Mixed Neuronal-Glial Tumor

1. Disease Information

Overview

Mixed neuronal-glial tumors (also termed glioneuronal tumors) are a heterogeneous group of rare primary central nervous system (CNS) neoplasms composed of both neuronal and glial cell populations in varying proportions (crainic2023rareneuronalglial pages 1-2). They represent less than 2% of all primary CNS tumors and predominantly affect children and young adults, with a strong predilection for the temporal and frontal lobes and a frequent association with epilepsy (crainic2023rareneuronalglial pages 1-2, vaz2022uncommonglioneuronaltumors pages 1-4). The 2021 WHO Classification of Tumors of the Central Nervous System (CNS5, 5th edition) reorganized these tumors into one of six families: "Glioneuronal and neuronal tumors," alongside closely related entities in the "Pediatric-type diffuse low-grade gliomas" and "Circumscribed astrocytic gliomas" families (bale2022the2021who pages 1-2, bale2022the2021who pages 2-3).

Key Identifiers

• MONDO ID: MONDO:0016729 (mixed neuronal-glial tumor) (OpenTargets Search: mixed neuronal-glial tumor,ganglioglioma,glioneuronal tumor)
• ICD-O-3 codes: Multiple codes apply depending on subtype (e.g., 9505/1 for ganglioglioma, 9413/0 for DNET)
• MeSH: Glioneuronal tumors / Neuronal and mixed neuronal-glial tumors
• Common Synonyms: Glioneuronal tumor, mixed glioneuronal neoplasm, neuronal-glial tumor

Subtypes per WHO 2021 Classification

The following table provides a comprehensive overview of subtypes, grades, molecular features, histopathology, age of onset, and clinical presentation:

Table: This table summarizes major mixed neuronal-glial and closely related neuroepithelial tumor subtypes relevant to the WHO 2021 CNS classification, with practical emphasis on grade, molecular drivers, pathology, age, and presentation. It is useful as a quick reference for disease characterization and knowledge-base curation.

2. Etiology

Disease Causal Factors

Mixed neuronal-glial tumors are primarily driven by somatic genetic alterations, particularly those activating the mitogen-activated protein kinase (MAPK) signaling pathway. Gene expression studies have identified alterations in the RAS–RAF–MAPK and PI3K–AKT–mTOR signaling pathways, which affect cell proliferation, differentiation, autophagy, protein synthesis, and cell survival (kobow2021moleculardiagnosticsin pages 2-4). Experimental evidence demonstrates that BRAF V600E mutations in neural progenitors during embryonic development can reproduce ganglioglioma histopathological features and lead to epileptic seizures (kobow2021moleculardiagnosticsin pages 2-4). The tumors are generally considered developmental or hamartomatous neoplasms arising from aberrant neurodevelopment rather than from acquired environmental exposures.

Genetic Risk Factors

• BRAF V600E: The most common somatic alteration, present in approximately 36.94% of gangliogliomas (528 of 1360 cases in a systematic review of 43 studies) (pereira2026molecularfeaturesin pages 1-2, pereira2026molecularfeaturesin pages 2-4). This glutamic acid-to-valine substitution causes constitutive activation of the serine/threonine kinase domain, promoting oncogenic transformation (pereira2026molecularfeaturesin pages 4-5).
• FGFR1: FGFR1 hotspot mutations (N546K and K656E) are the fifth most prevalent alteration in LGG/MNGT; among driver-unknown samples, up to 12% harbor these mutations (engelhardt2022frequentfgfr1hotspot pages 1-2). FGFR1 alterations are present in >75% of DNETs (crainic2023rareneuronalglial pages 6-8).
• NF1/PTPN11/KRAS: A subgroup of gangliogliomas with PTPN11/KRAS/NF1 alterations has been identified, showing adverse clinical outcomes and atypical histopathological features, with only 38% achieving Engel I seizure outcome compared to 85% for BRAF V600E-only gangliogliomas (pereira2026molecularfeaturesin pages 8-9).
• Neurofibromatosis type 1 (NF1): Germline NF1 mutations predispose to various glioneuronal tumors.

Environmental and Lifestyle Risk Factors

No specific environmental or lifestyle risk factors have been consistently identified for mixed neuronal-glial tumors. These tumors are not associated with known carcinogen exposures, ionizing radiation, or infectious agents based on current evidence. The primary etiologic mechanism appears to be somatic genetic alteration during neural development.

Gene-Environment Interactions

No well-established gene-environment interactions have been documented for this tumor group. The predominantly somatic, developmental nature of the underlying genetic alterations suggests limited environmental modulation.

3. Phenotypes

Primary Phenotypes

Seizures / Epilepsy (HP:0001250) - Type: Symptom (neurological) - Characteristics: Drug-resistant focal epilepsy is the hallmark presentation; seizures are present in the vast majority of cases, often with onset at a young age and a long-term history (crainic2023rareneuronalglial pages 1-2, vaz2022uncommonglioneuronaltumors pages 1-4). Ganglioglioma and DNET have been informally termed "epileptomas" due to their extremely high epileptogenic potential (crainic2023rareneuronalglial pages 1-2). - Onset: Childhood to young adulthood - Severity: Often medically refractory (drug-resistant) - Frequency: >80% of gangliogliomas and DNETs

Headache (HP:0002315) - Type: Symptom - Characteristics: Less common than seizures; may present in tumors causing mass effect or hydrocephalus - Frequency: Variable, more common in posterior fossa tumors (RGNT) and central neurocytoma

Focal neurological deficits (HP:0007340) - Type: Clinical sign - Characteristics: Depend on tumor location; may include motor weakness, sensory changes, visual field deficits - Onset: Variable; more common in aggressive subtypes (anaplastic ganglioglioma)

Hydrocephalus (HP:0000238) - Type: Clinical sign - Characteristics: Seen particularly with intraventricular tumors (central neurocytoma) and leptomeningeal spread (DLGNT)

Macrocephaly (HP:0000256) - Type: Physical manifestation - Characteristics: Particularly relevant to desmoplastic infantile ganglioglioma presenting in infancy

Quality of Life Impact: Chronic epilepsy significantly impairs quality of life, including cognitive development in children, educational achievement, employment, driving ability, and psychosocial functioning. Successful surgical resection with seizure freedom provides the greatest quality-of-life benefit.

4. Genetic/Molecular Information

Causal Genes and Pathogenic Variants

OpenTargets disease-target association analysis identified 8 key targets for mixed neuronal-glial tumor (MONDO:0016729), with PTEN (score 0.66), BRAF (score 0.63), FGFR1 (score 0.48), H3-3A (score 0.42), NTRK3 (score 0.38), IDH1 (score 0.37), ETV6 (score 0.37), and MUTYH (score 0.34) as the top associations (OpenTargets Search: mixed neuronal-glial tumor,ganglioglioma,glioneuronal tumor).

BRAF (HGNC:1097; ENSG00000157764): - V600E missense mutation: most frequent alteration in gangliogliomas at 36.32–36.94% (pereira2026molecularfeaturesin pages 1-2, pereira2026molecularfeaturesin pages 2-4) - Additional variants: duplications, in-frame insertions, and fusions including KIAA1549::BRAF (pereira2026molecularfeaturesin pages 2-4) - Somatic origin; constitutive activation of MAPK/ERK pathway - ClinVar: RCV000515781 for BRAF-mixed neuronal-glial tumor association

FGFR1 (HGNC:3688; ENSG00000077782): - Hotspot mutations N546K and K656E; present in 1.18% of gangliogliomas but dominant in DNETs (>75%) (engelhardt2022frequentfgfr1hotspot pages 1-2, pereira2026molecularfeaturesin pages 1-2, crainic2023rareneuronalglial pages 6-8) - FGFR activation phosphorylates kinase domains to activate Ras/Raf/MEK and PI3K-Akt pathways (engelhardt2022frequentfgfr1hotspot pages 1-2)

FGFR1::TACC1 fusion: Reported in approximately two-thirds of extraventricular neurocytomas (crainic2023rareneuronalglial pages 4-5)

SLC44A1::PRKCA fusion: Characteristic of papillary glioneuronal tumor (crainic2023rareneuronalglial pages 4-5, crainic2023rareneuronalglial pages 5-6, vaz2022uncommonglioneuronaltumors pages 4-6)

PDGFRA p.K385 mutation: Defining alteration for myxoid glioneuronal tumor (capper2023eanoguidelineon pages 11-12, bale2022the2021who pages 8-9)

Epigenetic Information

DNA methylation profiling has emerged as a critical diagnostic tool for classifying glioneuronal tumors. The DKFZ/Heidelberg CNS tumor classifier uses machine learning-based methylation analysis to distinguish tumor subtypes, and methylation classification confirmed or refined morphological diagnoses in a significant proportion of cases (singh2023currentstatusof pages 3-4). DLGNT shows two molecular subclasses (MC-1 and MC-2) based on distinct methylation profiles with different age presentations and survival outcomes (singh2023currentstatusof pages 3-4). DGONC is defined by a distinct methylation class associated with monosomy 14 (bale2022the2021who pages 1-2, xie2023lowgradeepilepsyassociatedneuroepithelial pages 2-3, bale2022the2021who pages 8-9).

Chromosomal Abnormalities

• 1p deletion: Characteristic of DLGNT
• Monosomy 14: Defining feature of DGONC (bale2022the2021who pages 1-2, bale2022the2021who pages 8-9)
• Chromosome 12 gains, NF1 CNV losses: Identified in PTPN11-altered gangliogliomas (pereira2026molecularfeaturesin pages 8-9)

5. Environmental Information

No specific environmental toxins, radiation exposures, or lifestyle factors have been established as causative or contributory for mixed neuronal-glial tumors based on current evidence. No infectious agents have been implicated in the pathogenesis of these tumors.

6. Mechanism / Pathophysiology

Molecular Pathways

The central pathogenic mechanism involves constitutive activation of the RAS–RAF–MEK–ERK (MAPK) signaling cascade (kobow2021moleculardiagnosticsin pages 2-4, pereira2026molecularfeaturesin pages 4-5). BRAF V600E mutations cause constitutive kinase activation, leading to uncontrolled cell proliferation and oncogenic transformation. BRAF inhibitors work by selectively binding to V600E-mutated B-Raf proteins and preventing MEK activation (pereira2026molecularfeaturesin pages 4-5).

The PI3K–AKT–mTOR pathway also plays a role, particularly through co-mutations in PIK3CA and PIK3R1 observed in rosette-forming glioneuronal tumors (crainic2023rareneuronalglial pages 4-5). FGFR1 activation simultaneously stimulates both Ras/Raf/MEK and PI3K-Akt cascades (engelhardt2022frequentfgfr1hotspot pages 1-2).

Relevant GO terms: - GO:0000165 (MAPK cascade) - GO:0043066 (negative regulation of apoptotic process) - GO:0008284 (positive regulation of cell population proliferation) - GO:0048015 (phosphatidylinositol-mediated signaling)

Cellular Processes

• Cell proliferation driven by constitutive MAPK activation
• Aberrant neural progenitor differentiation during development
• Epileptogenesis through cortical involvement and association with focal cortical dysplasia (FCD) (kobow2021moleculardiagnosticsin pages 2-4)

Relevant CL terms: - CL:0000540 (neuron) - CL:0000127 (astrocyte) - CL:0000128 (oligodendrocyte) - CL:0002319 (neural cell)

Causal Chain

Somatic mutation (e.g., BRAF V600E) in neural progenitor during embryonic development → constitutive MAPK/ERK pathway activation → aberrant cell proliferation and differentiation → formation of mixed neuronal-glial neoplasm in cortex → cortical disruption and epileptogenic zone formation → drug-resistant focal epilepsy (kobow2021moleculardiagnosticsin pages 2-4).

7. Anatomical Structures Affected

Primary Organs

• Brain (UBERON:0000955): Primary site of involvement
• Cerebral cortex (UBERON:0000956): Most common location, especially temporal lobe
• Temporal lobe (UBERON:0001871): Predilection site for ganglioglioma and DNET (vaz2022uncommonglioneuronaltumors pages 1-4)
• Fourth ventricle / Posterior fossa: Common site for RGNT (crainic2023rareneuronalglial pages 4-5)
• Septum pellucidum / Lateral ventricle: Characteristic for myxoid glioneuronal tumor (bale2022the2021who pages 8-9)
• Leptomeninges (UBERON:0000016): Involved in DLGNT
• Spinal cord (UBERON:0002240): Can be involved in DLGNT and rare glioneuronal tumors

Tissue and Cell Level

• Neuronal cells: Dysmorphic ganglion cells (ganglioglioma), floating neurons (DNET), neurocytic rosettes (RGNT)
• Glial cells: Astrocytic (GFAP+) and oligodendroglial (OLIG2+) components
• Progenitor cells: CD34+ ramified cells characteristically present (vaz2022uncommonglioneuronaltumors pages 1-4)

8. Temporal Development

Onset

• Typical age: Predominantly childhood to young adulthood (crainic2023rareneuronalglial pages 1-2, vaz2022uncommonglioneuronaltumors pages 1-4)
• Desmoplastic infantile ganglioglioma: Presents in infancy, usually first 2 years of life
• Onset pattern: Typically insidious, with chronic seizures developing over months to years before diagnosis

Progression

• Most subtypes (WHO grade 1): Slow-growing, indolent biological behavior with long-term seizure history (crainic2023rareneuronalglial pages 1-2)
• Anaplastic ganglioglioma (WHO grade 3): More aggressive course with potential for rapid progression (crainic2023rareneuronalglial pages 6-8, vaz2022uncommonglioneuronaltumors pages 1-4)
• Disease course: Generally stable or slowly progressive; recurrence possible, particularly with subtotal resection

9. Inheritance and Population

Epidemiology

According to the CBTRUS Statistical Report (2014–2018), neuronal and mixed neuronal-glial tumors had an annual average of 58 cases and 5-year total of 290 cases in the United States, with an age-adjusted incidence rate (AAAIR) of 0.05 per 100,000 population (95% CI: 0.04–0.06) (ostrom2021cbtrusstatisticalreport pages 50-51). These tumors represent less than 2% of all primary CNS tumors (crainic2023rareneuronalglial pages 1-2).

Population Demographics

• Age distribution: Predominantly affects children, adolescents, and young adults
• Sex ratio: Most subtypes show no strong sex predilection, though some series report slight male predominance
• Geographic distribution: No documented geographic clustering; reported worldwide
• Inheritance: Almost exclusively somatic (non-hereditary) mutations. No Mendelian inheritance pattern. Rare association with NF1 (autosomal dominant predisposition syndrome).

10. Diagnostics

Clinical Tests

Imaging (MAXO:0000387 - imaging study): - MRI is the cornerstone of neuroimaging. Gangliogliomas typically appear as cortical/subcortical cystic-solid lesions with enhancement. DNETs often show cortical "bubbly" T2-hyperintense lesions without mass effect. Genotype-neuroimaging correlations have been identified: BRAF V600E tumors show indistinct borders with iso-T1/high-T2 signal (93.8% sensitivity, 100% specificity), while FGFR1-mutant tumors show sharp borders with very high T2 signal and diffuse mass effect (100% sensitivity and specificity) (iijima2024genotyperelevantneuroimagingfeatures pages 9-9).

Histopathology and Immunohistochemistry: - Ganglioglioma: Synaptophysin+/Chromogranin A+ neuronal cells, GFAP+/OLIG2+ glial cells, eosinophilic granular bodies, CD34+ stellate cells, Ki67 <3% (crainic2023rareneuronalglial pages 6-8, vaz2022uncommonglioneuronaltumors pages 1-4) - DNET: "Floating neurons" in myxoid matrix, NeuN+/synaptophysin+ neurons, Olig2+ oligodendroglia-like cells (crainic2023rareneuronalglial pages 6-8) - RGNT: Synaptophysin+/MAP2+/NSE+ neurocytic rosettes, GFAP+/OLIG2+/S100+ glial component (vaz2022uncommonglioneuronaltumors pages 6-7)

Molecular/Genetic Testing: The EANO guideline recommends next-generation sequencing (NGS) panel diagnostics rather than sequential target-specific testing, given the low prevalence (<5%) of individual targets in CNS tumors (capper2023eanoguidelineon pages 3-4). DNA methylation profiling using the DKFZ/Heidelberg classifier is increasingly essential for accurate subtyping (singh2023currentstatusof pages 3-4). The 2023 EANO molecular diagnostic tools guideline systematically reviews methods including NGS for DNA and RNA, methylome profiling, and immunohistochemistry for marker assessment (capper2023eanoguidelineon pages 3-4).

Differential Diagnosis

Key differential diagnoses include: pilocytic astrocytoma, oligodendroglioma (IDH-mutant, 1p/19q-codeleted), pleomorphic xanthoastrocytoma, angiocentric glioma, focal cortical dysplasia, and diffuse low-grade glioma (vaz2022uncommonglioneuronaltumors pages 4-6, bale2022the2021who pages 3-5).

11. Outcome/Prognosis

Survival and Mortality

• Ganglioglioma (WHO grade 1): 10-year survival exceeds 80% with complete surgical resection (crainic2023rareneuronalglial pages 6-8). Gross total resection (GTR) improves both overall survival and seizure control compared to subtotal resection (STR) (crainic2023rareneuronalglial pages 6-8).
• Ganglioglioma with PTPN11/KRAS/NF1 alterations: Significantly worse seizure outcomes (38% Engel I) compared to BRAF V600E-only gangliogliomas (85% Engel I), suggesting a clinically relevant adverse subgroup (pereira2026molecularfeaturesin pages 8-9).
• DLGNT: Prognosis varies by methylation subclass; MC-1 and MC-2 have different survival outcomes (singh2023currentstatusof pages 3-4).
• Anaplastic ganglioglioma (WHO grade 3): More aggressive clinical course with shorter survival.

Prognostic Factors

• Extent of surgical resection (GTR vs. STR)
• Tumor location (temporal lobe more favorable than infratentorial) (crainic2023rareneuronalglial pages 6-8)
• Molecular subgroup (BRAF V600E-only more favorable; PTPN11/KRAS/NF1 subgroup worse) (pereira2026molecularfeaturesin pages 8-9)
• Ki67/MIB1 proliferation index (>2% associated with recurrence risk) (vaz2022uncommonglioneuronaltumors pages 9-10)
• WHO grade (grade 1 vs. grade 3)
• CDKN2A/B deletion status

12. Treatment

Surgical Management (MAXO:0000004 - surgical procedure)

Gross total resection is the cornerstone of treatment and is considered curative for most WHO grade 1 glioneuronal tumors (crainic2023rareneuronalglial pages 1-2, crainic2023rareneuronalglial pages 6-8). For epilepsy-associated tumors, extended resection including the epileptogenic zone improves seizure-free outcomes (crainic2023rareneuronalglial pages 6-8). Temporal lobe surgeries generally achieve better seizure control than extratemporal resections.

Targeted Therapies (MAXO:0001525 - targeted therapy)

The following table summarizes the molecular targets and therapeutic options:

Table: This table summarizes the main molecular alterations linked to mixed neuronal-glial tumors and maps them to current or emerging targeted treatment options. It emphasizes where evidence is strongest—especially for BRAF V600E—and where alterations are primarily diagnostic rather than therapeutically validated.

BRAF V600E-targeted therapy: The EANO guideline (2023) recommends that BRAF p.V600E targeted treatment should be considered part of the standard of care for patients with recurrent gliomas, pending regulatory approval (capper2023eanoguidelineon pages 2-3). FDA-approved BRAF inhibitors include vemurafenib (Zelboraf), dabrafenib (Tafinlar), and encorafenib (Braftovi) (pereira2026molecularfeaturesin pages 4-5). Combination BRAF/MEK inhibitor therapy (e.g., dabrafenib + trametinib) is preferred as it can overcome resistance to single-agent BRAF inhibitors and has been shown to produce durable responses (crainic2023rareneuronalglial pages 18-19, capper2023eanoguidelineon pages 9-10). In a multi-institutional study of BRAF-mutant pediatric high-grade gliomas (including anaplastic gangliogliomas) treated with upfront molecular targeted therapy, 3-year progression-free and overall survival were 65% and 82%, respectively, superior to historical controls (rosenberg2022upfrontmoleculartargeted pages 5-6).

NTRK inhibitors: Larotrectinib and entrectinib have received conditional tumor-agnostic approval for NTRK fusion-positive tumors (capper2023eanoguidelineon pages 6-7). However, evidence of clinical benefit specifically in adult CNS tumors remains limited, and treatment should preferably occur within clinical trials (capper2023eanoguidelineon pages 2-3, capper2023eanoguidelineon pages 11-12).

FGFR inhibitors: Clinical trials have evaluated FGFR inhibitors (e.g., pemigatinib, NCT05267106) for FGFR-altered CNS tumors, though activity has been modest (capper2023eanoguidelineon pages 2-3, capper2023eanoguidelineon pages 11-12). FGFR alterations are classified as ESCAT IIB in glioneuronal tumors (capper2023eanoguidelineon pages 11-12).

Radiotherapy (MAXO:0000015 - radiation therapy)

Radiotherapy is reserved for subtotal resection of aggressive tumors, tumors in eloquent brain areas, or recurrent disease (crainic2023rareneuronalglial pages 6-8, talloa2022brafandmek pages 10-11). Focal radiation therapy should be used cautiously in young children due to long-term cognitive side effects (talloa2022brafandmek pages 10-11).

Chemotherapy

Temozolomide has limited evidence for improving survival but may be considered for anaplastic features or inoperable recurrent tumors (crainic2023rareneuronalglial pages 6-8). For DLGNT, bevacizumab has been used successfully in some cases (crainic2023rareneuronalglial pages 18-19).

Clinical Trials

• NCT02684058: Dabrafenib + trametinib in pediatric BRAF V600 mutation-positive LGG/relapsed HGG (Phase 2, completed, 151 participants)
• NCT04923126: Mirdametinib (MEK inhibitor) in children/adolescents/young adults with low-grade glioma (Phase 1/2, recruiting, 132 participants)
• NCT05267106: Pemigatinib (FGFR inhibitor) in FGFR1-3 altered primary CNS tumors (Phase 2, terminated, 83 participants)
• NCT05259605: EORTC observational study assessing treatment and outcome using WHO 2021 classification (recruiting, 1650 participants)

13. Prevention

Primary Prevention

No established primary prevention strategies exist for mixed neuronal-glial tumors. As these tumors arise from somatic mutations during neural development, there are no modifiable risk factors or vaccination strategies available.

Secondary Prevention (Early Detection)

• Early neuroimaging (MRI) evaluation in children presenting with new-onset seizures
• Genetic counseling for families with NF1 or other cancer predisposition syndromes
• Epilepsy monitoring and evaluation for surgical candidacy in drug-resistant cases

Tertiary Prevention

• Post-surgical surveillance imaging to monitor for recurrence
• Long-term epilepsy follow-up and anti-seizure medication management
• Neurocognitive monitoring and rehabilitation, particularly in pediatric patients

14. Other Species / Natural Disease

Limited data exist on naturally occurring mixed neuronal-glial tumors in other species. Ganglioglioma-like tumors have been rarely reported in veterinary neuropathology in domestic animals. BRAF V600E-equivalent mutations and MAPK pathway alterations have been identified in canine tumors, supporting evolutionary conservation of oncogenic mechanisms. However, no systematic comparative pathology data specific to glioneuronal tumors are available in the current literature.

15. Model Organisms

Genetic Models

Experimental models have demonstrated that expression of BRAF V600E in neural progenitors during embryonic development reproduces ganglioglioma histopathological features and leads to epileptic seizures (kobow2021moleculardiagnosticsin pages 2-4). These models have been crucial for understanding the developmental origin of these tumors and the mechanism of epileptogenicity.

• Mouse models: Conditional BRAF V600E expression in neural progenitors (genetically engineered mouse models)
• Cell lines: Patient-derived primary tumor cultures have been used for drug sensitivity studies

Model Limitations

• Difficulty recapitulating the mixed neuronal-glial phenotype in full
• Limited availability of immortalized cell lines due to the low-grade, slow-growing nature of most subtypes
• Differences between murine and human neural development may affect translational relevance

Summary

Mixed neuronal-glial tumors are a diverse group of rare, predominantly low-grade CNS neoplasms characterized by dual neuronal-glial composition, strong association with epilepsy, and frequent MAPK pathway alterations. The WHO 2021 classification substantially expanded and refined this tumor family through integration of molecular markers and DNA methylation profiling. BRAF V600E is the most actionable therapeutic target, with dabrafenib/trametinib combination therapy approaching standard-of-care status for recurrent disease per EANO guidelines. Gross total surgical resection remains the primary curative modality, with excellent long-term survival exceeding 80% for WHO grade 1 subtypes. Ongoing molecular characterization continues to identify new tumor entities and refine prognostic stratification within this heterogeneous tumor group.

References

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18. (capper2023eanoguidelineon pages 11-12): David Capper, Guido Reifenberger, Pim J French, Leonille Schweizer, Michael Weller, Mehdi Touat, Simone P Niclou, Philipp Euskirchen, Christine Haberler, Monika E Hegi, Sebastian Brandner, Emilie Le Rhun, Roberta Rudà, Marc Sanson, Ghazaleh Tabatabai, Felix Sahm, Patrick Y Wen, Pieter Wesseling, Matthias Preusser, and Martin J van den Bent. Eano guideline on rational molecular testing of gliomas, glioneuronal, and neuronal tumors in adults for targeted therapy selection. Neuro-Oncology, 25:813-826, Jan 2023. URL: https://doi.org/10.1093/neuonc/noad008, doi:10.1093/neuonc/noad008. This article has 129 citations and is from a domain leading peer-reviewed journal.

19. (bale2022the2021who pages 5-6): Tejus A. Bale and Marc K. Rosenblum. The 2021 who classification of tumors of the central nervous system: an update on pediatric low‐grade gliomas and glioneuronal tumors. Brain Pathology, Feb 2022. URL: https://doi.org/10.1111/bpa.13060, doi:10.1111/bpa.13060. This article has 279 citations and is from a domain leading peer-reviewed journal.

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