Vascular malformations are disorders in which blood or lymphatic vessels develop abnormally, often causing serious health problems in children. A better understanding these conditions is essential for improving treatments and saving the lives of children with life-threatening vascular malformations or anomalies.
My research focuses on how blood and lymphatic vessels grow and what goes wrong when vascular diseases develop. By studying patient samples and cells, my team works to identify the key biological changes that drive these disorders and to discover new treatment options.
Working with colleagues at Cincinnati Children’s, we have also studied genetic changes that contribute to vascular malformations in children. Our research has helped uncover new approaches for targeted treatment.
A key strength of our work is our close collaboration with physicians at Cincinnati Children’s and other pediatric hospitals. These partnerships allow us to study patient blood samples and gain unique insights into disease processes.
I have more than 30 years of experience in vascular research and have been part of Cincinnati Children’s since 2001. My work has been published in leading medical and scientific journals and is focused on improving the diagnosis and treatment of vascular disorders in children.
Fellowship: Postdoctoral, University of Virginia, Charlottesville, VA, 1996
PhD: University of Cambridge, UK, 1992
BS: Biochemistry, Brunel University, London, UK, 1987
Pathogenesis of vascular anomalies; vascular malformations; kaposiform lymphangiomatosis; capillary lymphatic venous malformations; pulmonary hypertension; pulmonary vascular disease; bronchopulmonary dysplasia
NRASQ61R Expression in Lymphatic Endothelial Cells Causes Enlarged Vessels, Hemorrhagic Chylous Effusions, and High Mortality in a Mouse Model of Kaposiform Lymphangiomatosis. Pediatric Blood and Cancer. 2026; 73(7):e70339.
MEK Inhibition Reduces Vascular Malformations and Gene Dysregulation in NRASQ61R Human Endothelial Cells. Pediatric Blood and Cancer. 2026; 73(3):e70002.
Trametinib normalizes angiopoietin-2 levels and successfully treats kaposiform lymphangiomatosis. Journal of Vascular Anomalies. 2025; 6(4).
Use of angiopoietin-2 as a biomarker in vascular anomalies beyond complex lymphatic anomalies. Blood. 2025; 146(Supplement 1):4877.
Human Lymphatic Endothelial Cells Expressing NRASQ61R Model Characteristics of Kaposiform Lymphangiomatosis. Pediatric Blood and Cancer. 2025; 72(11):e31984.
RAS Pathway Mutations and Therapeutics in Vascular Anomalies. Pediatric Blood and Cancer. 2025; 72(5):e31605.
Lyve1-Driven NrasQ61R Causes Edema, Enlarged Lymphatic Vessels, and Hepatic Vascular Defects in Embryonic Mice. Pediatric Blood and Cancer. 2025; 72(3):e31492.
NRASQ61R mutation drives elevated angiopoietin-2 expression in human endothelial cells and a genetic mouse model. Pediatric Blood and Cancer. 2024; 71(7):e31032.
How we use angiopoietin-2 in the diagnosis and management of vascular anomalies. Pediatric Blood and Cancer. 2024; 71(5):e30921.
Kaposiform lymphangiomatosis: Diagnosis, pathogenesis, and treatment. Pediatric Blood and Cancer. 2023; 70(4):e30219.