Breast cancer cells (shown here) can break away from the original tumor and travel to the rest of the body. A new study shows how to stop them.
Almost 41,000 of these cases will result in death.
However, as the NCI show, the number of breast cancer deaths has been steadily decreasing since the early 1990s.
Overall, the 5-year survival rate for breast cancer is now close to 90 percent.
After receiving a breast cancer diagnosis, a person’s outlook is influenced by several factors — the most important of which is the extent of the cancer and whether it has spread beyond the original site of the tumor.
For instance, the 5-year survival rate for women with stage 2 breast cancer is approximately 93 percent. However, once the cancer has spread — or metastasized — this number drops to 22 percent.
As a result, more and more researchers have been focusing on the process of metastasis in the hope that a better understanding of it will lead to better strategies for prevention.
New research, published in the journal Nature Cell Biology, sheds such light on the process of metastasis in breast cancer, uncovering a previously unknown aspect of it.
Primary breast tumors, the new study shows, have the ability to stop themselves from spreading.
The scientists who conducted the research were jointly led by Dr. Sandra McAllister, from Brigham and Women’s Hospital and Harvard Medical School, both in Boston, MA, and Dr. Christine Chaffer, from the Garvan Institute of Medical Research in Sydney, Australia.
Tracking down ‘breakaway cancer cells’
With their team, Drs. McAllister and Chaffer conducted experiments in mice and human tumors. In a rodent model of breast cancer, they found that primary tumors have the ability to stop the “breakaway” cancer cells from traveling to other sites in the body.
The primary tumor does this by triggering an inflammatory response from the immune system. Once activated, the immune system dispatches “search patrols” of immune cells throughout the body. The main role of these cells is to find the locations where breakaway cells may be trying to settle and create new tumors.
According to Dr. Chaffer, “When these breakaway cells are settling, before they have established a new tumor, 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.”
The experiments showed that once the breakaway cells are tracked down, immune cells are able to “freeze” them, thereby stopping metastasis.
“When breakaway cells are forced to remain in the transition state, they don’t grow very well,” adds Dr. McAllister, “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.”
Dr. Sandra McAllister
‘Freezing’ secondary cancers in humans
The researchers were able to find confirmation for their initial findings in humans. An analysis of 215 people who had been diagnosed with advanced breast cancer revealed that those who displayed the same type of immune response had better survival rates than patients who did not exhibit the same immune response.
“We want to understand exactly what the tumor is releasing to activate this immune response, and how immune cells are targeting the secondary sites,” Dr. Chaffer says, going on to explain how the findings can be used to stop advanced breast cancer from spreading.
“In principle, all of these steps present therapeutic opportunities that could be used to stop a cancer from developing any further.”
“When you have a primary tumor,” she says, “there are untold numbers of breakaway cells that will travel throughout the body — but not all of them will form tumors.”
“By some estimates, less than 0.02 percent of breakaway cells will form secondary tumors, so we have a real opportunity to bring this number down to zero.”
“This new research has yielded that rare thing,” continues Dr. Chaffer, “— a clue from the cancer itself about new possibilities to fight its spread.”
“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.”
Dr. Christine Chaffer
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