Breast cancer cells can turn off key immune response

Breast cancer cells can destroy a powerful immune response in the body and allow the disease to spread to the patient's bones, researchers in Australia reported on Monday. They also experimented with two ways to reinstate this immune response to help patients fight breast cancer, but it will take more tests and several more years for these therapies to become routine treatments, they said. "We have identified a way that breast cancer cells can turn off the immune system, allowing them to spread to distant parts such as the bone," said Belinda Parker, a research fellow at the Peter MacCallum Cancer Centre in Melbourne, who led the study. "By understanding how this occurs, we hope to use existing and new therapies to restore this immune function and prevent the spread of cancer," she said by telephone. The study was published on Monday in the peer-reviewed journal Nature Medicine. In 2010, 1.5 million people were diagnosed with breast cancer, the top cancer in women around the world. Although it kills many women in developing countries, 89 percent of women diagnosed with breast cancer in western countries are still alive five years after diagnosis thanks to detection tests and treatment. Using tissue samples from breast cancer patients and experiments with mice, Parker and colleagues found that a gene called IRF7 is switched off in patients whose cancer spreads to other parts of the body. IRF7 controls the production of interferon, an important type of immune protein that fights viruses and bacteria apart from tumour cells "Usually when breast cancer cells leave the breast and travel in the bloodstream and into bone marrow, the release of interferons by IRF7 will cause the immune system to recognise those cells and eliminate them," Parker said. "But by losing IRF7, it prevents the stimulation of immune responses and allows those cells to hide from being recognised (and later spread)." Parker and her team tried two ways to revive this immune response in mice experiments and both appeared to work. "We put the gene back into cancer cells so it can't switch it (IRF7) off. We allowed the immune pathway to be stimulated and the cancer cells did not spread to the bone," Parker said. "The other way is to treat the animals with interferon, which is available for treating other diseases, like hepatitis. That also prevented the spread of cancer to the bone." Parker said they will study how best to use these two methods on patients in the next few years and plan to have a clinical trial in two to three years.