Dr. Haneline’s research focuses on two broad areas. First, using a murine model of Fanconi anemia, she identified redox signaling abnormalities in Fanconi anemia hematopoietic stem and progenitor cells, which lead to impaired proliferation and survival. These alterations in function are key mechanisms that contribute to bone marrow failure in Fanconi anemia patients. By dissecting the signaling abnormalities responsible for enhanced apoptosis of Fanconi anemia progenitors, she identified a potential molecular target for treatment of these patients, which is being explored in preclinical murine models. Second, Dr. Haneline expanded her research program to investigate whether pathologic oxidative stress encountered by a fetus leads to altered neonatal endothelial progenitor cell function. These studies demonstrated that endothelial colony forming cells from infants born to mothers with pre-gestational diabetes have increased oxidative damage and impaired function, including vessel forming ability in xenograft transplants. Ongoing studies are evaluating the molecular mechanisms involved. Additionally, her laboratory demonstrated that endothelial progenitor cells are reduced in cord blood and maternal blood samples from pregnancies complicated by gestational diabetes, supporting the concept that measuring endothelial progenitor cells during pregnancy could serve as a biomarker to identify those at highest risk for vascular dysfunction. Based on these studies, she is involved in an NIH-funded Obstetric-Fetal Pharmacologic Research Unit Network grant that proposes to conduct basic and translational pharmacologic studies of drug disposition and effect on endothelial progenitor cells during normal and abnormal pregnancies.