Evidence map›Paper›PMID 23103179›Full record

ReviewMolecular oncology2012

Trials with 'epigenetic' drugs: an update.

Angela Nebbioso, Vincenzo Carafa, Rosaria Benedetti, Lucia Altucci

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
9.9field-weighted citation impact, top 1% 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

99 citing papers in PubMed, 239 citations in OpenAlex.

  1. Article
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  6. Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024
    Review
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  17. Metabolic disorder in Alzheimer's disease.Metabolic brain disease · 2021
    Review
  18. Review
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  20. Review

39 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Angela NebbiosoDipartimento di Patologia Generale, Seconda Università degli Studi di Napoli, Vico L. de Crecchio 7, Napoli 80138, Italy.
Vincenzo Carafa
Rosaria Benedetti
Lucia Altucci
University of Naples Federico II · ITInstitute of Genetics and Biophysics · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic inactivation of pivotal genes involved in correct cell growth is a hallmark of human pathologies, in particular cancer. These epigenetic mechanisms, including crosstalk between DNA methylation, histone modifications and non-coding RNAs, affect gene expression and are associated with disease progression. In contrast to genetic mutations, epigenetic changes are potentially reversible. Re-expression of genes epigenetically inactivated can result in the suppression of disease state or sensitization to specific therapies. Small molecules that reverse epigenetic inactivation, so-called epi-drugs, are now undergoing clinical trials. Accordingly, the Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for cancer treatment have approved some of these drugs. Here, we focus on the biological features of epigenetic molecules, analyzing the mechanism(s) of action and their current use in clinical practice.

Indexed as

AnimalsAntineoplastic AgentsChromatinClinical Trials as TopicDNA Modification MethylasesEpigenesis, GeneticGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistonesHumansNeoplasmsRNA, UntranslatedSirtuinsAntineoplastic AgentsChromatinDNA Modification MethylasesHistone Deacetylase InhibitorsHistonesRNA, UntranslatedSirtuins

Identifiers

PMID23103179
PMCPMC5528349
OpenAlexW1975705914

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.