Evidence map›Paper›PMID 26022161›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

Loss of 5-hydroxymethylcytosine and intratumoral heterogeneity as an epigenomic hallmark of glioblastoma.

Theo F J Kraus, Gesa Kolck, Andrea Greiner, Katharina Schierl, Virginie Guibourt, Hans A Kretzschmar

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

  1. Loss ofJournal of Cancer · 2026
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  2. Ultra-Fast IntraoperativeInternational journal of molecular sciences · 2025
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  3. Review
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  5. Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Profiling of methylation and demethylation pathways during brain development and ageing.Journal of neural transmission (Vienna, Austria : 1996) · 2016
    Article
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Theo F J KrausCenter for Neuropathology and Prion Research (ZNP), Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, Munich, D-81377, Germany. theo.kraus@med.uni-muenchen.de.
Gesa KolckCenter for Neuropathology and Prion Research (ZNP), Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, Munich, D-81377, Germany.
Andrea GreinerCenter for Neuropathology and Prion Research (ZNP), Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, Munich, D-81377, Germany.
Katharina SchierlCenter for Neuropathology and Prion Research (ZNP), Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, Munich, D-81377, Germany.
Virginie GuibourtCenter for Neuropathology and Prion Research (ZNP), Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, Munich, D-81377, Germany.
Hans A KretzschmarCenter for Neuropathology and Prion Research (ZNP), Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, Munich, D-81377, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most malignant neoplasm with predominant astrocytic differentiation and the most frequent primary brain tumor of the adult. Here, we investigated 170 human GBM specimens deriving from 162 patients, as well as 66 healthy control tissue specimens deriving from 27 patients, and analyzed the amount of 5-hydroxymethylcytosine (5hmC) in GBMs compared to normal brain and tumor infiltration zones. Additionally, we correlated the amount of 5hmC with two different proliferation markers, Ki67 and H3S10p. Genetic characterization of GBMs enabled us to analyze the effect of isocitrate dehydrogenase 1 (IDH1) mutations, O6-methylguanin-DNA-methyltransferase (MGMT) promoter methylation, and loss of heterozygosity of chromosome 1p and 19q (LOH1p/19q) on 5hmC amount. We found that GBMs show a tremendous loss of 5hmC, and we observed that even the infiltration zones show reduced amounts of 5hmC. Interestingly, the amount of 5hmC was inversely proportional to the two investigated proliferation markers, Ki67 and H3S10p. Correlation of 5hmC amount and molecular genetic markers of GBMs showed that there are no correlations of 5hmC amount and IDH1 mutations, MGMT promoter methylation, and LOH1p/19q. Furthermore, we evaluated the intratumoral distribution of 5hmC in compact and infiltrating areas and found that the quantification of the 5hmC amount is a useful tool in evaluation of tumor infiltration. In summary, our data emphasize that GBMs show a disturbed hydroxymethylome that is disrupted by IDH1 independent pathways, and that loss of 5hmC shows astonishing intratumoral heterogeneity.

Indexed as

5-MethylcytosineAdultAgedAged, 80 and overCytosineDNA MethylationDNA Modification MethylasesDNA Repair EnzymesEpigenesis, GeneticFemaleGlioblastomaHistonesHumansIsocitrate DehydrogenaseKi-67 AntigenLoss of Heterozygosity5-hydroxymethylcytosine5-MethylcytosineCytosineDNA Modification MethylasesDNA Repair EnzymesHistonesIDH1 protein, humanIsocitrate DehydrogenaseKi-67 AntigenMGMT protein, humanTumor Suppressor Proteins5hmC5-hydroxymethylomeBrain tumorEpigeneticGBMGlioblastoma

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.