Cancer is bad enough in one spot, but the disease gets especially dangerous once it starts migrating throughout the body. Finding ways to stop this process, known as metastasis, is a key way to improve survival rates for patients. Now researchers have found that primary tumors have their own mechanism for slowing the growth of secondary cancers, which could be tapped into as a new potential treatment option.
Any treatment we throw at a tumor isn’t going to really help if cancer is just going to spring up again in a different part of the body. Metastasis, therefore, is one of the key areas of cancer research, and recent work has identified several mechanisms that allow cells to break off the main tumor, and proteins that protect the loose cells as they travel through the body. All of these are potential targets for future treatment.
Examining the process of metastasis, the researchers on the new study discovered a strange new “ecosystem” at play. In tests on mice, the team found that primary breast tumors can emit signals to “breakaway cells” that are traveling to other parts of the body. Interestingly, these messages are actively inhibiting the growth of secondary tumors.
Using an inflammatory response, the primary tumor provokes the immune system to launch an attack on the secondary tumors before they have a chance to take hold. Once the immune cells locate the rogues, they’re able to freeze their growth.
“When breakaway cells are forced to remain in the transition state, they don’t grow very well,” says Sandra McAllister, co-lead author of the study. “And their ability to form a new tumor is severely compromised. So, remarkably, by activating the immune response, the primary tumor essentially shuts down its own spread.”
Although this process was discovered in mice, the researchers say there is evidence that it does take place in humans as well. So far, the team has identified some of the signals used by the tumor to activate the immune system, as well as how the immune cells respond, but they plan to continue investigating to find other potential ways to manipulate the process to help stop cancer spreading.
“This new research has yielded that rare thing – a clue from the cancer itself about new possibilities to fight its spread,” says Christine Chaffer, co-lead author of the study. “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. We want to understand exactly what the tumor is releasing to activate this immune response, and how immune cells are targeting the secondary sites. In principle, all of these steps present therapeutic opportunities that could be used to stop a cancer from developing any further.”
If the new research pans out, the team says that it could improve the survival rates for patients, which often dips drastically once the cancer metastasizes. The next steps involve investigating whether the technique might apply to other kinds of breast cancer, and eventually other types of tumors as well.
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