A gene known as deleted colorectal carcinoma (DCC) could safeguard against the development of the colorectal cancer by inducing a process called apoptosis, or cell death.

Professor Patrick Mehlen and his team at the Lyon Cancer Research Center and Université de Lyon in France showed that apoptosis in mice with genetically modified DCC genes did not occur, and that they spontaneously developed colon cancer.

Professor Mehlen and his fellow researchers explained that the DCC gene usually protects against cancer by depriving cancer cell receptors of the signals that indicate that 'all is well' – without these the cell triggers a 'self-destruct' mechanism.

'The organism is naturally protected from the development of cancers thanks to the presence of this tumour-suppressing gene', said Professor Mehlen. 'Unfortunately, certain cancer cells escape from this control by blocking this 'dependence receptor' mechanism. That is how we know that the DCC gene is extinguished in most human cancers'.

The research group hopes to further its research in humans in the next three years. In particular, Professor Mehlen reports they have developed several candidate drugs that reactivate the cell death induced by the DCC receptor in animal models. These will be tested on humans to see if they represent possible cancer prevention treatments.

In a separate study, it has been found that cases of colorectal cancer rose by more than two percent in young adults in their 30s and 40s. The team, from the MD Anderson Cancer Center in Houston, Texas, USA, analysed data on 600,000 US patients collected between 1990 and 2007.

They believe the increase could be due to not recognising symptoms such as bleeding and abdominal pain, or a change in bowel habits. Doctors often do not suspect the disease in adults of this age either, they added. This research was published in the journal Archives of Internal Medicine.