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Epilepsy drug suppresses growth of nervous system tumors in mice


People with neurofibromatosis type 1 (NF1) develop tumor on nerves throughout their body. These tumors are usually benign – meaning they have not spread to other parts of the body and are not considered life-threatening – but they can still cause serious medical problems such as blindness. blindness, especially when they form in the brain and nerves.

Mouse in the laboratory.

Mouse in the laboratory. Image credit: Rama qua WikimediaCC-BY-SA-2.0-FR

Researchers at Washington University School of Medicine in St. Louis discovered that neurons carry mutations in Nf1 genes and suppressed this hyperactivity with lamotrigine, a drug approved by the Food and Drug Administration to treat epilepsy, suppressed tumor growth in mice.

“Tumors are very common in people with NF1,” said senior author David H. Gutmann, MD, PhDFamily Professor Donald O. Schnuck and director of University of Washington (NF) Neurofibromatosis Center. “We demonstrated that we can suppress NF1 tumor growth by blocking the neuron’s ability to excitability. We’ve done it a couple of different ways now, and there’s no doubt that resetting the antiepileptic drug is an effective way to inhibit tumor growth, at least in the mice. This highlights the important role of neurons in tumor biology. “

The study was published in the journal Nature Communications.

NF1 is a genetic disorder that affects one out of every 3,000 people worldwide. This condition is caused by a mutation in NF1 gene. Any part of the body can be affected, but the most common signs of this disorder are light brown spots on the skin, benign nerve tumors called neurofibromas, tumors of the brain and optic nerve, skeletal deformities, and cognitive differences such as autism, learning disabilities, and attention deficit hyperactivity disorder.

Last year, Gutmann and Michelle Monje, MD, PhD, a professor of neurology at Stanford University School of Medicine and an investigator Howard Hughes, shows that light increases neuronal activity in your eyes Nf1-mutant mice, then caused tumors to form on the optic nerve connecting the eye and brain. In the new study, they – along with the first author Corina Anastasaki, PhDassistant professor of neurology at the University of Washington, and co-author Lu Q. Le, MD, PhD, professor of dermatology at the University of Texas, Southwestern Medical Center – studied how increased activity of neurons that lead to tumors in people with NF1.

The researchers studied neurons from mice with and without Nf1 gene mutation. Initially, neurons from mice caused tumors Nf1 mutants fired electrical impulses more often than normal rat neurons. These excitable neurons then release molecules that promote the growth of brain and nerve tumours. The researchers discovered that this increased secretion is the result of a dysfunctional ion channel that alters the basic electrical activity inside nerve cells.

They also studied rats with a Nf1 mutations seen in people with NF1 who do not develop brain or nerve tumors. Anastasaki discovered that the neurons of the mice had Nf1 the mutation failed to reduce and did not grow tumors – providing the first explanation for why this group of NF1 patients lacked gliomas or neurofibromas.

Excitable neurons are also a feature of epilepsy, and the epilepsy drug lamotrigine targets the same ion channels disrupted during euphoria. Nf1-mutant neurons. The researchers gave lamotrigine to a group Nf1-The small mice developed optic nerve tumors. Compared with mice given a placebo, mice given the drug had smaller, no longer growing tumors.

In addition to suggesting a new approach to treat NF1 tumors, these findings also suggest a new way of thinking about the origins of cognitive dysfunction symptoms.

“The surge in Nf1 Gutmann says genes change the basic biology of neurons. “During development, neurons form first and tell the rest of the brain how to form. If you have a mutation that affects the way nerve cells work, that can change everything about how the brain is set up during development. To date, we have not attempted to effectively prevent learning disabilities. It is possible that this discovery could lead to new treatments for learning and cognitive problems in children with NF1.

“I am very excited about the scientific and medical implications of these findings. Not hypnotized,” he added, “but very excited. ”

The source: Washington University in St. Louis






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