Evidence map›Paper›PMID 24601786›Full record

ArticleOmics : a journal of integrative biology2014

An epigenetic biomarker panel for glioblastoma multiforme personalized medicine through DNA methylation analysis of human embryonic stem cell-like signature.

Jung-Hsien Chiang, Wan-Shu Cheng, Leroy Hood, Qiang Tian

Open access · greenAbstract read
In one paragraph

Article in Omics : a journal of integrative biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Evolutionary Origins of Metabolic Reprogramming in Cancer.International journal of molecular sciences · 2022
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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

4 authors at 3 institutions in 3 countries.

Jung-Hsien Chiang1 Department of Computer Science and Information Engineering, National Cheng Kung University , Tainan City, Taiwan .
Wan-Shu Cheng
Leroy Hood
Qiang Tian
National Cheng Kung University · TWInstitute for Systems Biology · USInSysBio (Russia) · RU

Funding

Quantitative Systems BiologyP50GM076547 · NIGMS · INSTITUTE FOR SYSTEMS BIOLOGY · PI BALIGA, NITIN S · 2006 to 2016
$30.6M
QUANTITATIVE IMAGE ANALYSIS SPECIALIZED RESOURCE COREU54CA119347 · NCI · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI HEATH, JAMES R. · 2005 to 2009
$17.8M
NCI NIH HHS U54 CA119347NIGMS NIH HHS P50GM076547
6 · The paper itself

Abstract

Alterations of DNA methylation occur during the course of both stem cell development and tumorigenesis. We present a novel strategy that can be used to stratify glioblastoma multiforme (GBM) patients through the epigenetic states of genes associated with human embryonic stem cell (hESC) identity in order to 1) assess linkages between the methylation signatures of these stem cell genes and survival of GBM patients, and 2) delineate putative mechanisms leading to poor prognosis in some patient subgroups. A DNA methylation signature was established for stratifying GBM patients into several hESC methylator subgroups. The hESC methylator-negative phenotype has demonstrated poor survival and upregulation of glioma stem cell (GSC) markers, and is enriched in one of the previously defined transcriptomic phenotypes-the mesenchymal phenotype. We further identified a refined signature of 36 genes as the gene panel, including SOX2, POU3F2, FGFR2, GAP43, NTRK2, NTRK3, and NKX2-2, which are highly enriched in the nervous system. Both signatures outperformed the O6-methylguanine-DNA methyltransferase (MGMT) methylation test in predicting patient's outcome. These findings were also validated through an independent dataset of patients. Furthermore, through statistical analyses, both signatures were examined significantly. Hypomethylation of hESC-associated genes predicted poorer clinical outcome in GBM, supporting the idea that epigenetic activation of stem cell genes contributes to GBM aggression. The gene panel presented herein may be developed into clinical assays for patient stratification and future personalized medicine interventions.

Indexed as

Area Under CurveBiomarkers, TumorBrain NeoplasmsDNA MethylationEmbryonic Stem CellsEpigenesis, GeneticGene Expression Regulation, NeoplasticGenetic MarkersGlioblastomaHomeobox Protein Nkx-2.2Homeodomain ProteinsHumansKaplan-Meier EstimateNeoplastic Stem CellsNuclear ProteinsPrecision MedicineBiomarkers, TumorGenetic MarkersHomeobox Protein Nkx-2.2Homeodomain ProteinsNKX2-2 protein, humanNuclear ProteinsTranscription Factors

Identifiers

PMID24601786
PMCPMC4012637
OpenAlexW1502259022

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.