Questions about COVID-19?

What Patients & Families Need to Know | New Visitor Policy | Guidance for Community Healthcare Providers

A photo of Elisa Boscolo.

Member, Division of Experimental Hematology & Cancer Biology

Assistant Professor, UC Department of Pediatrics

513-803-7267

513-636-3549

Biography & Affiliation

Biography

Elisa Boscolo received her PhD from the University of Padua, Italy. She completed her postdoctoral training and worked as instructor in Joyce Bischoff's laboratory where she investigated the cellular basis and the molecular signaling involved in infantile hemangioma formation. In May 2014, Dr. Boscolo moved to Cincinnati Children’s Hospital Medical Center to study vascular anomalies.

Research Interests

Vascular anomalies; endothelial cell biology; mTOR signaling.

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Departments

Experimental Hematology and Cancer Biology, Cancer and Blood Diseases

Education

BS: Molecular Biology, University of Padua, Padova, Italy.

PhD: Tissue Engineering, University of Padua, Padova, Italy.

Postdoctoral Fellowship: Vascular Biology, Boston Children’s Hospital, Harvard Medical School, Cambridge, MA.

Publications

Selected Publication

Constitutive Active Mutant TIE2 Induces Enlarged Vascular Lumen Formation with Loss of Apico-basal Polarity and Pericyte Recruitment. Cai, Y; Schrenk, S; Goines, J; Davis, GE; Boscolo, E. Scientific Reports. 2019; 9.

Ponatinib Combined With Rapamycin Causes Regression of Murine Venous Malformation. Li, X; Cai, Y; Goines, J; Pastura, P; Brichta, L; Lane, A; Le Cras, TD; Boscolo, E. Arteriosclerosis, Thrombosis, and Vascular Biology. 2019; 39:496-512.

A xenograft model for venous malformation. Goines, J; Li, X; Cai, Y; Mobberley-Schuman, P; Metcalf, M; Fishman, SJ; Adams, DM; Hammill, AM; Boscolo, E. Angiogenesis. 2018; 21:725-735.

Rapamycin improves TIE2-mutated venous malformation in murine model and human subjects. Boscolo, E; Limaye, N; Huang, L; Kang, K; Soblet, J; Uebelhoer, M; Mendola, A; Natynki, M; Seront, E; Dupont, S; et al. Journal of Clinical Investigation. 2015; 125:3491-3504.

AKT hyper-phosphorylation associated with PI3K mutations in lymphatic endothelial cells from a patient with lymphatic malformation. Boscolo, E; Coma, S; Luks, VL; Greene, AK; Klagsbrun, M; Warman, ML; Bischoff, J. Angiogenesis. 2015; 18:151-162.

Pericytes From Infantile Hemangioma Display Proangiogenic Properties and Dysregulated Angiopoietin-1. Boscolo, E; Mulliken, JB; Bischoff, J. Arteriosclerosis, Thrombosis, and Vascular Biology. 2013; 33:501-509.

VEGFR-1 Mediates Endothelial Differentiation and Formation of Blood Vessels in a Murine Model of Infantile Hemangioma. Boscolo, E; Mulliken, JB; Bischoff, J. The American journal of pathology. 2011; 179:2266-2277.

JAGGED1 Signaling Regulates Hemangioma Stem Cell-to-Pericyte/Vascular Smooth Muscle Cell Differentiation. Boscolo, E; Stewart, CL; Greenberger, S; Wu, JK; Durham, JT; Herman, IM; Mulliken, JB; Kitajewski, J; Bischoff, J. Arteriosclerosis, Thrombosis, and Vascular Biology. 2011; 31:2181-U91.

Corticosteroid Suppression of VEGF-A in Infantile Hemangioma-Derived Stem Cells. Greenberger, S; Boscolo, E; Adini, I; Mulliken, JB; Bischoff, J. The New England journal of medicine. 2010; 362:1005-1013.

Multipotential stem cells recapitulate human infantile hemangioma in immunodeficient mice. Khan, ZA; Boscolo, E; Picard, A; Psutka, S; Melero-Martin, JM; Bartch, TC; Mulliken, JB; Bischoff, J. Journal of Clinical Investigation. 2008; 118:2592-2599.