Abstract: As the most apical structure between epithelial and endothelial cells, Tight Junctions (TJ) are well known as functioning as a control for the paracellular diffusion of ions and certain molecules. It has however, become increasingly apparent that the TJ has a vital role in maintaining cell to cell integrity and that the loss of cohesion of the structure can lead to invasion and thus metastasis of cancer cells. We will present data showing how modulation of expression of TJ molecules results in key changes in TJ barrier function leading to the successful metastasis in breast and prostate cancer. It is apparent that changes in the function and regulation of TJ in cancer is not just a by-product of cancer progression but is integral to its formation and persistence, eventually enabling metastasis and secondary disease. As such, this area of research is of fundamental importance in the effort to understand and alleviate this terrible disease.

Brief Biography of the Speaker:
Following her first degree in Microbiology with Genetics, Dr Tracey Martin began her research career with a PhD in microbial molecular ecology at Cardiff University, Wales. In 1997, she became a research fellow at the Department of Surgery, Wales College of Medicine, where she still works. Initially working jointly with MARG and the Wound Healing Research Unit, in 2000 she moved fully to MARG and was appointed as a non-clinical lecturer in August 2003. She was a the recipient of an Astra-Zeneca Scholarship at the San Antonio Breast Cancer Symposium in 2002. Her main interests are how tight junctions function between normal and cancerous cells, and the interaction of cancer cells in cell-adhesion and cell-signalling; she is especially interested in VE-cadherin and how this molecule is involved in angiogenesis. In addition, she has also investigated the role of HGF/SF and other cytokines/growth factors in affecting angiogenesis and tight junction function of both endothelial and in breast & prostate cancers, together with the HGF/SF antagonist, NK4 and other anti-angiogenic molecules.