British scientists said on Tuesday they had identified subtle chemical changes that allow abnormal cells to multiply out of control, a finding that could help detect colon cancer earlier.

The researchers looked at changes affecting 18 genes that play a key role in the very early stages of colon cancer and found a pattern of chemical changes in people who had pre-cancerous polyps likely to develop into a tumour.

“This could help us to predict people more likely to get colon cancer in the future,” said Ian Johnson, a researcher at Britain’s Institute of Food Research, who worked on the study. “We might be able to apply the principle to other cancers.”

Colon cancer is one of the most common cancers, killing 655,000 people each year globally according to the World Health Organisation. It is strongly linked to both genes and diet.

The researchers focused on a chemical process called methylation, which turns genes on and off.

This process can go awry and switch off genes that normally direct abnormal cells - the ones that lead to tumours - to destroy themselves, Johnson said.

Small changes in methylation may help predict that such malfunctioning genes will allow cancer-causing cells to continue replicating, Johnson and colleagues reported in the British Journal of Cancer.

“We can show that patterns of methylation are associated with cancer,” Johnson said in a telephone interview.

Such processes are called epigenetic changes. While the chemical activity affects genes, the differences are not found in the DNA code itself, but in activity affecting how a cell “reads” its genetic instructions.

In their study, the team compared tissue taken from volunteers with cancer, people with pre-cancerous lesions and healthy individuals to see if these mistakes might begin to appear long before a tumour arises.

Some of these changes seem to occur naturally with age but the researchers said they were also exploring the possibility that diet, obesity and exercise can accelerate or delay this chemical process.

By Michael Kahn
LONDON (Reuters)