Radiation and chemotherapy damage DNA. If a cell can't repair itself, that can put a patient at risk for a tumor, in this case, a secondary TIHGG tumor.
"If we can prove efficacy of one of these drugs in preventing PNAC, it will dramatically alter the course of treatment for these infants and children."
A mutation that may increase a patient's risk for a secondary tumor doesn't warrant altering treatment independently. Providers would need to know that the mutation is responsible and how likely it is that it would cause a secondary tumor.
"If this mutation increased risk by a few percentage points, that may not be worth a potentially less effective treatment for a patient's initial cancer," says Dr. Green. "However, if it's a 75% increase in risk, then that may be worth it."
Exploring pathways for treating high-grade gliomas
By studying tumors in Children's Hospital Colorado's tumor bank from the last 20 years, Dr. Green's team has also found that TIHGG tumors fall into two groups based on expression of RNA. One of these groups appears to be driven by NF-κβ, a major oncogenic pathway.
"All cancer pathways have a normal function, but in patients with cancer, they're usually too active or don't respond to inhibitory signals," says Dr. Green. "If NF-κβ is driving the TIHGG in one of these groups, it could be disinhibited."