UK and Australian scientists have been able to show ways in which we can markedly improve drug targeting of solid tumours, using tiny 'biosensors' along with new advanced imaging techniques.
In real time and in three dimensions, these technologies can show us how cancers spread and how active cancer cells respond to a particular drug. They can also tell us how much, how often and how long to administer drugs. Finally, using preclinical models of the disease, they can guide the use of 'combination therapies', techniques that enhance drug delivery by breaking up the tissue surrounding a tumour.
The study was performed by Dr Paul Timpson of the Garvan Institute of Medical Research and Professor Kurt Anderson of the Beatson Institute for Cancer Research in Glasgow, UK. PhD student Max Nobis studied the signaling protein 'Src', which becomes activated to drive invasive pancreatic cancer, and looked at how it could best be deactivated by a small molecule inhibitor - currently in phase II clinical trials - known as 'dasatinib'. Their findings are published in the journal Cancer Research, now online.
"We have already shown that Src is activated in pancreatic tumours and we knew that dasatinib deactivates Src and could partially reduce the spread of this form of cancer. Through a collaborative partner in the US, we had access to FRET (Fluorescence Resonance Energy Transfer) imaging technology," said Dr Paul Timpson.
"Until now, we have been limited to studying tumour signalling in two dimensions - and lacked a dynamic way of reporting on drug targeting in live tumour tissue. Nanotechnology opens up a portal into living tissue that allows us to watch cancers spreading, and to determine which parts of a tumour we should be targeting with drugs."