We investigate the role of cyclin-dependent kinases (CDKs) in regulating hematopoietic stem and progenitor cell function, leukemic transformation, and disease maintenance. A major focus of our work is to understand the mechanisms underlying response and resistance to CDK inhibitors in hematologic malignancies and solid cancer. By defining the molecular pathways that drive therapeutic associated with CDK inhibition, we aim to develop more effective combination therapies and improve patient outcomes.

Environmental exposures can profoundly affect hematopoietic stem cell function and genomic integrity. We study how environmental toxins promote clonal expansion, alter stem cell fitness, and contribute to leukemogenesis. Our goal is to uncover the biological mechanisms linking environmental risk factors to blood cancer development and to identify biomarkers for exposure-associated disease risk.

Clonal hematopoiesis represents an early stage of hematologic disease development and is associated with an increased risk of leukemia and other age-related disorders. We investigate the molecular determinants of clonal fitness, evolution, and progression to overt malignancy. By integrating genomic analyses with functional studies, including 3D Bone marrow niche models,  and patient-derived samples, we aim to improve risk stratification and develop strategies for early intervention, disease prevention, and precision medicine.