Researchers unlock the key to the spread of breast cancer.
Breast cancer is the most common cancer among Australian women, with 36 women being diagnosed with the disease every day, according to Cancer Care. A key concern for these patients is the possibility that the cancer cells could spread and thrive in other tissues.
While survival rates for primary breast cancer have steadily increased (a five-year relative survival increased from 72.6% in 2000 to 88.3% in 2006), mortality rates remain high when cancer spreads to secondary sites such as the brain, bones and liver.
Researchers at the Peter MacCallum Cancer Centre and Monash Institute of Medical Research have identified the way breast cancer cells switch off the signal that tells the immune system to fight them, their results were published in the journal Nature Medicine. The researchers hope that this discovery will assist them in harnessing the same mechanisms to switch the immune system back on to prevent metastasis, the spread of cancer.
“We’ve found a way that breast cancer cells can hide from the immune system to enable them to spread to other parts of the body, such as the bone,” Belinda Parker, lead researcher at Peter MacCallum Cancer Centre said. “We’re quite excited by this because therapies that are currently available can be used to switch this immune signal back on, and we’ve found that that actually prevents the spread of cancer to bone.”
The researchers conducted the experiment on mice using tissue samples from breast cancer patients. They found that a gene called IRF7 is switched off in patients whose cancer metastasised 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 utilise this discovery on patients and plan to have a clinical trial in the next few years.
Source: Peter MacCallum Cancer Centre