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- Bone Oncology Research Group
Associate Professor of 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, where I am an Associate Professor 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
Diet-induced obesity promotes a myeloma-like condition in vivo.
Lwin ST. et al, (2015), Leukemia, 29, 507 - 510
Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease.
Fowler JA. et al, (2011), Blood, 118, 5872 - 5882
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
Increasing Wnt signaling in the bone marrow microenvironment inhibits the development of myeloma bone disease and reduces tumor burden in bone in vivo.
Edwards CM. et al, (2008), Blood, 111, 2833 - 2842
A loss of host-derived MMP-7 promotes myeloma growth and osteolytic bone disease in vivo.
Lwin ST. et al, (2017), Mol Cancer, 16
Tumour-derived alkaline phosphatase regulates tumour growth, epithelial plasticity and disease-free survival in metastatic prostate cancer.
Rao SR. et al, (2017), Br J Cancer, 116, 227 - 236
The Role of the Microenvironment in Prostate Cancer-Associated Bone Disease.
Turner CJ. and Edwards CM., (2016), Curr Osteoporos Rep, 14, 170 - 177
The role of bone marrow adipocytes in bone metastasis.
Morris EV. and Edwards CM., (2016), J Bone Oncol, 5, 121 - 123
New approaches to targeting the bone marrow microenvironment in multiple myeloma.
Gooding S. and Edwards CM., (2016), Curr Opin Pharmacol, 28, 43 - 49