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Staining shows collagen deposit, in blue, within a residual bad tumor following Her2 inhibition. Image credit: Duke Health
For many women who thought they had beaten bad cancer, the news that it has gotten back to life.
Now a team of Duke Cancer Institute researchers has written in a few words that could lead to potential strategies to halt the process.
Experimenting in mice, the researchers tracked a series of events that enable a small reservoir of cancer-resistant cancer cells to grow dormancy, grow and spread. The findings appear online in eLife.
"These are the cells that are left over following therapy, and we do not know much about them because we can not see them. There are so many of them to show up in PET scans, "said senior author James V. Alvarez, Ph.D., badistant professor in Duke's Department of Pharmacology & Cancer Biology.
"But using mouse models that replicate recurrent HER2-positive bad cancers, which afflicts about 20 percent of women, we were able to locate the residual cancer cells that survive after treatment and study them," he said.
Alvarez and colleagues, including lead author Andrea Walens, found that these residual cancer-cell-resistant cancer cells are rapidly growing.
Instead, they lay low and begin an intricate interaction with surrounding cells, especially those of the immune system. Over time, they switch over to small signaling proteins called cytokines that are vital communicators with immune cells.
Responding to the cytokines, immune cells as rushing to the tumor sites. Among the most abundant of these immune cells are macrophages, a type of white blood cells that have been shown to be deformable and have been shown to be prominent.
In mapping this route to recurrence, Alvarez and Walens noted that macrophages might be targetable by current drugs. They showed that one particular type of cytokine – CCL5 – is able to accelerate tumor recurrence, and blocking it might delay or halt the process.
"There are drugs already approved or under development that inhibit macrophages in general or specifically CCL5 function," Walens said. "Our next step is to test these macrophage inhibitors to see whether they can delay or prevent recurrence in mice and kill the residual, dormant tumor cells.
"We are doing these experiments now and then," said Walens said, "we would be able to test these tests in conjunction with anti-HER2 therapies.
This article has been reprinted by Duke Health. Note: material may have been edited for length and content. For further information, please contact the cited source.
Reference:
Walens, A., et al. (2019). CCL5 promotes bad cancer recurrence through macrophage recruitment in residual tumors. eLIFE DOI: 10.7554 / eLife.43653
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