Meningioma scan Credit Raleigh lab / UCSF
UC San Francisco scientists have uncovered a common genetic driver of aggressive meningiomas, which could help clinicians detect such dangerous cancers earlier and lead to new therapies aimed at curing these difficult-to-treat tumors.
Meningiomas are tumors that grow from the layer of tissue that surrounds the brain and spinal cord and are the most common central nervous system tumor in the United States. Although the vast majority are benign and grow slowly, over time they can lead to headaches, seizures, neurological deficits and even death.
Most meningiomas are treatable with radiation therapy or surgery. However, approximately twenty percent of meningiomas are aggressive and can recur even after surgery and radiation therapy. In the new study, published online March 27, 2018, in Cell Reports, a team led by UCSF’s David Raleigh, MD, PhD, found that increased activity of a gene known as FOXM1 appears to be responsible for the aggressive growth and frequent recurrence of these tumors.
Raleigh, an assistant professor of radiation oncology and of neurological surgery and member of the UCSF Helen Diller Family Comprehensive Cancer Center, hopes the finding will be an important step towards correctly diagnosing these more aggressive tumors: “There haven’t been as many studies on what drives ‘problem’ meningiomas,” he said. “For clinicians, patients, and families, these are the most heartbreaking cases because we expect to cure meningiomas, but sometimes we can’t and we don’t always do a good job of differentiating ‘good’ and ‘bad’ meningiomas ahead of time.”
In order to investigate what might be driving aggressive meningioma, Raleigh’s group examined 280 human meningioma samples collected by Michael McDermott, MD, and other faculty members in the Department of Neurological Surgery at UCSF between 1990 and 2015. Using an array of techniques, including RNA sequencing and targeted gene expression profiling, the researchers searched for links between gene activity and protein production in these tumors and the clinical outcomes of patients.
Read more at UCSF.edu