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DURHAM, NC – For many women who thought they had conquered bad cancer, the news that he came back years later is a particularly cruel diagnosis, with no clear answer as to why or why. its recurrence.
Now, a team of researchers at the Duke Cancer Institute has provided extremely unknown details that could lead to potential strategies to end the process.
By experimenting on mice, the researchers followed a series of events that allowed a small reservoir of cancer-resistant cancer cells to break dormancy, grow, and spread. The results appear online in eLife.
"These are the cells that remain after the treatment, and we know little about them because we do not see them.There are too few of them to appear in mammography or PET," said lead author James V Alvarez, Ph.D., badistant professor in the Duke Department of Pharmacology and Cancer Biology.
"But by using murine models that reproduce recurrent HER2 positive bad cancers, which affect about 20% of women, we have been able to locate residual cancer cells that remain after treatment and study them," he said.
Alvarez and colleagues, including lead author Andrea Walens, found that these treatment-resistant residual tumor cells did not look like the original cancer cells that grow and proliferate quickly.
Instead, they rest low and begin a complex interaction with the surrounding cells, particularly those of the immune system. Over time, they activate a horde of small signaling proteins, called cytokines, which are vital communicators of immune cells.
In response to cytokines, immune cells rush to tumor sites. Macrophages, a type of white blood cell that digest cellular debris and deposit a form of collagen, are among the most abundant immune cells. It has been proven that it is important that dormant cells wake up and develop.
Alvarez, Walens and colleagues noted that macrophages could be targeted by current drugs. They have shown that a particular type of cytokine – CCL5 – is able to accelerate the recurrence of the tumor, and its blockage could delay or stop the process.
"There are drugs already approved or under development that inhibit macrophages in general or specifically the function of CCL5," said Walens. "Our next step is to test these macrophage inhibitors to see if they can delay or prevent recurrence in mice and if they can kill residual dormant tumor cells.
"We are currently performing these experiments on mice and if it worked, we could start trying to go to a clinical trial to test these drugs in combination with anti-HER2 treatments," said Walens.
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Among the authors of the study are Ashley V. DiMarco, Ryan Lupo, Benjamin R. Kroger and Jeffrey S. Damrauer.
The authors do not report any conflict.
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