Cancer cells may find a hideout in the body’s immune system, researchers said on Thursday in a study that may help explain why tumors can come back after rounds of toxic chemotherapy.

Tests on mice showed that the stress of chemotherapy drives some tumor cells into the thymus, the gland that produces immune cells known as T-cells.

The gland bathes these rogue tumor cells with protective agents, the researchers at the Massachusetts Institute of Technology reported in the journal Cell. The findings suggest that cancer treatments need to attack this hiding place.

“Successful cancer therapy needs to involve a component that kills tumor cells as well as a component that blocks pro-survival signals,” MIT’s Michael Hemann said in a statement.

“Current cancer therapies fail to target this survival response.”

Hemann and colleagues tested mice with a type of cancer called Burkitt’s lymphoma. They were treated with doxorubicin, a standard chemotherapy drug.

The drug worked, as expected - the tumors regressed. The mice were killed and examined.

“To analyze the effect of drug treatment on specific tumor niches, we harvested all primary lymphoid organs, including peripheral lymph nodes, thymus, spleen and bone marrow, following doxorubicin treatment,” the researchers wrote.

Most of these were clear, too - except for the thymus. In fact, there were more tumor cells in the thymus after chemotherapy than there had been before.

“Thus, the thymus represents a chemoprotective niche that protects lymphoma cells from doxorubicin-induced cell death,” the researchers wrote.

Mice genetically engineered to have tiny and dysfunctional thymuses survived better when infected with Burkitt’s lymphoma and then treated, so it appeared the thymus was doing something to protect the tumor cells.

Lab tests suggested that the thymus secretes chemicals that protect immature cells from toxins, and the cancer cells were just taking advantage of this, Hemann said.

More tests will be required to see if the same thing happens in people, they said, but it may be necessary to attack certain immune system compounds such as IL-6 and one called Bcl2.

SOURCE:  Cell, online October 29, 2010.