Stopping tumours from hijacking the blood supply
Professor Robert Kerbel is using funding from Worldwide Cancer Research to work out how breast tumours that have spread to the lungs connect themselves to the blood supply. The team hopes this will lead to the development of an entirely new way of targeting the tumour’s vasculature to treat cancer that has spread.
Mouse models of cancer are currently the most common and initial way to test whether or not new treatments may be safe and effective to trial in patients. But we know that these models often can’t tell us exactly what will happen and so many drugs that show promise in such preclinical studies fail to work as effectively in patients once they enter advanced clinical trials.
One type of approved treatment that has partially fallen victim to this is a class of drugs called anti-angiogenics. These drugs are aimed at blocking the growth of new blood vessels from existing ones in a tumour (“tumour angiogenesis”) in the hope of cutting off the supply of oxygen nutrients that tumours need to keep growing and spreading. However, with some exceptions, these drugs have not worked as well in patients as originally anticipated, especially when treating metastatic disease that has spread to sites such as the lungs.
Professor Robert Kerbel and others have shown previously that this may be because secondary tumours connect to the blood supply in a different way to the primary tumour in that they can hijack the existing blood vessel supply. Now Professor Kerbel wants to understand how much this different process contributes to anti-angiogenic drugs not working optimally. He and his team also want to work out what the molecular features are of this process in the hope that it will help them identify whole new ways to target advanced cancers by selective targeted therapy of the hijacked blood vessels in tumours such as lung metastases.