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Decoding Epileptogenic Glioma Networks Using Forebrain Assembloids

Project description

Neuron-glioma interactions for better treatments

Brain tumours are a leading cause of cancer-related deaths in children, with certain aggressive types linked to specific genetic mutations. Among them, H3G34-mutant diffuse hemispheric gliomas (DHGs) affect the cerebral hemispheres and often lead to seizures, making the disease even more devastating. Research suggests that gliomas disrupt neural connections, creating a feedback loop where increased neuronal activity accelerates tumour growth. Despite this, little is known about how neuron-glioma interactions contribute to disease progression. Supported by the Marie Skłodowska-Curie Actions programme, the GLIO-NET project aims to develop patient-derived models of DHGs using cerebral organoids. It will map neuron-glioma synapses and test targeted interventions to uncover new therapeutic strategies to slow tumour growth and reduce seizures.

Objective

Pediatric-type diffuse high-grade gliomas are the primary cause of cancer-related mortality in children and adolescents. The most common and aggressive forms harbor mutually exclusive mutations in histone 3 (H3), involving distinct brain regions and developmental origins. In contrast to other gliomas, GABAergic interneuron progenitors are implicated as the cells of origin for H3G34-mutant diffuse hemispheric gliomas (DHGs), which almost exclusively affect the cerebral hemispheres.

Seizures are a common comorbidity in patients with cortical gliomas, with evidence suggesting that gliomas alter synaptic structures to induce hyperexcitability. Neuronal activity, in turn, accelerates glioma progression through paracrine signaling and neuron-to-glioma synapses. Despite their cortical involvement, high seizure incidence, and poor prognosis, neuron-glioma interactions in DHGs remain understudied.

Human cerebral organoids, pioneered by the Knoblich Lab, recapitulate early brain architecture and circuit assembly via excitatory neurogenesis (dorsal forebrain) and interneuron development (ventral forebrain). Ultimately leading to functional network activity with complex oscillatory dynamics, organoids provide the ideal platform to study brain tumors in the context of network pathologies.

In this project, I will develop patient-derived models of seizure-associated DHGs in brain region specific cerebral organoids to examine neuron-glioma synapses. Using barcoded viral tracing and genetic perturbation screening, I will identify synaptic interaction partners and tumor-specific anti-connectivity targets. Electrophysiological recordings will assess the effects of anti-epileptogenic and anti-tumorigenic perturbations. This work will provide critical insights into neuron-glioma communication and its role in epileptogenesis during tumor progression, with important therapeutic implications.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2024-PF-01

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Coordinator

INSTITUT FUER MOLEKULARE BIOTECHNOLOGIE GMBH
Net EU contribution

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€ 230 184,72
Address
DR BOHRGASSE 3
1030 WIEN
Austria

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Region
Ostösterreich Wien Wien
Activity type
Private for-profit entities (excluding Higher or Secondary Education Establishments)
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Total cost

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