IEC 2025 | Identifying therapeutic markers and mechanisms related to developmental glioneuronal tumors
Silvia Cases-Cunillera, PhD, Institut de Psychiatrie et Neuroscience de Paris (IPNP), Paris, France, discusses a project focused on identifying therapeutic markers and mechanisms related to developmental glioneuronal tumors, which are associated with epilepsy. Dr Cases-Cunillera’s work combines two molecular alterations, the B600E mutation and activated AKT, to create a mouse model that develops tumors early in life, which can lead to alterations in neuronal activity and epilepsy. This interview took place at the 36th International Epilepsy Congress (IEC) in Lisbon, Portugal.
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Transcript
So my project is related to a glioneuronal developmental tumor which is associated with epilepsy. These are very benign tumors however they are the most common tumors in young patients who undergo surgery for the control of temporal lobe epilepsy and therefore there is a high need to find new therapeutic options for these children and young adults. In my project, we developed a mouse model for ganglioglioma based on two molecular alterations that have been described in human tissue...
So my project is related to a glioneuronal developmental tumor which is associated with epilepsy. These are very benign tumors however they are the most common tumors in young patients who undergo surgery for the control of temporal lobe epilepsy and therefore there is a high need to find new therapeutic options for these children and young adults. In my project, we developed a mouse model for ganglioglioma based on two molecular alterations that have been described in human tissue. These are B600E mutation. This is a missense mutation that causes an over-activation of the MAP kinase signaling pathway, which regulates cell growth and cell proliferation. And also we use an activated form of AKT, which triggers an activation of mTOR. And both pathways are critical for oncogenesis, cell growth, cell proliferation. In our work, we combine them and we introduce them to the brain of the mice at developmental time points by using intraventricular and in utero electroporation, which is a technique that allows to manipulate the brain genome during embryonic times. So when we do so, the mice develop tumors very early, actually already at postnatal stages, these mice suffer from tumors. and the tumors expand or the tumors let’s say they are the same until adult stages so they remain the same. Which is one of the main characteristics and main power aspects of this model because they don’t grow they have the same size the same phenotype but this is the reason why these tumors actually have a long time period or a long time window to alter the brain in another fashion. And one of them is by causing alterations in the neuronal activity and leading to epilepsy. So therefore, our project is a focus on finding therapeutic markers or the underlying mechanisms to treat both the tumor per se, but also and most importantly, the epileptic related aspects. And I say importantly because the surgical resection has been shown that it gives a very good outcome for the tumor, so it can be very well resected. However, these patients still have epilepsy after the tumor resection. Therefore, we think that it’s more important for them to find new options for the treatment of epilepsy-associated processes.
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