecular switches that control how genes are turned on and off, to fuel their growth. These same mechanisms may also create opportunities for better and more precise therapies. My research program seeks to understand how epigenetic changes allow leukemia cells to activate harmful gene programs, why some patients respond to epigenetic drugs while others do not, and how we can use this knowledge to improve treatment. To address these questions, my laboratory uses innovative and unbiased discovery tools and integrates multiple scientific approaches, including the study of chromatin biology, chemical and structural biology, advanced genetics and genomics, and computational analyses. Our work focuses on four major goals: identifying abnormal gene programs that drive leukemia, uncovering the epigenetic machinery that keeps these programs active, understanding why certain epigenetic therapies work in some patients but fail in others, and developing strategies to improve the effectiveness of emerging targeted treatments. Together, these efforts aim to reveal new weaknesses in leukemia cells and translate those insights into more effective and mechanism-based therapies. By deepening our understanding of the epigenetic processes that sustain AML, my research has strong potential to guide the development of safer and more durable treatment options for patients.