One of the most exciting strategies researchers are pursuing in the fight against cancer is to cut off the blood supply of cancerous cells.

However, many initially-promising therapies have failed in part because tumour cells counteract these therapies by increasing their production of "pro-angiogenic" proteins that promote new blood vessel growth and boost tumour blood supply.

In a new study, researchers have found a way to turn the tables on this process by disrupting the ability of vascular endothelial cells (blood vessel-forming cells) to respond to these pro-angiogenic signals from tumours.

Brant Weinstein will present this research during the Haematopoeisis and Vascular Biology session as part of The Allied Genetics Conference.

The findings could open the door to new cancer treatments with a lower risk of drug resistance.

The study was conducted by an international team of researchers from the National Institutes of Health, the Chinese Academy of Sciences and Shanghai Jiao Tong University, and the University of Missouri.

Their innovative approach inhibits the replenishment of an intracellular substrate vascular endothelial cells need to respond to pro-angiogenic signals.

As the substrate gets used up, this reduces the ability of endothelial cells to respond to a pro-angiogenic agent called vascular endothelial growth factor, or VEGF, thus limiting the growth of new blood vessels.

What's more, when tumor cells attempt to overcome the therapy by increasing VEGF production, endothelial cells only consume the substrate faster, enhancing the effectiveness of the therapy and further reducing tumour blood supply.

The approach has been successful in initial tests using mice, zebrafish and cell culture.

Source: The Allied Genetics Conference