Brain cancer treatments have made considerable advances, but doctors have struggled to understand why therapies that have been very successful for one patient may not work for another.
In a new study published in Nature Scientific Reports, Cedars-Sinai investigators identified ZEB1, a gene that affects tumor growth and could help better predict the prognosis of patients with brain tumors.
Why is ZEB1 important?
- It plays an important role in what makes some brain tumors more aggressive than others.
- It could help develop more personalized treatments for patients with brain tumors.
- It influences the survival rate of patients.
ZEB1 is able “turn off” a gene that causes tumor cells to grow like stem cells do—quickly and uncontrollably.
“Patients without the gene in their tumors have more aggressive cancers that act like stem cells by developing into an uncontrollable number of cell types,” said Dr. John Yu, vice chair of Neurosurgical Oncology in the Department of Neurosurgery and senior author of the study. “This new information could help us to measure the mutation in these patients so that we are able to provide a more accurate prognosis and treatment plan.”
Tumors without the gene tend not to respond to common chemotherapies—and brain cancer patients who don’t have the gene tend to have a lower rate of survival.
The study focused on a specific kind of brain tumor—glioma, one of the most common brain cancers. To better understand how glioma cancer stem cells reproduce and how they affect patient survival, investigators spent three years analyzing the genetic makeup of more than 4,000 brain tumors.
Identifying specific genes and how they affect cancer cells is a crucial part of precision medicine. Understanding how ZEB1 affects the growth of brain tumors may help in creating individualized treatments and determining which treatments are most likely to be effective for brain cancer patients.
The study was funded by FasterCures, a center of the Milken Institute, and the National Institutes of Health grant #NS048959.