Coloured scanning electron micrograph of solon cancer cells

Some colon tumours contain two distinct populations of cells, each resistant to a key class of drugs. Credit: Dr Gopal Murti/SPL


A double-pronged attack on colon tumours succeeds where one doesn’t

Two populations of colon-cancer cells form a seamless and deadly partnership.

Colon-cancer treatment could be improved by targeting two signalling systems in tumour cells simultaneously, studies in mice suggest.

Most colon tumours use a signalling system called NOTCH, which is associated with cancer progression. David Horst at the Ludwig Maximilians University in Munich, Germany, and his colleagues analysed 328 human colorectal tumours and found that they tend to have high levels of NOTCH activity at their centres. But cells at the tumours’ edges typically had lower NOTCH activity than central cells. On the other hand, edge cells showed higher activity of a different signalling pathway, called MAPK, which is also tied to cancer progression.

In studies of mice, drugs that block MAPK signalling caused tumour cells with high NOTCH activity to flourish. And in reverse, drugs that blocked NOTCH allowed cancer cells with high MAPK activity to thrive. Targeting both proteins slowed colon-cancer growth better than targeting either alone.