CHARLOTTESVILLE, Va. (CBS19 NEWS) -- Researchers at the University of Virginia School of Medicine think they have found out why so-called "killer T cells" are unable to destroy cancer tumors.
Scientists have found a defect in these kinds of immune cells, and they believe repairing this defect will make the cells better at killing cancer.
They also think this discovery could be used within three to five years to help identify patients who would best respond to cancer therapies.
According to a release, this research could be a significant boost to the growing field of immunotherapy, which aims to harness the body's own immune defenses to defeat cancer and it could let doctors better predict and assess how well a patient responds to treatment.
"For a long time, the presence of immune cells in cancer has been associated with a better outcome in patients, but it's not really been clear why the immune cells haven't been able to control the cancer," said Timothy Bullock, PhD, of the UVA Cancer Center. "What is the cancer doing? This [finding] gives us plenty of opportunity to come in with interventions to invigorate these T cells and level the playing field substantially so they're much more competitive."
The release says killer T cells often become inactive in solid tumors, which the scientists determined is due to a dysfunctional enzyme called enolase 1.
Without that enzyme, the cells cannot use a vital nutrient, glucose, because they cannot break it down and use it so they can proliferate and become functional.
The researchers think that by increasing the effectiveness of the enzyme, they can make the cells better at killing cancer cells.
They also believe doctors will be able to examine the enzyme to see how well a patient will respond to treatment.
"I think that there is an opportunity to actually use this enzyme as a read-out for the quality of the T cells that are in the tumor, so that when a physician comes in with a clinical trial, we can theoretically analyze how the T cells metabolically compare within the tumor," said Bullock. "It's almost a biomarker of immune function and fitness within the tumor."
He also hopes that by confronting the defect, this discovery will complement emerging treatments and make them more effective, such as a clinical trial underway on pediatric acute lymphoblastic leukemia.
Bullock adds these finding may also be used to dampen excessive immune response, such as people with autoimmune disorders see, in the future.
These findings have been published in the journal Science Immunology.