Funded Research 2006

Endogemous anti-angiogenic tumour suppressing VEGF splice variants in the treatment of prostate cancer.
Dr Steven Harper, David Gillatt & Dr Dave Bates, Bristol Urological Institute

It is a reality that no cell can survive if it is more than one fifth of a millimetre from a vessel. For cancers to grow from an initial cell to the size of a golf ball thousands of new vessels have to be created. Cancers use a vessel growth factor to achieve this called Vascular Endothelial Growth Factor or VEGF for short. VEGF is also produced in large quantities by normal human kidney but without any new vessel growth. While investigating this paradox we have discovered that many human tissues including kidney and prostate, in health, produce an inhibitory form of VEGF called VEGF165b. This is almost identical to conventional VEGF but crucially has completely different properties. We have shown that VEGF165b is reduced in prostate cancer and that by manipulating prostate cancer cells to over-express this inhibitory form then tumour growth can be significantly reduced.

The award recently granted to Drs Harper, Gillatt and Bates shall test whether VEGF165b over-expression in established (rather than de novo) tumours can slow tumour growth and will test whether the administration of VEGF165b protein produces a similar effect. Finally the efficacy of VEGF165b will be compared with that of a VEGF antibody, a form of which was recently licensed for use in bowel cancer.

Should these experiments confirm tumour regression in response to VEGF165b peptide it would provide the final functional proof required to justify Phase I trials of VEGF165b peptide in human prostate cancer.

 

Project commenced
March 2006

Length of project
2 years

Amount Supported
£82,000

 

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