Cedars-Sinai investigators have identified a stem cell–regulating gene that affects tumor growth in patients with brain cancer and can strongly influence survival rates of patients. The findings, published by Edwards et al in Nature Scientific Reports, could move physicians closer to their goal of better predicting the prognosis of patients with brain tumors and developing more personalized treatments for them.
To enhance understanding of how glioma cancer stem cells reproduce and how they affect patient survival, investigators spent 3 years analyzing the genetic makeup of more than 4,000 brain tumors. During their investigation, they identified a gene, called ZEB1, that regulates tumor growth. The investigators’ analysis suggests that patients who don’t have the gene tend to have lower survival rates.
“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 John Yu, MD, 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.”
Dr. Yu and fellow researchers noted that while some brain cancer patients are born without the gene, others who have it experience the gene becoming less powerful as time progresses—which could have had a role in causing the disease.
“We found an 8.5-month shorter survival rate in lower-grade glioma patients with the ZEB1 gene mutation compared to those individuals who have the gene,” said Dr. Yu, who also serves as Director of Surgical Neuro-Oncology. “We are learning that some chemotherapies are not effective in the population of individuals who have the gene deletion, so we have to treat them with different medications.”
The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.