Eileen M. Shore, Ph.D.
Research Associate Professor of Orthopaedic SurgeryResearch Associate Professor of Genetics
HOMETOWN
EDUCATION
Ph.D., Cell and Molecular Biology, University of Pennsylvania, 1987
M.A., Biology, Indiana University, 1978
B.S., Biology, University of Notre Dame, 1976
AREAS OF EXPERTISE
Genetic diseases of bone formation and development. Molecular biology and genetics of bone formation
AREAS OF SPECIAL INTEREST
Research is focused on genetic diseases of bone formation, mainly fibrodysplasia ossificans progressiva (FOP) and progressive osseous heteroplasia (POH). Both of these rare disorders are characterized by de novo formation of bone: in FOP, the ectopic bone forms in deep connective tissues such as muscle; and in POH, bone formation initiates within the skin. Our goals are to identify the genetic causes of these conditions and the cellular pathways that are involved in the induction of bone development and formation, and to use this information to develop treatments for these and other disorders of bone.
RECENT PUBLICATIONS
- Kaplan, F.S. and E.M. Shore (2000). Progressive osseous heteroplasia: a perspective. J. Bone Min. Res. 15, 2084-2094.
- Shore, E.M., J. Ahn, S. Jan de Beur, M. Li, M. Xu, R.J.M. Gardner, M.A. Zasloff, M.P. Whyte, M.A. Levine, and F.S. Kaplan (2002). Paternally inherited inactivating mutations of the GNAS1 gene in progressive osseous heteroplasia (POH). New Engl. J. Med. 346, 99-106.
- Olmsted, E.A., F.S. Kaplan, and E.M. Shore (2003). Bone morphogenetic protein 4 regulation in fibrodysplasia ossificans progressiva. Clin. Ortho. Rel. Res. 408, 331-343.
- Glaser, D.L., Economides, A.N., L. Wang, X. Liu, R. Kimble, J. P. Fandl, J.M. Wilson, N. Stahl, F.S. Kaplan, E.M. Shore (2003). In Vivo Somatic Cell Gene Transfer of an Engineered Noggin Mutein Prevents BMP4-Induced Heterotopic Ossification in the Mouse. JBJS 85-A (12), 2332-2342.
- Serrano de la Pena, L., P.C. Billings, J.L. Fiori, J. Ahn, F.S. Kaplan, E.M. Shore (2005). Fybrodysplasia ossificans progressiva (FOP), a disorder of ectopic osteogenesis, misregulates cell surface expression and trafficking of BMPRIA. J. Bone Min. Res. 20 (7), 1168-1176.

