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Co-culture of Glutamatergic Neurons and Pediatric High-Grade Glioma Cells Into Microfluidic Devices to Assess Electrical Interactions
Published on: November 17, 2021
Pediatric gliomas
1Department of Pediatric Hematology, Heidelberg University Hospital, Im Neuenheimer Feld 153, Heidelberg 69120, Germany. stefan.pfister@med.uniheidelberg.de
Insights
Pediatric gliomas are diverse brain tumors differing from adult types. Understanding molecular pathways like MAPK and PI3K/AKT is key for new treatments and better patient risk stratification.
Area of Science:
- Pediatric neuro-oncology
- Cancer molecular biology
- Genomics and epigenetics
Background:
- Pediatric gliomas are a heterogeneous group of central nervous system (CNS) tumors.
- They differ significantly from adult gliomas despite similar histology and WHO classification.
- Pilocytic astrocytoma is common in children, while glioblastoma multiforme is prevalent in adults.
Purpose of the Study:
- To investigate the molecular pathogenesis of pediatric gliomas.
- To identify key signaling pathways involved in tumor development.
- To explore potential targets for future therapeutic strategies and improve patient stratification.
Main Methods:
- Genome-wide analyses including DNA copy-number aberrations, mRNA expression, and methylation patterns.
- Microarray-based techniques were employed.
- Identification of involved oncogenic signaling pathways.
Main Results:
- Mitogen-activated protein kinase (MAPK) and PI3K/AKT signaling pathways are prominently implicated in pediatric astrocytic tumors.
- NOTCH signaling pathway is involved in a subset of intracranial ependymomas.
- Molecular analyses reveal distinct pathogenic mechanisms in pediatric gliomas.
Conclusions:
- Targeting identified oncogenic pathways (e.g., MAPK, PI3K/AKT) and epigenetic modifications offers potential for improved treatment of unresectable or disseminated pediatric gliomas.
- Molecular markers are crucial for accurate outcome prediction and risk-based treatment stratification.
- Further research into pediatric glioma molecular biology is essential for advancing patient care.
Abstract:
Pediatric gliomas comprise a clinically, histologically, and molecularly very heterogeneous group of CNS tumors. In addition, these tumors are largely different from their counterparts occurring in adults, although they are histologically indistinguishable and uniformly classified by the current WHO classification for CNS tumors. Pilocytic astrocytoma (WHO grade I), mainly arising in the posterior fossa, is the most common representative in children, whereas glioblastoma multiforme (WHO grade IV) predominates in adults. When radical surgical resection is possible in low-grade gliomas, it will likely cure the patient. If complete surgical resection is not possible, however, for example in brainstem gliomas, which are defined by their anatomic localization rather than by their histological or molecular features, therapeutic options are limited and prognosis is usually poor. Recent genome-wide analyses applying different microarray-based methods to investigate DNA copy-number aberrations, mRNA expression signatures, and methylation patterns have shed some light on the pathways involved in the pathogenesis of pediatric glio-mas. Mitogen-activated protein kinase (MAPK) and PI3K/AKT signaling were identified as prominent oncogenic pathways in astrocytic tumors in several studies, whereas NOTCH signaling was implicated in the pathogenesis of a subset of intracranial ependymomas. Future therapeutic strategies targeting these (and other) pathways or conferring epigenetic modifications in the tumor might contribute to a better treatment outcome of patients with unresectable or disseminated tumors at diagnosis. Consideration of reliable molecular markers for outcome prediction will most likely result in a better stratification of patients into different risk groups with adjusted treatment intensity in the future.
