Evidence map›Paper›PMID 24382114›Full record

ReviewAntioxidants & redox signaling2015

Targeting Histone Deacetylases in Diseases: Where Are We?

Rosaria Benedetti, Mariarosaria Conte, Lucia Altucci

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. Article
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  12. Article
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  14. Article
  15. Article
  16. Article
  17. The role of histone deacetylase 3 in breast cancer.Medical oncology (Northwood, London, England) · 2022
    Review
  18. Article
  19. Review
  20. Cereblon: promise and challenges for combating human diseases.Pflugers Archiv : European journal of physiology · 2021
    Review

1 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

3 authors at 1 institution in 1 country.

Rosaria Benedetti1 Department of Biochemistry, Biophysics, and General Pathology, Seconda Università degli Studi di Napoli , Napoli, Italy .
Mariarosaria Conte1 Department of Biochemistry, Biophysics, and General Pathology, Seconda Università degli Studi di Napoli , Napoli, Italy .
Lucia Altucci1 Department of Biochemistry, Biophysics, and General Pathology, Seconda Università degli Studi di Napoli , Napoli, Italy .
Institute of Genetics and Biophysics · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

significanceEpigenetic inactivation of pivotal genes involved in cell growth is a hallmark of human pathologies, in particular cancer. Histone acetylation balance obtained through opposing actions of histone deacetylases (HDACs) and histone acetyltransferases is one epigenetic mechanism controlling gene expression and is, thus, associated with disease etiology and progression. Interfering pharmacologically with HDAC activity can correct abnormalities in cell proliferation, migration, vascularization, and death. RECENT ADVANCES: Histone deacetylase inhibitors (HDACi) represent a new class of cytostatic agents that interfere with the function of HDACs and are able to increase gene expression by indirectly inducing histone acetylation. Several HDACi, alone or in combination with DNA-demethylating agents, chemopreventive, or classical chemotherapeutic drugs, are currently being used in clinical trials for solid and hematological malignancies, and are, thus, promising candidates for cancer therapy. CRITICAL ISSUES: (i) Non-specific (off-target) HDACi effects due to activities unassociated with HDAC inhibition. (ii) Advantages/disadvantages of non-selective or isoform-directed HDACi. (iii) Limited number of response-predictive biomarkers. (iv) Toxicity leading to dysfunction of critical biological processes. FUTURE DIRECTIONS: Selective HDACi could achieve enhanced clinical utility by reducing or eliminating the serious side effects associated with current first-generation non-selective HDACi. Isoform-selective and pan-HDACi candidates might benefit from the identification of biomarkers, enabling better patient stratification and prediction of response to treatment.

Indexed as

Histone Deacetylase InhibitorsHistone DeacetylasesHumansNeoplasmsHistone Deacetylase InhibitorsHistone Deacetylases

Identifiers

PMID24382114
PMCPMC4492558
OpenAlexW2092000241

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.