Clare Isacke
Team Leader
Molecular Cell Biology
The Institute Of Cancer Research
United Kingdom
Biography
Professor Clare Isacke studied for her BA in Biochemistry and DPhil in Developmental Biology with John Heath at the University of Oxford. She then moved to Tony Hunter's laboratory at the Salk Institute in San Diego to work on growth factor receptor signalling as a postdoctoral fellow. On returning to England, she started her own research laboratory first in the Department of Biochemistry and then in the Department of Biology at Imperial College London. She was appointed Professor of Molecular Cell Biology in 2000. In 2001, Professor Isacke moved to The Institute of Cancer Research in London to take up an appointment as Professor of Molecular Cell Biology in the Breast Cancer Now Breast Cancer Research Centre. In 2004, Professor Isacke was appointed Deputy Director of the Centre and from 2011–2013 she was the Interim Director of the Breast Cancer Now Breast Cancer Research Centre and the Interim Head of the Division of Breast Cancer Research. In 2013, she was appointed Academic Dean at the ICR.
Research Interest
Cancer as a disease can be regarded as having three broad stages: - uncontrolled growth of primary tumour - invasion into adjacent tissues - metastasis, in which tumour cells escape from the primary site and re-establish growth at distant, secondary locations In breast cancer, as in other cancers of epithelial origin, it is well recognised that these proliferative, invasive and metastatic events do not result solely from rogue cancer cells acquiring additional properties and behaving abnormally within 'normal' surroundings. Rather, all three stages rely on the ability of the tumour cells to recruit and activate neighbouring non-tumour (stromal) cells and to respond to the signals that these stromal cells produced. In addition, there is now increasing evidence that these stromal cells can modulate the response of tumour cells to both targeted therapies and cytotoxic chemotherapy. Consequently, in our laboratory, a focus is placed on tumour cells in the context of their cellular and non-cellular environments. Our goal is to identify the pathways and processes that that can be targeted for the prevention or suppression of secondary disease or which are responsible for treatment-resistant tumour progression.
Publications
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Morandi, A. & Isacke, C.M. (2014). Targeting RET–interleukin-6 crosstalk to impair metastatic dissemination in breast cancer. Breast cancer research, Vol.16(1), p. 301.
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Isacke, C.M. & Barcellos-Hoff, M.H. (2014). Soil Amendments That Slow Cancer Growth. Cancer discovery, Vol.4(6), pp. 637-639.
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Soady, K.J., Kendrick, H., Gao, Q., Tutt, A., Zvelebil, M., Ordonez, L.D., Quist, J., Tan, D.W., Isacke, C.M., Grigoriadis, A., et al. (2015). Mouse mammary stem cells express prognostic markers for triple-negative breast cancer. Breast cancer research, Vol.17(1), p. 31.
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Bacci, M., Giannoni, E., Fearns, A., Ribas, R., Gao, Q., Taddei, M.L., Pintus, G., Dowsett, M., Isacke, C.M., Martin, L.-., et al. (2016). miR-155 Drives Metabolic Reprogramming of ER + Breast Cancer Cells Following Long-Term Estrogen Deprivation and Predicts Clinical Response to Aromatase Inhibitors. Cancer research, Vol.76(6), pp. 1615-1626
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Isacke, C., viski, C., konig, C., Kijewska, M., Mogler, C. & Augustin, H. (2016). Endosialin-Expressing Pericytes Promote Metastatic Dissemination. Cancer research, Vol.76(18), pp. 5313-5325
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Locard-Paulet, M., Lim, L., Veluscek, G., McMahon, K., Sinclair, J., van Weverwijk, A., Worboys, J.D., Yuan, Y., Isacke, C.M. & Jorgensen, C., et al. (2016). Phosphoproteomic analysis of interacting tumor and endothelial cells identifies regulatory mechanisms of transendothelial migration. Science signaling, Vol.9(414), pp. ra15-ra15.
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Thway, K., Robertson, D., Jones, R.L., Selfe, J., Shipley, J., Fisher, C. & Isacke, C.M. (2016). Endosialin expression in soft tissue sarcoma as a potential marker of undifferentiated mesenchymal cells. British journal of cancer, Vol.115(4), pp. 473-479.
