As anyone who’s fond (or not so fond) of clothes-shopping will know, the idea that “one size fits all” is a myth. And the same is true of cancer treatment.

Fundamentally, cancer is due to faulty genes – this is usually a combination of genetic variations inherited from our parents, topped with the random mistakes that happen during a lifetime’s wear and tear. But the distinct signature of gene faults in an individual tumour also affects how the disease responds to treatment.

Increasingly, scientists and doctors are working together to make “personalised medicine” a reality, as it becomes clear that all cancers are not the same. The idea is that a patient will get a treatment tailored to the genetic makeup of their cancer, which is more likely to work than a “one size fits all” standard treatment.

For example, in the case of breast cancer, the disease can be broken down into several different sub-types, depending on the genes that are active within a tumour. And each subtype may require a slightly different treatment approach.

Cancer Research UK scientists from Edinburgh have just announced an important step forward in this area, discovering that a genetic test (already used in breast cancer diagnosis) can predict whether an individual patient will benefit from certain chemotherapy drugs or not. And we could see it become standard clinical practice within a couple of years.

The story starts with Professor John Bartlett and his team, who were searching for genetic ‘markers’ that could help to identify women with breast cancer who would benefit from anthracycline drugs, such as the commonly used epirubicin.

While these drugs are very effective in some women, they can cause unpleasant side effects, and this has limited its use. So identifying people who won’t get any benefit from it would be a good thing.

A NEAT finding
The scientists trawled through tumour samples taken from more than 2,500 women who had been taking part in clinical trials of breast cancer chemotherapy, including the UK’s NEAT (National Epirubicin Adjuvant Trial).

After painstaking analysis, they found that if a woman’s tumour had extra copies (duplication) of a certain region of DNA found on chromosome 17, they were likely to respond to the treatment. But this wasn’t the case for women with the normal complement of DNA.

Duplication of chromosome 17 is already known to be involved in breast cancer – it harbours HER2, the gene that makes the molecule targeted by Herceptin. And there’s an effective test to look for duplications of the chromosome, which is routinely used by doctors to find out if a woman will benefit from Herceptin treatment.

What does it mean?
The great thing about this finding, presented at the San Antonio Breast Cancer Symposium, is that both the duplication test and the drug are already available here in the UK for doctors to use.

The team are still waiting for the results of one final clinical trial to confirm the accuracy of the test. But if all goes well, we should see this becoming clinical practice, and directly benefitting patients, within a year or two.

Listen to an interview with Professor Bartlett, talking about this research.