Improving treatments for ovarian cancer
Professor Jonathan Ledermann is leading an international clinical trial of a new treatment for women with ovarian cancer. This disease often becomes resistant to chemotherapy, making it difficult to treat. The new drug could help to block blood vessel growth in the tumour, starving the cancer cells.
Targeting new blood vessel growth
Like all cancers, ovarian cancer depends on the formation of new blood vessels to supply the tumour with essential nutrients and oxygen. Molecules released by the cancer cells act on endothelial cells encouraging the growth of new vessels. This process of blood vessel growth is called angiogenesis.
One of the most important of these 'signal' molecules is a protein called vascular endothelial growth factor (VEGF). Levels of VEGF are often high in ovarian cancer patients. Targeting VEGF to block blood vessel growth offers a potential new way to treat this disease.
Professor Jonathan Ledermann and his team are carrying out a trial called ICON-6 testing a new drug called Cediranib. This blocks the action of VEGF by targeting its receptor on the surface of endothelial cells.
Women from several countries including the UK and Canada are currently being recruited for the trial. Patients will receive chemotherapy with or without Cediranib to see if the new drug improves the current standard treatment. Some patients will also receive cediranib after chemotherapy to see if it helps stop the cancer returning.
The results of this trial could lead to much-needed new ways to treat ovarian cancer more successfully.
Listen to an audio package featuring Professor Ledermann talking about the importance of clinical trials for cancer research, and how they are carried out:
Other research projects by Jonathan Ledermann
CRUK/07/025: ICON6: An international randomised trial of molecular targeted therapy with AZD2171 with Pt-based chemotherapy for patients with ovarian cancer relapsing more than 6 months following completion of first line Pt-based
Funding period: 01 July 2007 to 30 June 2014
Funding period: 01 October 2008 to 30 September 2013
MDM2 interacts with NME2 (non-metastatic cells 2, protein) and suppresses the ability of NME2 to negatively regulate cell motility
Combined p53 and MDM2 biomarker analysis shows a unique pattern of expression associated with poor prognosis in patients with renal cell carcinoma undergoing radical nephrectomy