Immune System “Double Agent” Fuels Colon Cancer Stem Cells, New Study Finds

Researchers have discovered that a type of cell normally tasked with defending the body against foreign invaders actually spurs the development of colon cancer stem cells. This discovery, published in the journal Immunity, offers new insight into why some forms of cancer come back again and again—even in the face of aggressive treatment.

Led by University of Michigan Medical School’s Dr. Weiping Zou, the research team uncovered how a subset of the human immune system is actually working against itself—by turning run-of-the-mill colon cancer cells into the far more dangerous cancer stem cells.

Cancer stem cells are a subpopulation of cancer cells that can self-renew, and transform into the many types of cells that are found in a tumor. They are a relatively new concept and are not quite fully understood—or even accepted at all—by researchers. But as Zou explained in today’s news release, they may hold the key to controlling aggressive cancers:

“If you want to control cancer stem cells through new therapies, then you need to understand what controls the cancer stem cells.”

The human body’s defense mechanism—its immune system—is managed by several types of T cells. In some forms of cancer, such as colon cancer, the T cells’ job is to attack and destroy the tumor cells.

But in this study, Zou and his team found one type of T cell that was going rogue. The Th22 T cell, rather than working with other T cells to target the tumor for destruction, Th22 actually acts as a ‘tumor helper,’ keeping the cells alive and helping them replicate—causing the tumor to grow.

Upon closer examination, the researchers identified a specific molecule within the Th22 cell, called DOT1L, which was the underlying culprit. In tumor samples taken from patients, the team found that when the samples had higher levels of DOT1L the patients had a survival time. According to the research team, these results suggest first of all that DOT1L could be used as a marker for colon cancer progression.

And if DOT1L levels could be artificially manipulated, Zou and his team foresee a way to halt Th22’s effects on tumor cells—thereby curbing the cells’ rogue tendencies.

Want to learn more about cancer stem cells? Check out our Spotlight on Cancer Stem Cells from our video archive.

Anne Holden