Sturge, Justin - University of Hull - Department of Biology / Biomedical Sciences

个人简介

Senior Lecturer in Biomedical Science (2012–present): Dept. Biological Sciences, University of Hull, UK. Honorary Lecturer, Imperial College London (October 2011-) Lecturer, Imperial College London (2006-2011). Post-doctoral Research Fellow, Breakthrough Breast Cancer Research Centre, Institute of Cancer Research (Chester Beatty Laboratories) (2001-2006) Post-doctoral Research Assistant, The Randall Centre for Molecular Mechanisms of Cell Function, King's College London (1998-2001) PhD, Cardiovascular Science, School of Medicine, Imperial College London (1996-1998) Research Assistant in Histopathology & Cardiovascular Science, Department of Medicine, King’s College London (1992-1995) Training Fellow of Higher Education Academy (2008) Certificate for Advanced Study in Learning & Teaching (CASLAT), Imperial College London (2008) Upper Second class BSc (Hons) in Pharmacology, University of Portsmouth (1992)

研究领域

Bidirectional communication between tumour cells and the stromal compartment – which comprises fibroblasts, immune cells and the extracellular matrix (ECM) – is a key driver of metastatic progression. Tumour cells located in the primary tissue site – like the breast or prostate gland – or a distant secondary tissue site – like the bone – directly respond to signals generated by their immediate microenvironment. Conversely the cells located in the stromal compartment that normally function to maintain homeostasis of the ECM become dysregulated by signals induced by the adjacent tumour cells. The biological transmitters able to communicate these signals include: (a) soluble factors released by tumour cells and/or adjacent stromal cells; (b) cell-cell adhesion receptors that form molecular complexes between adjacent tumour cells and/or stromal cells; and (c) cell-matrix adhesion receptors that form molecular complexes between tumour and stromal cells with their surrounding ECM. The complex network of homo- and hetero- typical interactions between tumour cells and stromal cells – and tumour/stromal cell-matrix interactions – results in the formation of a ‘vicious-cycle’ where each component can direct the other to drive pathological change and further disease progression. Work in my laboratory has defined critical roles for the multidomain type I membrane receptor Endo180 (CD280; MRC2; urokinase plasminogen activator receptor associated protein, uPARAP) in the tumour and stromal compartment in carcinomas of the breast and prostate; as well as their associated secondary tumours that have established in bone. Ongoing studies aim to define the role of Endo180, its interaction partners and a number of newly identified factors in the progression of metastatic prostate and breast cancer.

近期论文

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Palmieri C, Caley MP, Purshouse K, Fonseca A-V, Rodriguez-Teja M, Kogianni G, Woodley L, Odendaal J, Elliott K, Waxman J, Sturge J. (2012). Endo180 modulation by bisphosphonates and diagnostic accuracy In metastatic breast cancer. British Journal of Cancer (accepted Nov 8 2012) Caley MP, Kogianni G, Adamarek A, Gronau JH, Rodriguez-Teja M, Fonseca A-V, Mauri F, Sandison A, Rhim JS, Palmieri C, Cobb JP, Waxman J, Sturge J. (2012). TGFβ1-Endo180 dependent collagen deposition is dysregulated at the tumour-bone stromal interface in bone metastases. Journal of Pathology, 226 (5), 775-783 http://www.ncbi.nlm.nih.gov/pubmed/22072289 Sturge J, Caley MP, Waxman J. (2011). Bone metastases - progress and challenges in treatment. Nature Reviews in Clinical Oncology, 8, 357-368 http://www.ncbi.nlm.nih.gov/pubmed/21556025 Kogianni G, Walker MM, Waxman J, Sturge J. (2009). Endo180 expression with cofunctional partners MT1-MMP and uPAR-uPA is correlated with prostate cancer progression. European Journal of Cancer, 45, 685-693 http://www.ncbi.nlm.nih.gov/pubmed/19112015 Sturge J, Wienke D, Isacke CM. (2006). Endosomes generate localized Rho-ROCK-MLC2-based contractile signals via Endo180 to promote adhesion disassembly. Journal of Cell Biology, 175, 337-347 http://www.ncbi.nlm.nih.gov/pubmed/17043135 Sturge J, Wienke D, East L, Jones GE, Isacke CM. (2003). GPI-anchored uPAR requires Endo180 for rapid directional sensing during chemotaxis. Journal of Cell Biology, 162, 789-794 http://www.ncbi.nlm.nih.gov/pubmed/12952933