A trial to see if p53 gene damage can predict how well different chemotherapy drugs will work for breast cancer (EORTC 10994)

Cancer type:

Breast cancer




Phase 3

This trial tried to find out if there was a link between damage to the p53 gene and how cancer responded to different types of chemotherapy.

Doctors usually treat breast cancer with surgery, radiotherapy and chemotherapy. Chemotherapy works very well for some cancers, but unfortunately not all. No one knows exactly why this is.

A gene called p53 Open a glossary item stops cells multiplying. It is a tumour suppressor gene and should stop cancers growing. When this gene works normally it helps the chemotherapy drugs kill the cancer cells. But the p53 gene is often damaged (mutated) or missing from cancer cells. This may be part of the reason some cancers are resistant to certain chemotherapy drugs.

Drugs called anthracyclines (such as epirubicin) are used to treat breast cancer. From previous research doctors thought that anthracyclines may kill more cells with a normal p53 gene than cells with a damaged p53 gene.

Laboratory studies Open a glossary item also suggested that a group of drugs called taxanes Open a glossary item (such as docetaxel) might kill cancer cells with both a normal and a damaged p53 gene. This trial compared 2 combinations of chemotherapy before surgery for people with breast cancer who had not had chemotherapy. The standard arm included an anthracycline. The experimental arm included both an anthracycline and a taxane. The doctors looked at the p53 gene in each person’s cancer to see if it was normal or damaged.

The aims of this trial were to see if there is a link between p53 damage and how well different combinations of chemotherapy worked. And to see which treatment worked best.

Summary of results

The trial found that there was no clear link between p53 damage and how well the 2 combinations of chemotherapy worked.

This trial recruited 1,856 people.  They were put into 1 of 2 treatment groups

  • 928 had fludarabine, epirubicin and cyclophosphamide
  • 928 had epirubicin and docetaxel

After 5 years follow up the researchers found little difference between the numbers of people in both groups whose cancer had started to grow again.

Of the 1,856 people, the researchers were able to look at the p53 gene of 1,469 people.

After 5 years the researchers found little difference between how well the chemotherapy worked for those who had p53 damage and those who did not.

The trial team concluded that there was no clear link between damage to the p53 gene and how well the 2 chemotherapy combinations worked.

We have based this summary on information from the team who ran the trial. The information they sent us has been reviewed by independent specialists (peer reviewed Open a glossary item) but may not have been published in a medical journal.  The figures we quote above were provided by the trial team. We have not analysed the data ourselves.

Recruitment start:

Recruitment end:

How to join a clinical trial

Please note: In order to join a trial you will need to discuss it with your doctor, unless otherwise specified.

Please note - unless we state otherwise in the summary, you need to talk to your doctor about joining a trial.

Chief Investigator

Mr David Cameron

Supported by

Anglo Celtic Cooperative Oncology Group
European Organisation for Research and Treatment of Cancer (EORTC)
Experimental Cancer Medicine Centre (ECMC)
National Institute for Health Research Cancer Research Network (NCRN)

Freephone 0808 800 4040

Last review date

CRUK internal database number:

Oracle 364

Please note - unless we state otherwise in the summary, you need to talk to your doctor about joining a trial.

Harriet wanted to try new treatments

Picture of Harriet

“I was keen to go on a clinical trial. I wanted to try new cancer treatments and hopefully help future generations.”

Last reviewed:

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