Evidence map›Paper›PMID 26451167›Full record

ArticleClinical epigenetics2015

Selective increase in subtelomeric DNA methylation: an epigenetic biomarker for malignant glioma.

Samrat Roy Choudhury, Yi Cui, Jacob R Milton, Jian Li, Joseph Irudayaraj

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Potential Epigenetic-Based Therapeutic Targets for Glioma.Frontiers in molecular neuroscience · 2018
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Let-7a suppresses glioma cell proliferation and invasion through TGF-β/Smad3 signaling pathway by targeting HMGA2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

5 authors at 2 institutions in 2 countries.

Samrat Roy ChoudhuryDepartment of Biological Engineering, Center for Cancer Research, Purdue University, West Lafayette, IN 47906 USA.
Yi CuiDepartment of Biological Engineering, Center for Cancer Research, Purdue University, West Lafayette, IN 47906 USA.
Jacob R MiltonDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47906 USA.
Jian LiDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008 China.
Joseph IrudayarajDepartment of Biological Engineering, Center for Cancer Research, Purdue University, West Lafayette, IN 47906 USA.
Purdue University West Lafayette · USCentral South University · CN

Funding

Transgenic Mouse Core Facility Shared Resource (TMCF-SR)P30CA023168 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI John Tesmer · 1985 to 2026
$43.4M
NCI NIH HHS P30 CA023168
6 · The paper itself

Abstract

backgroundSubtelomeric regions dynamically change their epigenetic pattern during development and progression of several malignancies and degenerative disorders. However, DNA methylation of human subtelomeres and their correlation to telomere length (TL) remain undetermined in glioma.

resultsHerein, we report on the selective changes in subtelomeric DNA methylation at the end of five chromosomes (Chr.) (7q, 8q. 18p, 21q, and XpYp) and ascertain their correlation with TL in patients with glioma. Subtelomeric methylation level was invariably higher in glioma patients compared to the control group, irrespective of their age and tumor grade. In particular, a significant increase in methylation was observed at the subtelomeric CpG sites of Chr. 8q, 21q, and XpYp in tissues, obtained from the brain tumor of glioma patients. In contrast, no significant change in methylation was observed at the subtelomere of Chr. 7q and 18p. Selective changes in the subtelomeric methylation level, however, did not show any significant correlation to the global TL. This observed phenomenon was validated in vitro by inducing demethylation in a glioblastoma cell line (SF-767) using 5-azacytidine (AZA) treatment. AZA treatment caused significant changes in the subtelomeric methylation pattern but did not alter the TL, which supports our hypothesis.

conclusionsDNA methylation level dramatically increased at the subtelomere of Chr.8q, 21q, and XpYp in malignant glioma, which could be used as an early epigenetic diagnostic biomarker of the disease. Alterations in subtelomeric methylation, however, have no effects on the TL.

Indexed as

Epigenetic biomarkerGliomaSubtelomeric DNA methylationTelomere length

Identifiers

PMID26451167
PMCPMC4597615
OpenAlexW1834490057

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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.