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研究领域

As animals grow and develop their tissues are re-organised in a highly ordered way. Central to this remodeling is the balance between apoptosis and cell survival/proliferation signals that ultimately determines the composition and size of tissues. Appropriate regulation of these signals is important not only for the efficient removal of supernumerary, potentially harmful, cells but also for the maintenance of pluripotent cells (eg. stem cells) necessary for tissue expansion. The consequences of errors in these cell death/survival signals can be severe, and may lead to major developmental defects, immune diseases or cancer. My lab focuses on how the aberrant regulation of these processes might contribute to breast cancer. Using the mouse mammary gland as our principal model, we identified a number of candidate genes that appear to play a role in the re-organisation of different cell types during tissue morphogenesis. We have since found that some of these genes have disease-modifying effects on the establishment or progression of breast cancers, either by altering the proportion of tumour initiating cells (cancer stem cells) within the tumour or by directly affecting tumour malignancy – such as promoting the migration of cancer cells to other sites within the body. Work in our laboratory is directed at using conditional gene technology to regulate these disease modifiers in order to establish whether altering their expression could have beneficial effects on the development and progression of breast cancers. Our ongoing studies include efforts to identify novel therapeutic and diagnostic strategies that target these novel disease modifiers. This has led to the development of an experimental pharmacological agent that potently suppresses the spread of tumour cells in pre-clinical models of metastatic breast cancer.

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Yeo, S.et al. 2017. Opposing roles of Nfkb2 gene products p100 and p52 in the regulation of breast cancer stem cells. Breast Cancer Research and Treatment pdf Yeo, S.et al. 2016. Bisabolene, a sesquiterpene from the essential oil extract of opoponax (Commiphora guidottii), exhibits cytotoxicity in breast cancer cell lines. Phytotherapy Research 30(3), pp. 418-425. (10.1002/ptr.5543) pdf French, R.et al. 2015. Cytoplasmic levels of cFLIP determine a broad susceptibility of breast cancer stem/progenitor-like cells to TRAIL. Molecular Cancer 14(1), article number: 209. (10.1186/s12943-015-0478-y) pdf Piggott, L.et al. 2015. Erratum to: Suppression of apoptosis inhibitor c-FLIP selectively eliminates breast cancer stem cell activity in response to the anti-cancer agent, TRAIL. Breast Cancer Research 17(1), pp. 96. (10.1186/s13058-015-0597-9) pdf Ali, A.et al. 2015. Anti-metastatic and cytotoxic properties of frankincense and scented myrrh. Anticancer Research 35(7), pp. 4310-4311. Cowley, M.et al. 2014. Developmental programming mediated by complementary roles of imprinted Grb10 in mother and pup. PLoS Biology 12(2), pp. e1001799. (10.1371/journal.pbio.1001799) pdf Wakefield, A.et al. 2013. Bcl3 selectively promotes metastasis of ErbB2-driven mammary tumors. Cancer Research 73(2), pp. 745-755. (10.1158/0008-5472.CAN-12-1321) Smalley, M. J., Piggott, L. and Clarkson, R. W. E. 2013. Breast cancer stem cells: obstacles to therapy. Cancer Letters 338(1), pp. 57-62. (10.1016/j.canlet.2012.04.023) Soukupova, J.et al. 2012. Inhibitors of Bcl-3 as a novel therapeutic strategy for HER2+ breast cancer. European Journal of Cancer 48(5), pp. S225-S225. Piggott, L.et al. 2011. Suppression of apoptosis inhibitor c-FLIP selectively eliminates breast cancer stem cell activity in response to the anti-cancer agent, TRAIL. Breast Cancer Research 13(5), article number: R88. (10.1186/bcr2945) pdf Knight, J.et al. 2011. Evaluation of a fluorescent derivative of AMD3100 and its interaction with the CXCR4 chemokine receptor. ChemBioChem 12(17), pp. 2692-2698. (10.1002/cbic.201100441)

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