Study found that by activating the immune response, the primary tumour essentially shuts down its own spread.
A new discovery has now revealed how breast cancer tumours can stop themselves from spreading.
According to a story published in MailOnline, when breast cancer cells break away from a tumour and travel to new parts of the body, the tumour triggers an immune response. This in turn, causes the release of immune cells that ‘freeze’ cancer cells preventing them from getting established in new areas.
Speaking about the study, lead author of the research Dr Christine Chaffer, from the Garvan Institure of Medical Research in Sydney said that by activating the immune response, the primary tumour essentially shuts down its own spread.
The researchers hope they can one day mimic this cancer cell 'freezing' to prevent all breast cancers from spreading.
Study indicates that those with cancer that is growing but still confined to the breast or nearby lymph nodes have a five-year survival rate of 93 percent, however, this falls to just 22 percent once the tumour has spread.
The researchers, which also included scientists from Harvard, analysed breast-cancer tumours in humans and mice.
In rodents, they discovered tumours that have not spread away from the breast have the ability to stop 'breakaway' cancer cells from travelling to other parts of the body.
Thus occurs by such tumours triggering an inflammatory response via the immune system, which causes immune cells to be released.
These immune cells find out where 'breakaway' cancer cells may be settling and trying to create new tumours and subsequently 'freeze' these cancer cells.
According to Dr Chaffer when these breakaway cells are settling, before they have established a new tumour, they are particularly vulnerable, because they are in an intermediate state and their identity isn't very solid.
“It's at this point that the immune system can intervene,” she said.
After analysing mice, the researcher assessed 215 people who had been diagnosed with advanced breast cancer and found those who had the same sort of 'breakaway' immune cell response were more likely to survive than those without it.
Speaking of future research, Dr Chaffer said that they want to understand exactly what the tumour is releasing to activate this immune response and how immune cells are targeting the secondary sites.
“Our goal is to work out how we can mimic this "freezing" of secondary cancers, so that one day we might influence all breast cancers to keep their secondary tumors in check,” she said.