Blocking bio-parcels to stop breast cancer spreading

Professor Ed Tate is studying how breast cancer spreads to other organs. He hopes that blocking a protein involved in messaging between cells could prevent this happening and potentially be an effective new treatment for patients.

Hope for the future

Breast cancer is the most common cancer in women in the world. In 2020, almost 685,000 women worldwide died of breast cancer. A lot of progress has been made in treating breast cancer if caught early, however it is much harder to treat once it has spread to other organs. 

Breast tumours are able to send signals to other organs around the body, making it easy for new tumours to develop there. Professor Ed Tate and his team are studying how blocking these signals could stop breast cancer spreading with the hope of being able to develop new treatment options. 

Meet the scientist

Prof Ed Tate studied chemistry at the University of Durham before carrying our a PhD at the University of Cambridge. After a period working in Paris he moved to Imperial College London where he leads a team of over 60 researchers. 

The science

Breast tumours can communicate with other organs around the body and make them more receptive to hosting new tumours as the cancer spreads. They do this by sending tiny parcels of genetic information, proteins and fats, called exosomes, which can travel between cells. The exosomes sent by breast tumours make things easier for cancer cells to seed a new tumour by altering the immune response in the target organ. 

Professor Tate and his team recently found that mice lacking a protein called Rab27 were less likely to have breast cancer spread to other organs. For the first time, Professor Tate and his team found a way to block Rab27 with drugs and believe this has potential as a new treatment to stop breast cancer spreading. 

The researchers now aim to develop these new drugs further, and will test how well they can target Rab27 and block it in cells in the lab. The team hope this will reveal important new insights into the role of Rab27 in the spread of breast cancer, and lay the groundwork for future trials blocking Rab27.