Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas
Open accessAbstract
To identify somatic mutations in pediatric diffuse intrinsic pontine glioma (DIPG), we performed whole-genome sequencing of DNA from seven DIPGs and matched germline tissue and targeted sequencing of an additional 43 DIPGs and 36 non-brainstem pediatric glioblastomas (non-BS-PGs). We found that 78% of DIPGs and 22% of non-BS-PGs contained a mutation in H3F3A, encoding histone H3.3, or in the related HIST1H3B, encoding histone H3.1, that caused a p.Lys27Met amino acid substitution in each protein. An additional 14% of non-BS-PGs had somatic mutations in H3F3A causing a p.Gly34Arg alteration.
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Single allele mutations of histone H3.3 lysine27-to-methionine (H3.3K27M) occur in a subtype of aggressive pediatric brain cancers.
“Histone H3 lysine27-to-methionine (H3K27M) gain-of-function mutations occur in highly aggressive pediatric gliomas.”
From Histone H3 lysine-to-methionine mutants as a paradigm to study chromatin signaling (2014) · cites this paper as [4]
The Abstract reports monoallelic p.K27M substitutions in histone H3 genes, including H3F3A (H3.3), in pediatric high-grade gliomas. It says these substitutions suggest a gain-of-function effect, but that further studies are required to determine their functional impact; the citing sentence states gain of function as established. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe K27M mutation has been observed to occur in genes encoding all forms of histone H3 (H3.1, H3.2, and H3.3) in human glioma.
“Indeed, the K27M mutation has been observed to occur in genes encoding all forms of histone H3 (H3.1, H3.2, and H3.3) in human glioma (1,10,24).”
From <i>S</i> -adenosyl methionine is necessary for inhibition of the methyltransferase G9a by the lysine 9 to methionine mutation on histone H3 (2016) · cites this paper as [24]
The Abstract reports K27M mutations in genes encoding H3.1 and H3.3 in paediatric gliomas. It does not support the H3.2 part: the paper says it found no K27 mutations in the other 14 histone H3 genes it tested. No page number is provided in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredDespite reports supporting a higher affinity of PRC2 for H3K27M as compared with wild-type H3, H3K27M was often inversely correlated with PRC2 occupancy, challenging the idea that H3K27M sequesters PRC2 on chromatin.
“Despite reports supporting a higher affinity of PRC2 for H3K27M as compared with wild-type H3 108-110 , H3K27M was often inversely correlated with PRC2 occupancy, challenging the idea that H3K27M sequesters PRC2 on chromatin 111,112 .”
From The roles of DNA, RNA and histone methylation in ageing and cancer (2019) · cites this paper as [108]
A heterozygous histone H3 point mutation causing a lysine-to-methionine substitution at position 27 (H3K27M) is present in more than 80% of diffuse intrinsic pontine gliomas.
“A heterozygous point mutation of histone H3 occurs in more than 80% of these tumors, and results in a lysine-to-methionine substitution (H3K27M)2,3.”
From Therapeutic targeting of polycomb and BET bromodomain proteins in diffuse intrinsic pontine gliomas (2017) · cites this paper as [3]
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- Authors
- St. Jude Children's Research Hospital–Washington University Pediatric Cancer Genome Project
- Venue
- Nature Genetics
- Published
- 2012-01-29
- Volume
- 44
- Issue
- 3
- Pages
- 251-253
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3288377
- OpenAlex
- W2062062519
- Cited by
- 1,724
- References
- 14
- Citations by year
- 2026: 68 · 2025: 84 · 2024: 113 · 2023: 155 · 2022: 123 · 2021: 160 · 2020: 171 · 2019: 126 · 2018: 109 · 2017: 133 · 2016: 113 · 2015: 101 · 2014: 115 · 2013: 97 · 2012: 54
- FWCI
- 56.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- St. Jude Children's Research Hospital
- Cure Starts Now Foundation
- American Lebanese Syrian Associated Charities
- National Institutes of Health (CA096832)
- National Cancer Institute (R01CA129541, CA 096832, R01CA135554, P01CA096832)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- diffuse intrinsic pontine glioma, pediatric glioblastoma, somatic mutations, histone H3.3, H3F3A, histone H3.1, H3K27M mutation, brainstem glioma, pediatric brain tumors
- MeSH terms
- Base Sequence, Glioblastoma, Histones, Humans, Molecular Sequence Data, Pons, Genome, Human, Sequence Analysis, DNA, Mutation, Missense, Brain Stem Neoplasms
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