Scientists have discovered a ‘hidden’ mechanism which could explain why some cancer therapies which aim to starve the tumour of its blood supply are failing cancer trials.

Numerous angiopoietin-blocking therapies are currently in clinical trials for ovarian cancer and other cancers.

But despite promising earlier results, some of these therapies are not improving patient survival as much as was expected.

Many current angiopoietin-blocking therapies work by inhibiting a specific cell pathway which promotes blood vessel growth.

The pathway involves angiopoietin-1 and angiopoietin-2 proteins and also another protein, called Tie-2.

However this latest research, supported by Worldwide Cancer Research and published in Nature Communications suggests the existence of an alternative angiopoietin-mediated mechanism which ‘bypasses’ Tie-2.

Lead researcher, Dr Pipsa Saharinen, at the University of Helsinki said: “What we have found in our studies on cells and in mice, is another angiopoietin-2 cell pathway which could promote blood vessel growth. This pathway is not necessarily targeted by current angiopoietin-blocking therapies, and this could help explain why some of the trials have not produced as much benefit as we might have hoped.”

“We still need to confirm what we’re seeing in normal cells is happening in tumours as well” says Dr Saharinen.

“And we have to figure out what actually happens inside the body. Then we can work out for sure how blocking this new angiopoietin‑2 pathway affects tumour blood vessels. Ultimately, I think these results could help explain some of the confusing trial results we’ve seen.”

Dr Helen Rippon, Head of Research at Worldwide Cancer Research said: “Around 19 women in the UK are diagnosed with ovarian cancer every day, and better treatments are desperately needed. There is still a lot of work to do to, but this finding could ultimately help us develop more effective anticancer treatments which work by blocking a tumour’s blood supply.”

Reference

Hakanpaa et al, 2015. Endothelial destabilisation by angiopoietin-2 via integrin β1 activation. Nature Communications

Source: Worldwide Cancer Research