Professor Claire Edwards

Professor Claire Edwards (née Shipman) obtained a first class honours degree and PhD from the University of Sheffield, where she began her career in cancer-induced bone disease. Following postdoctoral studies at the University of Sheffield and the University of Oxford, Prof. Edwards moved to the United States in 2004 to take up assistant professor positions at the University of Texas Health Science Center at San Antonio and subsequently at Vanderbilt University. Prof. Edwards is the recipient of multiple awards and fellowships, including most recently, the Iain T Boyle Award from the European Calcified Tissue Society.

Prof. Edwards relocated her lab to the University of Oxford as an Associate Professor of Bone Oncology, with a joint appointment in the Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS) and the Nuffield Dept of Surgical Sciences. She leads the bone oncology research group, focused upon the pathogenesis of cancer-induced bone disease. Specific interests include the contributions of the host bone marrow microenvironment and the role of obesity, adipocytes and adipokines.

Lwin, S.T., Olechnowicz, S.W.Z., Fowler, J.A., Edwards, C.M. Diet-induced obesity promotes a myeloma-like condition in vivo. (2014) Leukemia (in press)

Webb, S.L., Edwards C.M. Novel therapeutic targets in myeloma bone disease. (2014) British Journal of Pharmacology 171: 3765 – 3776

Olechnowicz, S.W.Z., Edwards, C.M. Contributions of the host microenvironment to cancer-induced bone disease. (2014) Cancer Research, 74(6): 1625-31.

Edwards, C.M. BTK inhibition in myeloma: targeting the seed and the soil. (2012) Blood, 120(9): 1757-9.

Fowler J.A., Mundy G.R., Lwin S.T., Edwards C.M. Bone marrow stromal cells create a permissive microenvironment for myeloma development: a new stromal role for Wnt inhibitor Dkk1. (2012) Cancer Research, 72(9): 2183-9.

Fowler, J.A., Lwin, S.T., Drake, M.T., Edwards, J.R., Kyle, R.A., Mundy, G.R., Edwards, C.M. Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease. (2011) Blood 118; 5872-82.

Yang, L., Edwards, C.M., Mundy, G.R. GR-1+ CD11b+ myeloid-derived immune suppressor cells: Formidable partners in tumor metastasis. (2010) Journal of Bone and Mineral Research 25; 1701-6.

Ayati, B.P., Edwards, C.M., Webb, G.F., Wikswo, J.P. A mathematical model of bone remodelling dynamics for normal bone cell populations and myeloma bone disease (2009). Biology Direct 5; 28.

Fowler, J.A., Mundy, G.R., Lwin, S.T., Edwards, C.M. A murine model of myeloma that allows genetic manipulation of the host microenvironment (2009) Disease Models & Mechanisms 2; 604-611.

Edwards, C.M., Lwin, S.T., Fowler, J.A., Oyajobi, B.O., Bates, A.L., Mundy, G.R. Myeloma cells exhibit an increase in proteasome activity and an enhanced response to proteasome inhibition in the bone marrow microenvironment in vivo. (2009) American Journal of Hematology 84; 268-72.

Edwards, C.M. (2008) Wnt signaling; Bone’s defense against myeloma. Blood 112; 216-217.

Edwards, C.M., Edwards, J.R., Esparza, J., Oyajobi, B.O., McCluskey, B., Munoz, S., Grubbs, B., Mundy, G.R. (2008) Increasing Wnt signaling in the bone marrow microenvironment inhibits the development of myeloma bone disease and reduces tumor burden in bone in vivo. Blood 111; 2833-2842.