Stopping prostate cancer growing and spreading by targeting blood vessels

University of BristolProfessor David Bates£98,8892010 - 2013

Why we funded it

New therapies for prostate cancer are needed to address the growing level of resistance to existing treatments. The pathway Professor Bates and his team have identified is a completely new way of blocking cancer growth, but is as yet untested in prostate cancer. If they can successfully show that this pathway - the splicing pathway - is effective in prostate cancer it can be used to develop new drugs that target this pathway.


Scientific title

Alternative splicing as a novel drug for prostate cancer

Research project summary

Although there are only 20,000 human genes, they can generate over 1 million different proteins because the messages they give out are edited in many different ways.  Professor Bates's group has already found that a key protein involved in growing new blood vessels within tumours, VEGF, is a gene that produces different forms of message.

One of these VEGF messages encourages blood vessel growth into tumours, another suppresses it.  As prostate cancer progresses, there is a switch towards the form that encourages blood vessel growth, so feeding the tumour with nutrients and oxygen.  This project will study why this switch happens and whether it can be prevented by manipulating two proteins, ASF and SRPK1, which appear to control it.

Using prostate cancer cells cultured in the laboratory, rodent models and samples of human prostate tumours the student working on this project will manipulate these proteins to see whether this causes the blood vessel suppressing form of VEGF to be produced in cancer cells.  If so, there are already chemicals that block ASF and SRPK1 which could form the beginnings of a new therapy for prostate cancer.

Professor Bates hopes that by the end of this project the research will be at a stage for drug companies to further develop these chemicals into effective treatments for advanced prostate cancer.