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GliomaSignals

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Oncometabolitic control of tumor growth and epileptogenesis in IDH mutated gliom...

Oncometabolitic control of tumor growth and epileptogenesis in IDH mutated gliomas D2HG signaling mechanism. Dysregulated growth processes of gliomas interact with pro-epileptic plasticity of brain circuits in such a way that the excitatory transmitter glutamate promotes autocrine tumor invasion as well as epileptic synchrony in surround... see more

31/05/2026

INSERM

2M€

Project Budget: 2M€

Project leader

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHER... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

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Financing granted El organismo H2020 notifico la concesión del proyecto The day 2020-04-16

ERC-2019-COG: ERC Consolidator Grant Scope:Objectives

I+D

Cerrada does 6 years

0% 100% 100%

characteristics of the participant

Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

Private Information

No hay información privada compartida para este proyecto. Habla con el coordinador.

2 Participantes

INSERM

1.88M€ | Leader

INDUSTRIAS QUIMICAS DEL VALL...

452.64K€ | participant

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Project duration: 73 months Date Start: 2020-04-16
End date: 2026-05-31

Project leader

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHER... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 2M€

participation deadline Sin fecha límite de participación.

Project description Dysregulated growth processes of gliomas interact with pro-epileptic plasticity of brain circuits in such a way that the excitatory transmitter glutamate promotes autocrine tumor invasion as well as epileptic synchrony in surrounding cortical regions. Most low-grade gliomas are associated with mutations of Isocitrate DesHydrogenase (IDH) genes which lead to an excess of the oncometabolite D-2-Hydroxyglutarate (D2HG). With a structure mimicking glutamate, D2HG is thought to participate in both epileptogenic and oncologic processes. Importantly, while epileptic activity is accentuated, tumor prognosis is improved in affected people. My preliminary data now suggest a dual function for D2HG, acting as a glutamatergic agonist at high levels, but as an antagonist in the presence of glutamate. Solving this paradox will be a step forward in glioma science. The GliomasSignals project will examine the role of D2HG in the neurobiology of gliomas bringing electrophysiology concepts and tools to neuro-oncology, seeking to transform our understanding. It seeks to better understand how D2HG modulates glutamatergic signaling, affects neuronal excitability and tumor growth, and to detect the extent to which tumor infiltration colocalizes with epileptic remodeling. In vivo and in vitro work mostly on human tissue will aim at: 1- Map biomarkers of epileptic activity / tumor infiltration by cortical recordings during surgery using unique next generation Neurogrid electrodes. 2- Correlate D2HG levels, glutamate concentrations and tumor infiltration with recordings in peritumoral cortex at an unprecedented resolution. 3- Identify D2HG effects on glutamate signaling in human tissue slices producing epileptic activities and in a rodent model. 4- Explore D2HG long-term effects on epileptic activity and tumor growth / infiltration in co-cultures of tumors with surrounding peritumoral cortex by exploiting our unique capabilities for long-term human cortex organotypic cultures.

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