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- Bone Oncology Research Group
- University Lecturer in Bone Oncology
I obtained a first class honours degree and Ph.D. from the University of Sheffield, where I began my career in cancer-induced bone disease. Following postdoctoral studies at the University of Sheffield and the University of Oxford, i 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. I am the recipient of multiple awards and fellowships, including most recently, the Iain T. Boyle Award from the European Calcified Tissue Society. I relocated my lab to the University of Oxford as a University Lecturer in Bone Oncology, with a joint appointment in NDS and the Nuffield Dept. of Orthopaedics, Rheumatology and Musculoskeletal Sciences, and a fellowship at St. Edmund Hall.
Cancer-induced bone disease is a characteristic feature of several types of cancer, including the haematological malignancy multiple myeloma, and other tumours that metastasise to bone such as breast, prostate and lung. In addition to the development of debilitating skeletal complications, the bone marrow provides a unique hospitable microenvironment, and once tumours become established in bone, they are largely unresponsive to treatment.
The overall goal of our research is to elucidate the cellular and molecular mechanisms that contribute to disease pathogenesis, and so identify and validate novel therapeutic approaches. Our focus is on the role of the tumour microenvironment and tumour-host interactions.
Major themes include; Obesity and adipokines in cancer-induced bone disease, MMPs in myeloma bone disease, miRNA in prostate cancer bone metastases and bone marrow stromal cells in the pathogenesis of cancer-induced bone disease
Bisphosphonates induce apoptosis in human myeloma cell lines: a novel anti-tumour activity.
Shipman CM. et al, (1997), Br J Haematol, 98, 665 - 672
The bisphosphonate, zoledronic acid, induces apoptosis of breast cancer cells: evidence for synergy with paclitaxel.
Jagdev SP. et al, (2001), Br J Cancer, 84, 1126 - 1134
Osteoprotegerin inhibits the development of osteolytic bone disease in multiple myeloma
Croucher PI. et al, (2001), Bone, 28, S81 - S81
The bisphosphonate incadronate (YM175) causes apoptosis of human myeloma cells in vitro by inhibiting the mevalonate pathway.
Shipman CM. et al, (1998), Cancer Res, 58, 5294 - 5297
Zoledronic acid treatment of 5T2MM-bearing mice inhibits the development of myeloma bone disease: evidence for decreased osteolysis, tumor burden and angiogenesis, and increased survival.
Croucher PI. et al, (2003), J Bone Miner Res, 18, 482 - 492
Novel therapeutic targets in myeloma bone disease.
Webb SL. and Edwards CM., (2014), Br J Pharmacol
Contributions of the host microenvironment to cancer-induced bone disease.
Olechnowicz SW. and Edwards CM., (2014), Cancer Res, 74, 1625 - 1631
The role of microRNAs in functional osteomimicry in prostate cancer cells
Rao SR. et al, (2013), International Journal of Experimental Pathology, 94, A10 - A10
BTK inhibition in myeloma: targeting the seed and the soil.
Edwards CM., (2012), Blood, 120, 1757 - 1759
Bone marrow stromal cells create a permissive microenvironment for myeloma development: a new stromal role for Wnt inhibitor Dkk1.
Fowler JA. et al, (2012), Cancer Res, 72, 2183 - 2189