Here’s one way triple-negative cancer works, according to researchers at the University of Michigan Rogel Cancer Center:
Tumor cells reprogram metabolic pathways to gain control over a type of immune cell that allows cancer growth.
Here’s the technical explanation: Myeloid-derived suppressor cells that live in and around a cancerous tumor encourage a stem cell-like growth that’s linked to TNBC. The more of these suppressor cells a patient has, the worse the outcome. This means the patient’s immune system isn’t strong enough to fight against the tumor.
And when there are a large number of myeloid-derived suppressor cells, immunotherapy treatments tend to be ineffective because the immune T-cells that immunotherapy targets are suppressed.
By looking at triple-negative breast cancer cells, researchers found that the metabolic process by which cells break down glucose also regulates the expression of a specific isoform that in turn causes more suppressor cells to develop. The immune system can’t mount enough of an assault on the tumor cells, which translates to poor outcomes in some TNBC patients.
“We hope that by understanding the biology better, it may lead to new ways to help these patients,” says Weiping Zou, M.D., Ph.D., the Charles B. de Nancrede Professor of Surgery, Pathology, Immunology and Biology at the University of Michigan.
Looking at samples from 250 triple-negative breast cancer patients, researchers found that when the metabolic pathway for glycolysis was enriched, so were the immune suppressor cells — and this linked with worse overall survival. In contrast, tumors with a high T-cell signature exhibited fewer of these suppressor cells and the patients had better outcomes.
The study is published in Cell Metabolism.
