Evidence map›Paper›PMID 19560734›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2009

Molecular epigenetics and genetics in neuro-oncology.

Raman P Nagarajan, Joseph F Costello

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  13. Differential expression and clinical significance of glioblastoma mRNA expression profiles in Uyghur and Han patients in Xinjiang province.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  14. Article
  15. Article
  16. Epigenetics and ncRNAs in brain function and disease: mechanisms and prospects for therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013
    Review
  17. Review
  18. Article
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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

2 authors at 1 institution in 1 country.

Raman P NagarajanBrain Tumor Research Center, Department of Neurosurgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94143, USA.
Joseph F Costello
University of California, San Francisco · US

Funding

Complex role of DNA hypomethylation in glioblastoma multiformeF32CA141799 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NAGARAJAN, RAMAN P · 2009 to 2010
$81k
NCI NIH HHS F32 CA141799
6 · The paper itself

Abstract

Gliomas arise through genetic and epigenetic alterations of normal brain cells, although the exact cell of origin for each glioma subtype is unknown. The alteration-induced changes in gene expression and protein function allow uncontrolled cell division, tumor expansion, and infiltration into surrounding normal brain parenchyma. The genetic and epigenetic alterations are tumor subtype and tumor-grade specific. Particular alterations predict tumor aggressiveness, tumor response to therapy, and patient survival. Genetic alterations include deletion, gain, amplification, mutation, and translocation, which result in oncogene activation and tumor suppressor gene inactivation, or in some instances the alterations may simply be a consequence of tumorigenesis. Epigenetic alterations in brain tumors include CpG island hypermethylation associated with tumor suppressor gene silencing, gene-specific hypomethylation associated with aberrant gene activation, and genome-wide hypomethylation potentially leading to loss of imprinting, chromosomal instability, and cellular hyperproliferation. Other epigenetic alterations, such as changes in the position of histone variants and changes in histone modifications are also likely to be important in the molecular pathology of brain tumors. Given that histone deacetylases are targets for drugs that are already in clinical trial, surprisingly little is known about histone acetylation in primary brain tumors. Although a majority of epigenetic alterations are independent of genetic alterations, there is interaction on specific genes, signaling pathways and within chromosomal domains. Next-generation sequencing technology is now the method of choice for genomic and epigenome profiling, allowing more comprehensive understanding of genetic and epigenetic contributions to tumorigenesis in the brain.

Indexed as

Epigenesis, GeneticAnimalsBiomarkersBrainBrain NeoplasmsChromosome MappingDNADNA MethylationDNA Modification MethylasesDNA Repair EnzymesGene Expression Regulation, NeoplasticGliomaHistonesHumansNeoplasm StagingTrinucleotide RepeatsBiomarkersDNADNA Modification MethylasesDNA Repair EnzymesHistonesMGMT protein, humanTumor Suppressor Proteins

Identifiers

PMID19560734
PMCPMC3981537
OpenAlexW2004062257

What OpenQuestion holds

Textmetadata
LicenceTDM
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.