Diffuse hemispheric glioma, H3 G34-mutant

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

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(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)*

Xiaolin Hu, PhD, Sema4 OpCo Inc.

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 Paediatric-type diffuse high-grade gliomas
Subtype(s) Diffuse hemispheric glioma, H3 G34-mutant

WHO Essential and Desirable Genetic Diagnostic Criteria

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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


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.


Add content below into table above -      

Oncogenic amplifications in G34-DHG have been shown to be negative prognostic markers, as documented below [1].

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
PDGFRA Amp chr4:54,229,293-54,298,245 [hg38] 4q12 Unk Yes Unk 27% cases of G34-DHG; overrepresented in cases with GBM-like morph [2]
CCND2 Amp 12:4,273,762-4,305,353 12p13.32 Unk Yes Unk 10% cases of G34-DHG; overrepresented in cases with embryonal-like morph [2]
CDK6 Amp 7:92,604,921-92,836,573 7q21.2 Unk Yes Unk 10% cases of G34-DHG; overrepresented in cases with GBM-like morph [2]
CDKN2A Homoz del 9:21,967,752-21,995,324 9p21.3 Unk Unk Unk 14% case of G34-DHG [2]

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

Add content below into table above -      

Chromosomal Pattern Diagnostic Significance (Yes, No or Unknown) Prognostic Significance (Yes, No or Unknown) Therapeutic Significance (Yes, No or Unknown) Notes
4q loss Yes N/A N/A Found in 70% of cases of G34-DHG [2]
3q loss Yes No No Found in 67% of cases of G34-DHG[2]
13q loss Yes No No Found in 57% of cases of G34-DHG [2]
7q gain Yes No No Found in 48% of cases of G34-DHG [2]
1q gain Yes No No Found in 44% of cases of G34-DHG [2]

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.


Add content below into table above -      

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
H3-3A p.G35R/V chromosome modification p.G35R 94%

p.G35V 6% [3]

TP53 mutations 90%;

ATRX mutations 95%

MGMT promoter methylation 70%-74% [4][1]

PDGFRA mutations 50-70%[5] [6]

IDH1

IDH2

H3 p.K28M/I [7]

TERT promoter

Yes
MGMT promoter methylation 70%-74% of G34-DHG [4][1] Yes (longer overall survival)

Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.

Epigenomic Alterations

Put your text here

Genes and Main Pathways Involved

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Gene; Genetic Alteration Pathway Pathophysiologic Outcome
EXAMPLE: BRAF and MAP2K1; Activating mutations EXAMPLE: MAPK signaling EXAMPLE: Increased cell growth and proliferation
EXAMPLE: CDKN2A; Inactivating mutations EXAMPLE: Cell cycle regulation EXAMPLE: Unregulated cell division
EXAMPLE: KMT2C and ARID1A; Inactivating mutations EXAMPLE: Histone modification, chromatin remodeling EXAMPLE: Abnormal gene expression program

Epigenomic Alterations

  • H3.3 G34R/V/D mutations impair di- or tri- methylation of lysine 36 by blocking the access to its lysine methyltransferase SETD2 and lysine demethylase KDM2A [8][9]. This attenuated interaction alters genome wide methylation level and promote tumorigenesis.
  • G34-DHG demonstrates global hypomethylation pattern but MGMT promoter is frequently methylated [10][11][12]
  • MGMT promoter methylation is seen between 70 and 74% of cases (ref 4, 5) and is associated with significantly longer overall survival [4][1].

Genes and Main Pathways Involved

Gene; Genetic Alteration Pathway Pathophysiologic Outcome
H3-3A; p.G35/R/V Histone modification, chromatin remodeling Altered methylation and gene expression
MGMT; promoter methylation DNA repair Sensitize tumor cells to chemo- or radiotherapy.
TP53; mutation Genome guardian, apoptosis Apoptosis resistance
ATRX; mutation Chromatin remodeling, alternative telomeres lengthening repression Facilitate alternative lengthening of telomeres

Genetic Diagnostic Testing Methods

  • Targeted sequencing to identify c.103G>A p.G35R (G34R), c.103G>C p.G35R (G34R), or c.104G>T p.G35V (G34V) is diagnostic for G34-DHG.
  • Pan-cancer sequencing will likely detect concurrent mutations in TP53, ATRX, PDGFRA etc.
  • DNA methylation and gene expression profiling can be used to differentiate G34-DHG with other glioma subgroups.
  • MGMT promoter methylation can be assessed by methylation specific polymerase chain reaction analysis (bisulfite treated DNA undergoes real-time PCR)

Familial Forms

N/A

Additional Information

This disease is defined/characterized as detailed below:

  • Diffuse hemispheric glioma, H3 G34–mutant (G34-DHG) is a newly recognized tumor entity that is characterized by point mutations in the H3-3A (H3-3A) gene, encoding for histone variant H3.3 [13][14]. Point mutations tend to be clustered at codon 34 including c.103G>A p.G35R (G34R), c.103G>C p.G35R (G34R), or rarely c.104G>T p.G35V (G34V) [13]. This distinct tumor entity is an aggressive glioma arising from the cerebral hemispheres. G34-DHG is designated as CNS WHO grade 4 in in the WHO 5th edition [3].
  • Please note that historically, numbering of the amino acid sequences of histone genes has begun at the second codon, as the amino acid encoded by the first codon (methionine) is cleaved post-translationally. Therefore, H3.3 G34 represents the legacy nomenclature of what is now referred to as H3.3 G35 [15].

The epidemiology/prevalence of this disease is detailed below:

  • G34-DHG is reported to account for approximately 15% of high grade gliomas (HGSs) and typically affect adolescents and young adults with a median age at diagnosis of 15.8 years old [16][4]. Studies have shown that there is a gender difference with male to female ratio of 1.4:1 [1][17].

The clinical features of this disease are detailed below:

  • Site dependent neurological symptoms including epileptic seizure, focal deficit, increased intracranial hypertension (headache, nausea and vomiting) [18].
  • Signs and symptoms - epileptic seizure, focal deficit, increased intracranial hypertension

The sites of involvement of this disease are detailed below:

  • sually involves cerebral hemispheres
  • Occasionally across the midline and disseminate to leptomeningeal structures.
  • MRI typically shows a bulky cortical mass, most commonly seen in the parietal or temporal lobe. Multifocal lesions and/or leptomeningeal dissemination can be seen along with necrosis, cysts, hemorrhage and calcification [19].

The morphologic features of this disease are detailed below:

  • Usually involves cerebral hemispheres
  • Occasionally across the midline and disseminate to leptomeningeal structures.
  • MRI typically shows a bulky cortical mass, most commonly seen in the parietal or temporal lobe. Multifocal lesions and/or leptomeningeal dissemination can be seen along with necrosis, cysts, hemorrhage and calcification [19]

The immunophenotype of this disease is detailed below:

Positive (universal) - MAP2, FOXG1, p53

Positive (subset) - GFAP (GBM-like morphology), synaptophysin (embryonal-like morphology)

Negative (universal) - ATRX, Olig2

Links

None

References

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Notes

*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.

Prior Author(s): *Citation of this Page: “Diffuse hemispheric glioma, H3 G34-mutant”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 03/27/2025, https://ccga.io/index.php/CNS5:Diffuse hemispheric glioma, H3 G34-mutant.

  1. ↑ Jump up to: 1.0 1.1 1.2 1.3 1.4 Korshunov, Andrey; et al. (2016-01). "Histologically distinct neuroepithelial tumors with histone 3 G34 mutation are molecularly similar and comprise a single nosologic entity". Acta Neuropathologica. 131 (1): 137–146. doi:10.1007/s00401-015-1493-1. ISSN 1432-0533. PMID 26482474. Check date values in: |date= (help)
  2. ↑ Jump up to: 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Korshunov, Andrey; et al. (2016-01). "Histologically distinct neuroepithelial tumors with histone 3 G34 mutation are molecularly similar and comprise a single nosologic entity". Acta Neuropathologica. 131 (1): 137–146. doi:10.1007/s00401-015-1493-1. ISSN 1432-0533. PMID 26482474. Check date values in: |date= (help)
  3. ↑ Jump up to: 3.0 3.1 Ellison, DW, Korshunov A, Northcott PA, Taylor MD, Kaur K, Clifford SC. Medulloblastoma, WNT-activated. In: WHO Classification of Tumours Editorial Board. Central nervous system tumours. Lyon (France): International Agency for Research on Cancer; 2021. (WHO classification of tumours series, 5th ed.; vol. 6). https://publications.iarc.fr/601.
  4. ↑ Jump up to: 4.0 4.1 4.2 4.3 Crowell, Cameron; et al. (2022-01). "Systematic review of diffuse hemispheric glioma, H3 G34-mutant: Outcomes and associated clinical factors". Neuro-Oncology Advances. 4 (1): vdac133. doi:10.1093/noajnl/vdac133. ISSN 2632-2498. PMC 9466272 Check |pmc= value (help). PMID 36105387 Check |pmid= value (help). Check date values in: |date= (help)
  5. ↑ Chen, Carol C. L.; et al. (2020-12-10). "Histone H3.3G34-Mutant Interneuron Progenitors Co-opt PDGFRA for Gliomagenesis". Cell. 183 (6): 1617–1633.e22. doi:10.1016/j.cell.2020.11.012. ISSN 1097-4172. PMC 7791404 Check |pmc= value (help). PMID 33259802 Check |pmid= value (help).
  6. ↑ Lucas, Calixto-Hope G.; et al. (2021-11-02). "Diffuse hemispheric glioma, H3 G34-mutant: Genomic landscape of a new tumor entity and prospects for targeted therapy". Neuro-Oncology. 23 (11): 1974–1976. doi:10.1093/neuonc/noab184. ISSN 1523-5866. PMC 8628364 Check |pmc= value (help). PMID 34519829 Check |pmid= value (help).
  7. ↑ Sturm, Dominik; et al. (2012-10-16). "Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma". Cancer Cell. 22 (4): 425–437. doi:10.1016/j.ccr.2012.08.024. ISSN 1878-3686. PMID 23079654.
  8. ↑ Shi, Leilei; et al. (2018-05-25). "Histone H3.3 G34 Mutations Alter Histone H3K36 and H3K27 Methylation In Cis". Journal of Molecular Biology. 430 (11): 1562–1565. doi:10.1016/j.jmb.2018.04.014. ISSN 1089-8638. PMC 6450091. PMID 29689253.
  9. ↑ Cheng, Zhongjun; et al. (2014-08-15). "A molecular threading mechanism underlies Jumonji lysine demethylase KDM2A regulation of methylated H3K36". Genes & Development. 28 (16): 1758–1771. doi:10.1101/gad.246561.114. ISSN 1549-5477. PMC 4197961. PMID 25128496.
  10. ↑ Sturm, Dominik; et al. (2012-10-16). "Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma". Cancer Cell. 22 (4): 425–437. doi:10.1016/j.ccr.2012.08.024. ISSN 1878-3686. PMID 23079654.
  11. ↑ Mackay, Alan; et al. (2017-10-09). "Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma". Cancer Cell. 32 (4): 520–537.e5. doi:10.1016/j.ccell.2017.08.017. ISSN 1878-3686. PMC 5637314. PMID 28966033.
  12. ↑ Wan, Yi Ching Esther; et al. (2018). "Histone H3 Mutations in Cancer". Current Pharmacology Reports. 4 (4): 292–300. doi:10.1007/s40495-018-0141-6. ISSN 2198-641X. PMC 6061380. PMID 30101054.
  13. ↑ Jump up to: 13.0 13.1 Schwartzentruber, Jeremy; et al. (2012-01-29). "Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma". Nature. 482 (7384): 226–231. doi:10.1038/nature10833. ISSN 1476-4687. PMID 22286061.
  14. ↑ Wu, Gang; et al. (2012-01-29). "Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas". Nature Genetics. 44 (3): 251–253. doi:10.1038/ng.1102. ISSN 1546-1718. PMC 3288377. PMID 22286216.
  15. ↑ Leske, Henning; et al. (2021-06). "A common classification framework for histone sequence alterations in tumours: an expert consensus proposal". The Journal of Pathology. 254 (2): 109–120. doi:10.1002/path.5666. ISSN 1096-9896. PMID 33779999 Check |pmid= value (help). Check date values in: |date= (help)
  16. ↑ Picart, Thiébaud; et al. (2021-01). "Characteristics of diffuse hemispheric gliomas, H3 G34-mutant in adults". Neuro-Oncology Advances. 3 (1): vdab061. doi:10.1093/noajnl/vdab061. ISSN 2632-2498. PMC 8156974 Check |pmc= value (help). PMID 34056608 Check |pmid= value (help). Check date values in: |date= (help)
  17. ↑ Mackay, Alan; et al. (2017-10-09). "Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma". Cancer Cell. 32 (4): 520–537.e5. doi:10.1016/j.ccell.2017.08.017. ISSN 1878-3686. PMC 5637314. PMID 28966033.
  18. ↑ Picart, Thiébaud; et al. (2021). "Characteristics of diffuse hemispheric gliomas, H3 G34-mutant in adults". Neuro-Oncology Advances. 3 (1): vdab061. doi:10.1093/noajnl/vdab061. ISSN 2632-2498. PMC 8156974 Check |pmc= value (help). PMID 34056608 Check |pmid= value (help).
  19. ↑ Jump up to: 19.0 19.1 Vettermann, Franziska J.; et al. (2018-12). "Characterization of Diffuse Gliomas With Histone H3-G34 Mutation by MRI and Dynamic 18F-FET PET". Clinical Nuclear Medicine. 43 (12): 895–898. doi:10.1097/RLU.0000000000002300. ISSN 1536-0229. PMID 30358620. Check date values in: |date= (help)
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