Ganglioglioma

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Central Nervous System Tumours(WHO Classification, 5th ed.)

(General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). Use HUGO-approved gene names and symbols (italicized when appropriate), HGVS-based nomenclature for variants, as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples); to add (or move) a row or column in a table, click nearby within the table and select the > symbol that appears. Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support.)

Primary Author(s)*

Dr Leila Moayed Alaei, Royal Prince Alfred Hospital

WHO Classification of Disease

Structure Disease
Book Central Nervous System Tumours (5th ed.)
Category Gliomas, glioneuronal tumours, and neuronal tumours
Family Gliomas, glioneuronal tumours, and neuronal tumours
Type Glioneuronal and neuronal tumours
Subtype(s) Ganglioglioma

WHO Essential and Desirable Genetic Diagnostic Criteria

(Instructions: The table will have the diagnostic criteria from the WHO book autocompleted; remove any non-genetics related criteria. If applicable, add text about other classification systems that define this entity and specify how the genetics-related criteria differ.)

WHO Essential Criteria (Genetics)*
WHO Desirable Criteria (Genetics)*
Other Classification

*Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the WHO Classification of Tumours.

Related Terminology

(Instructions: The table will have the related terminology from the WHO autocompleted.)

Acceptable
Not Recommended

Gene Rearrangements

Put your text here and fill in the table (Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Driver Gene Fusion(s) and Common Partner Genes Molecular Pathogenesis Typical Chromosomal Alteration(s) Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE: ABL1 EXAMPLE: BCR::ABL1 EXAMPLE: The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1. EXAMPLE: t(9;22)(q34;q11.2) EXAMPLE: Common (CML) EXAMPLE: D, P, T EXAMPLE: Yes (WHO, NCCN) EXAMPLE:

The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference). BCR::ABL1 is generally favorable in CML (add reference).

EXAMPLE: CIC EXAMPLE: CIC::DUX4 EXAMPLE: Typically, the last exon of CIC is fused to DUX4. The fusion breakpoint in CIC is usually intra-exonic and removes an inhibitory sequence, upregulating PEA3 genes downstream of CIC including ETV1, ETV4, and ETV5. EXAMPLE: t(4;19)(q25;q13) EXAMPLE: Common (CIC-rearranged sarcoma) EXAMPLE: D EXAMPLE:

DUX4 has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references).

EXAMPLE: ALK EXAMPLE: ELM4::ALK


Other fusion partners include KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1

EXAMPLE: Fusions result in constitutive activation of the ALK tyrosine kinase. The most common ALK fusion is EML4::ALK, with breakpoints in intron 19 of ALK. At the transcript level, a variable (5’) partner gene is fused to 3’ ALK at exon 20. Rarely, ALK fusions contain exon 19 due to breakpoints in intron 18. EXAMPLE: N/A EXAMPLE: Rare (Lung adenocarcinoma) EXAMPLE: T EXAMPLE:

Both balanced and unbalanced forms are observed by FISH (add references).

EXAMPLE: ABL1 EXAMPLE: N/A EXAMPLE: Intragenic deletion of exons 2–7 in EGFR removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways. EXAMPLE: N/A EXAMPLE: Recurrent (IDH-wildtype Glioblastoma) EXAMPLE: D, P, T


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Chromosomal Rearrangement Genes in Fusion

(5’ or 3’ Segments)

Structural variation Prevalence Diagnostic Significance (Yes, No or Unknown) Prognostic Significance (Yes, No or Unknown) Therapeutic Significance (Yes, No or Unknown) Notes
t(7;7)(q34;q34)[1][2] KIAA1549::BRAF[1][3] duplication   16.7%[3] Yes[4][1] No Yes[5] - also seen in PLNTY, ganglioglioma, and pilocytic astrocytoma; can distinguish by methylation signature[4]

- in-frame fusion[1]

t(8;8)(p11.23;p11.22)[1][2] FGFR1::TACC1[1] inversion 2.5% (1/40)[1] Unknown Unknown Unknown   - in-frame fusion[1]

- no FDA-approved anti-FGFR therapy for ganglioglioma at present

t(10;10)(q26.13;q25.3)[1][2] FGFR2::KIAA1598[1] deletion 2.5% (1/40)[1] Unknown Unknown Unknown - in-frame fusion[1]


t(10;10) (q26.13;q24.3)[1][2] FGFR2::INA[1] inversion 2.5% (1/40)[1] Unknown Unknown Unknown - in-frame fusion[1]


t(3;3)(p14.3;p25.2)[1][2] ERC2::RAF1[1] deletion 2.5%(1/40)[1] Unknown Unknown Yes (potential)[5] - in-frame fusion[1]


t(14;7)(q32.32;7q34)[1][2] CDC42BPB::BRAF[1] translocation 2.5% (1/40)[1] Unknown Unknown Yes (potential)[5] - in-frame fusion[1]


t(7;7)(p15.3;q34)[1][2] KLHL7::BRAF[1] inversion 2.5% (1/40) [1]


Unknown Unknown Yes (potential)[5] - in-frame fusion[1]


t(1;11)(q25.2;q14.1)[1][2] ABL2::GAB2[1] translocation 2.5% (1/40)[1]


Unknown Unknown Yes (potential)[5] - in-frame fusion[1]



Individual Region Genomic Gain/Loss/LOH

Put your text here and fill in the table (Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.)

Chr # Gain, Loss, Amp, LOH Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size] Relevant Gene(s) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:

7

EXAMPLE: Loss EXAMPLE:

chr7

EXAMPLE:

Unknown

EXAMPLE: D, P EXAMPLE: No EXAMPLE:

Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference).  Monosomy 7/7q deletion is associated with a poor prognosis in AML (add references).

EXAMPLE:

8

EXAMPLE: Gain EXAMPLE:

chr8

EXAMPLE:

Unknown

EXAMPLE: D, P EXAMPLE:

Common recurrent secondary finding for t(8;21) (add references).

EXAMPLE:

17

EXAMPLE: Amp EXAMPLE:

17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb]

EXAMPLE:

ERBB2

EXAMPLE: D, P, T EXAMPLE:

Amplification of ERBB2 is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined.

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Chr #   Gain/Loss/Amp/LOH Minimal Region Genomic Coordinates [Genome Build] Minimal Region Cytoband Diagnostic Significance (Yes, No or Unknown) Prognostic Significance

(Yes, No or Unknown)  

Therapeutic Significance

(Yes, No or Unknown)

Notes
1 loss Chr1:1- 248956422


Chr1 Unknown Unknown Unknown This constellation of chromosomal abnormalities was found in a case series of 40 gangliogliomas[8].

It is unknown if the abnormalities are either diagnostic, prognostic or therapeutic.  

3 gain Chr3:1- 198295559


Chr3 Unknown Unknown Unknown
4 gain Chr4:1- 190214555 Chr4 Unknown Unknown Unknown
5 gain Chr5:1- 181538259 Chr5 Unknown Unknown Unknown
6 gain Chr6:1- 170805979 Chr6 Unknown Unknown Unknown
7 gain Chr7:1- 159345973 Chr7 Unknown Unknown Unknown
8 gain Chr8:1- 145138636 Chr8 Unknown Unknown Unknown
9 gain Chr9:1- 138394717 Chr9 Unknown Unknown Unknown
10 loss (segmental) Chr10:1- 133797422 Chr10 Unknown Unknown Unknown
11 gain Chr11:1- 135086622 Chr11 Unknown Unknown Unknown
12 gain Chr12:1- 133275309 Chr12 Unknown Unknown Unknown
15 gain Chr15: 1- 101991189 Chr15 Unknown Unknown Unknown
16 Gain   Chr16:1-90338345


Chr16 Unknown Unknown Unknown
16 loss Chr16:1-90338345


Chr16 Unknown Unknown Unknown
17 loss Chr17:1- 83257441 Chr17 Unknown Unknown Unknown
18 gain Chr18:1- 80373285 Chr18 Unknown Unknown Unknown
19 gain Chr19:1- 58617616 Chr19 Unknown Unknown Unknown
20 gain Chr20:1- 64444167 Chr20 Unknown Unknown Unknown
21 gain Chr21:1- 46709983 Chr21 Unknown Unknown Unknown
22 gain Chr22:1- 50818468 Chr22 Unknown Unknown Unknown


Characteristic Chromosomal or Other Global Mutational Patterns

Put your text here and fill in the table (Instructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Chromosomal Pattern Molecular Pathogenesis Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:

Co-deletion of 1p and 18q

EXAMPLE: See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). EXAMPLE: Common (Oligodendroglioma) EXAMPLE: D, P
EXAMPLE:

Microsatellite instability - hypermutated

EXAMPLE: Common (Endometrial carcinoma) EXAMPLE: P, T

Gene Mutations (SNV/INDEL)

Put your text here and fill in the table (Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.)

Gene Genetic Alteration Tumor Suppressor Gene, Oncogene, Other Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T   Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
EXAMPLE:EGFR


EXAMPLE: Exon 18-21 activating mutations EXAMPLE: Oncogene EXAMPLE: Common (lung cancer) EXAMPLE: T EXAMPLE: Yes (NCCN) EXAMPLE: Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references).
EXAMPLE: TP53; Variable LOF mutations


EXAMPLE: Variable LOF mutations EXAMPLE: Tumor Supressor Gene EXAMPLE: Common (breast cancer) EXAMPLE: P EXAMPLE: >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer.
EXAMPLE: BRAF; Activating mutations EXAMPLE: Activating mutations EXAMPLE: Oncogene EXAMPLE: Common (melanoma) EXAMPLE: T

Note: A more extensive list of mutations can be found in cBioportal, COSMIC, and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.


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Gene; Genetic Alteration Presumed Mechanism (Tumor Suppressor Gene (TSG)/Oncogene/Other) Prevalence (COSMIC/ TCGA/Other) Concomitant Mutations Mutually Exclusive Mutations Diagnostic Significance (Yes, No or Unknown) Prognostic Significance

(Yes, No or Unknown)  

Therapeutic Significance

(Yes, No or Unknown)

Notes
BRAF p.V600E[4][1] oncogene 10-60%[4] Homozygous deletion of CDKN2A[1][8]


H3-3A p.K27M[6]

KRAS, RAF1, NF1, FGFR1, and FGFR2[1] Yes[4][1] Yes[7] Yes[8] FDA-approved therapy includes dabrafenib-trametinib[8]


BRAF indel events: p.L505delinsLEYLS p.R506delinsRVLR p.R506delinsRSTQ p.T599_W604delinsTDG) [1] oncogene 10%[1] KRAS, RAF1, NF1, FGFR1, and FGFR2[1] Yes[4][1] Unknown Unknown  
KRAS p.Q61K[1] oncogene 5%[1] KRAS, RAF1, NF1, FGFR1, and FGFR2[1] Yes[4][1] No[1][7] No
FGFR2 exon 17 splicesite mutation[1] oncogene 2.5%[1]


KRAS, RAF1, NF1, FGFR1, and BRAF[1] Yes[4][1] No[1][7] No - no FDA-approved anti-FGFR therapy for ganglioglioma at present


FGFR1 p.N546K[1] oncogene 2.5%[1]


KRAS, RAF1,

 NF1, BRAF, and FGFR2[1]

Yes[4][1] No[1][7] No - no FDA-approved anti-FGFR therapy for ganglioglioma at present


Epigenomic Alterations

Methylation profiling can be used in the diagnosis of ganglioglioma, however low tumour cellularity can impact on feasibility in the diagnostic setting[4].

Genes and Main Pathways Involved

90% of gangliogliomas harbor genetic alterations activating the MAPK signaling pathway, with non-MAPK signaling seen in 10% of cases (e.g. ABL2::GAB2 gene fusion)[1].  

Gene; Genetic Alteration Pathway Pathophysiologic Outcome
BRAF; activating alterations MAPK signaling Increased cell growth and proliferation
RAF1; activating alterations MAPK signaling Increase cell growth and proliferation
KRAS; activating mutations MAPK signaling Increase cell growth and proliferation
NF1; inactivating mutations MAPK signaling   Increase cell growth and proliferation
FGFR1/2/3; activating alterations MAPK signaling Increase cell growth and proliferation

Genetic Diagnostic Testing Methods

  • Chromosome microarray  
  • Next generation sequencing  
  • DNA methylation profiling

Familial Forms

Inactivating germline mutations or deletions of NF1, as occurs in neurofibromatosis type 1, can be associated with a minor proportion of gangliogliomas[1][9]

Additional Information

This disease is defined/characterized as detailed below:

  • This is a distinct entity in the World Health Organization (WHO) classification system within the section of Gliomas, Glioneuronal and neuronal tumours. This is a well-differentiated glioneuronal tumour with low proliferative activity, comprised of mixed neoplastic neuronal and glial cell components. It is molecularly characterized by genomic aberrations causing MAPK pathway activation (CNS WHO grade 1)[4].

The epidemiology/prevalence of this disease is detailed below:

  • Gangliogliomas are generally tumours of adolescent/young adults with a median age of 12 years at the time of diagnosis. However, the tumour has been reported in wider range of age from 0 to 70 years of age[10][11]. The tumour is more prevalent in male patients (59.8%) than in female patients (40.2%)[12].

The clinical features of this disease are detailed below:

  • The clinical features are dependent on the tumour location and size. If located in the cerebrum, the most common presentation is with focal seizures[4][13], with up to 23.6% of surgical epilepsy specimens harbouring gangliogliomas[14]. The mean duration of symptoms prior to diagnosis is also dependent on location. For tumours located in the cerebrum, the duration of symptoms prior to diagnosis ranges between 5 and 10 years, whereas in the brainstem and spinal cord, the mean duration of symptoms pre-diagnosis ranges between 1.25 years and 1.4 years, respectively[13][15].
  • The archetypal radiological features are of a circumscribed, solid/cystic mass, although varied appearances are the norm, ranging from presentation as a small cyst to a solid mass[16].  Patterns of contrast enhancement can also vary, including enhancement of the cystic wall to a markedly enhanced nodule[16].
  • Signs and symptoms - Intracerebral ganglioglioma: Seizure; chronic temporal lobe epilepsy[13]; Brain stem ganglioglioma: blurry vision, loss of memory, syncope spells, cranial nerve deficits, headache, and gait instability[17]; Spinal cord ganglioglioma:  acute onset paraparesis[18]
  • Laboratory findings - Classic imaging features: T1 iso- to hypointense solid component, T2-hyperintense solid component with varied signal within the cystic component; nodule and cyst wall show variable contrast enhancement[16]

The sites of involvement of this disease are detailed below:

  • Most common location: temporal lobes (>70%)[13][15][19]
  • Other locations: cerebrum, brainstem, cerebellum, spinal cord, and optic nerves, lateral ventricle[11][13][15][19]

The morphologic features of this disease are detailed below:

  • Ganglioglioma is a biphasic tumor composed of a neoplastic neuronal and a neoplastic glial component[11][19]. The neoplastic neuronal component is comprised of dysmorphic ganglion cells showing cytomegaly, binucleation and perimembranous aggregation of Nissl substance. Disorganized cytoarchitecture is also observed, with clustering of neurons. The neoplastic glial component can resemble a diffuse glioma or pilocytic astrocytoma; the glial component harbors the proliferative component of the tumor, which can show infiltration on microscopy. Proliferative activity is usually low to absent. The two components can be intermingled or geographically distinct. Other pertinent histological features include Rosenthal fibres, eosinophilic granular bodies and perivascular lymphoid infiltration[11][19]. An association with focal cortical dysplasia is a commonly reported finding[20].

The immunophenotype of this disease is detailed below:

  • Positive (universal) - CD34 expressed in expressed in ramified tumor cells[21]
  • Neoplastic neuronal component – MAP2, neurofilament, synaptophysin, chromogranin A (No definitive markers for neoplastic neuronal component; Typical profile: chromogranin A+, NeuN-, synaptophysin+, neurofilament+, MAP2+ (but MAP2 - in glial component)[4][22])
  • Neoplastic glial component – GFAP, OLIG2 (MAP2 -) (Ki-67 <5%[23])
  • Positive (subset) - BRAF VE1 (+ in BRAF-mutant gangliogliomas)[4]
  • Negative (universal) - IDH1 R132H, ATRX (normal retained pattern of staining)[4]
  • Negative (subset) - BRAF VE1 (- in BRAF-wildtype gangliogliomas)[4]

Links

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References

  1. ↑ Jump up to: 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 1.41 1.42 1.43 1.44 1.45 1.46 1.47 1.48 1.49 1.50 1.51 1.52 1.53 1.54 1.55 1.56 Pekmezci, Melike; et al. (2018-06-07). "The genetic landscape of ganglioglioma". Acta Neuropathologica Communications. 6: 47. doi:10.1186/s40478-018-0551-z. ISSN 2051-5960. PMC 5992851. PMID 29880043.
  2. ↑ Jump up to: 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Kim, Pora; et al. (2018-11-08). "FusionGDB: fusion gene annotation DataBase". Nucleic Acids Research. 47 (D1): D994–D1004. doi:10.1093/nar/gky1067. ISSN 0305-1048.
  3. ↑ Jump up to: 3.0 3.1 Appay, Romain; et al. (2018-10). "Duplications of KIAA1549 and BRAF screening by Droplet Digital PCR from formalin-fixed paraffin-embedded DNA is an accurate alternative for KIAA1549-BRAF fusion detection in pilocytic astrocytomas". Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc. 31 (10): 1490–1501. doi:10.1038/s41379-018-0050-6. ISSN 1530-0285. PMID 29802359. Check date values in: |date= (help)
  4. ↑ Jump up to: 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 Solomon D.A. et al. (2021). Ganglioglioma, in "World Health Organization Classification of Central Nervous System Tumours" (5th edition). pp.111-115.
  5. ↑ Jump up to: 5.0 5.1 5.2 5.3 5.4 Schreck, Karisa C.; et al. (2019-08-28). "BRAF Mutations and the Utility of RAF and MEK Inhibitors in Primary Brain Tumors". Cancers. 11 (9): E1262. doi:10.3390/cancers11091262. ISSN 2072-6694. PMC 6769482. PMID 31466300.
  6. ↑ Pagès, Mélanie; et al. (2018-01). "Co-occurrence of histone H3 K27M and BRAF V600E mutations in paediatric midline grade I ganglioglioma". Brain Pathology (Zurich, Switzerland). 28 (1): 103–111. doi:10.1111/bpa.12473. ISSN 1750-3639. PMC 8028391 Check |pmc= value (help). PMID 27984673. Check date values in: |date= (help)
  7. ↑ Jump up to: 7.0 7.1 7.2 7.3 Ryall, Scott; et al. (2020-04-13). "Integrated Molecular and Clinical Analysis of 1,000 Pediatric Low-Grade Gliomas". Cancer Cell. 37 (4): 569–583.e5. doi:10.1016/j.ccell.2020.03.011. ISSN 1878-3686. PMC 7169997 Check |pmc= value (help). PMID 32289278 Check |pmid= value (help).
  8. ↑ Jump up to: 8.0 8.1 Kowalewski, Adam; et al. (2020-08). "Clinical Relevance of BRAF V600E Mutation Status in Brain Tumors with a Focus on a Novel Management Algorithm". Targeted Oncology. 15 (4): 531–540. doi:10.1007/s11523-020-00735-9. ISSN 1776-260X. PMC 7434793 Check |pmc= value (help). PMID 32648041 Check |pmid= value (help). Check date values in: |date= (help)
  9. ↑ Rodriguez, Fausto J.; et al. (2008-03). "Gliomas in neurofibromatosis type 1: a clinicopathologic study of 100 patients". Journal of Neuropathology and Experimental Neurology. 67 (3): 240–249. doi:10.1097/NEN.0b013e318165eb75. ISSN 0022-3069. PMC 3417064. PMID 18344915. Check date values in: |date= (help)
  10. ↑ Lang, Shih-Shan; et al. (2012-07). "Surgical treatment of brain tumors in infants younger than six months of age and review of the literature". World Neurosurgery. 78 (1–2): 137–144. doi:10.1016/j.wneu.2011.09.012. ISSN 1878-8769. PMC 3292637. PMID 22120270. Check date values in: |date= (help)
  11. ↑ Jump up to: 11.0 11.1 11.2 11.3 Blumcke, Ingmar; et al. (2017-10-26). "Histopathological Findings in Brain Tissue Obtained during Epilepsy Surgery". The New England Journal of Medicine. 377 (17): 1648–1656. doi:10.1056/NEJMoa1703784. ISSN 1533-4406. PMID 29069555.
  12. ↑ Dudley, Roy W. R.; et al. (2015-03). "Pediatric low-grade ganglioglioma: epidemiology, treatments, and outcome analysis on 348 children from the surveillance, epidemiology, and end results database". Neurosurgery. 76 (3): 313–319, discussion 319, quiz 319–320. doi:10.1227/NEU.0000000000000619. ISSN 1524-4040. PMC 4333003. PMID 25603107. Check date values in: |date= (help)
  13. ↑ Jump up to: 13.0 13.1 13.2 13.3 13.4 Prayson, R. A.; et al. (1995-07). "Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors". Journal of Neuropathology and Experimental Neurology. 54 (4): 513–520. doi:10.1097/00005072-199507000-00005. ISSN 0022-3069. PMID 7541447. Check date values in: |date= (help)
  14. ↑ Blumcke, Ingmar; et al. (2017-10-26). "Histopathological Findings in Brain Tissue Obtained during Epilepsy Surgery". The New England Journal of Medicine. 377 (17): 1648–1656. doi:10.1056/NEJMoa1703784. ISSN 1533-4406. PMID 29069555.
  15. ↑ Jump up to: 15.0 15.1 15.2 Lang, F. F.; et al. (1993-12). "Central nervous system gangliogliomas. Part 2: Clinical outcome". Journal of Neurosurgery. 79 (6): 867–873. doi:10.3171/jns.1993.79.6.0867. ISSN 0022-3085. PMID 8246055. Check date values in: |date= (help)
  16. ↑ Jump up to: 16.0 16.1 16.2 Zhang, D.; et al. (2008-01). "Intracranial ganglioglioma: clinicopathological and MRI findings in 16 patients". Clinical Radiology. 63 (1): 80–91. doi:10.1016/j.crad.2007.06.010. ISSN 0009-9260. PMID 18068794. Check date values in: |date= (help)
  17. ↑ Mpairamidis, Evriviadis; et al. (2008-12). "Brainstem ganglioglioma". Journal of Child Neurology. 23 (12): 1481–1483. doi:10.1177/0883073808319316. ISSN 1708-8283. PMID 19073857. Check date values in: |date= (help)
  18. ↑ Cruz, Thainá Zanon; et al. (2021). "Ganglioglioma of the cervicothoracic spinal cord in a patient with neurofibromatosis type 1: A case report". Surgical Neurology International. 12: 313. doi:10.25259/SNI_192_2021. ISSN 2229-5097. PMC 8326088 Check |pmc= value (help). PMID 34345454 Check |pmid= value (help).
  19. ↑ Jump up to: 19.0 19.1 19.2 19.3 Wolf, H. K.; et al. (1994). "Ganglioglioma: a detailed histopathological and immunohistochemical analysis of 61 cases". Acta Neuropathologica. 88 (2): 166–173. doi:10.1007/BF00294510. ISSN 0001-6322. PMID 7985497.
  20. ↑ Blümcke, Ingmar; et al. (2011-01). "The clinicopathologic spectrum of focal cortical dysplasias: a consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission". Epilepsia. 52 (1): 158–174. doi:10.1111/j.1528-1167.2010.02777.x. ISSN 1528-1167. PMC 3058866. PMID 21219302. Check date values in: |date= (help)
  21. ↑ Blümcke, Ingmar; et al. (2002-07). "Gangliogliomas: an intriguing tumor entity associated with focal epilepsies". Journal of Neuropathology and Experimental Neurology. 61 (7): 575–584. doi:10.1093/jnen/61.7.575. ISSN 0022-3069. PMID 12125736. Check date values in: |date= (help)
  22. ↑ Blümcke, Ingmar; et al. (2002-07). "Gangliogliomas: an intriguing tumor entity associated with focal epilepsies". Journal of Neuropathology and Experimental Neurology. 61 (7): 575–584. doi:10.1093/jnen/61.7.575. ISSN 0022-3069. PMID 12125736. Check date values in: |date= (help)
  23. ↑ Prayson, R. A.; et al. (1995-07). "Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors". Journal of Neuropathology and Experimental Neurology. 54 (4): 513–520. doi:10.1097/00005072-199507000-00005. ISSN 0022-3069. PMID 7541447. Check date values in: |date= (help)


Notes[edit | edit source]

*Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the Associate Editor or other CCGA representative.  When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.

*Citation of this Page: “Ganglioglioma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 03/27/2025, https://ccga.io/index.php/CNS5:Ganglioglioma.

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