Genes guide cancer treatment

CANCER is the disease for which scientists are furthest advanced in defining novel drugs to exploit genetic variations between individuals.

The breast cancer drug Herceptin works only in women whose tumour over-expresses a protein called HER2, which is controlled by a common genetic mutation.

The drug, which targets the rogue protein, was first shown to improve survival - by as much as several months - in women whose cancer was otherwise considered terminal. Its use is now being expanded to women in earlier stages of the disease, with results showing it can slow tumour growth or in some cases even shrink cancers.

Because cancer is so common, and because it remains fatal for a significant proportion of people, there is always a pool of patients for whom an experimental treatment is their only hope, and whose treatment with such unproven drugs raises few ethical dilemmas.

The Australian company ChemGenex last week detailed preliminary results for its new cancer drug, Quinamed. In a 50-person trial patients with metastatic cancer were shown to require different doses of the drug, according to variations in the NAT2 gene. NAT2 controls a liver enzyme that influences metabolic speed.

The results, presented at an American Society for Clinical Oncology meeting in Chicago, mean it should be possible to treat patients without risking severe side effects, says Greg Collier, the company's chief executive and managing director.

But although genetic status might be increasingly helpful in guiding treatment protocols, cancer scientists are still a long way from being able to use genetics to pinpoint who will develop the disease.

Particular gene mutations are implicated in a minority of inherited breast cancers and in a form of bowel cancer that runs in families. But many other cases are thought to be linked to gene variations that have a much smaller but incremental effect on cancer risk.

An international study, published last week in Nature, identifies four new breast cancer genes - the biggest genetic discovery in the high-profile disease for more than a decade. But together the genes accounted for an increase in disease risk of only 3.6 per cent.

source:www.smh.com.au