The findings presented by researchers at the European Breast Cancer Conference in Spain on Thursday, mean doctors should be able to test patients, tailor treatment to them and avoid giving them toxic drugs that will not help.
By conducting a study called a meta-analysis of four large breast cancer trials including nearly 3,000 patients, the researchers found that an abnormality on chromosome 17, called CEP17, is a highly significant indicator that the tumor will respond to chemotherapy drugs called anthracyclines.
Anthracyclines are anti-tumor antibiotics that interfere with enzymes involved in DNA replication. They are widely used against a variety of cancers.
Our aim was to identify patients for whom anthracyclines provided benefit ... and to seek to ensure that future treatment was targeted to this group, John Bartlett of Britain's Edinburgh University, who led the study, said in a statement.
After adjusting for factors relating to the tumor and its treatment, the researchers found that if patients with CEP17 were treated with anthracyclines, they were around two-thirds more likely to survive, and to survive without a recurrence of cancer, than those not treated with anthracyclines.
This suggests that only those patients with CEP17 tumors should receive anthracyclines, Bartlett said.
The results provide more tools for doctors to make personalized, or tailored, medicine a reality in cancer care.
CEP17 is on the same chromosome as other genes known to be involved in breast cancer, such as HER-2, and can be detected with a simple test called fluorescent in situ hybridization, or FISH, which is carried out routinely in breast cancer patients.
Doctors can already also test for certain genes to tell whether a woman's breast cancer is sensitive to estrogen and likely to benefit from hormone-blocking drugs like tamoxifen.
And patients whose breast tumors are HER-2 positive are often given the drug Herceptin, made by Roche Holding AG, which only works against these kinds of tumors.
Bartlett said the existence of a readily available test for CEP17 meant doctors could immediately start to better tailor chemotherapy to patient needs. He said extra work on CEP17 was needed to see if it could reveal more about breast cancers.
It (CEP17) works as a biomarker for predicting response to anthracyclines, but we don't know why it works. So our next step is to discover this and to try to make the cancers that don't have the marker behave like the ones that do, he said.
U.S. researchers published a study in January that found that changes in two genes on a small region of chromosome 8q made tumors resistant anthracyclines, but not other types of chemotherapy drug.