Evidence map›Paper›PMID 24512308›Full record

ReviewAntioxidants & redox signaling2015

Mechanisms of Histone Deacetylase Inhibitor-Regulated Gene Expression in Cancer Cells.

Anderly C Chueh, Janson W T Tse, Lars Tögel, John M Mariadason

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 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 93 citations in OpenAlex.

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  16. Epigenetic mechanisms differentially regulate blood pressure and renal dysfunction in male and female Npr1 haplotype mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    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

4 authors at 1 institution in 1 country.

Anderly C ChuehLudwig Institute for Cancer Research , Olivia Newton John Cancer and Wellness Centre, Austin Health, Melbourne, Australia .
Janson W T TseLudwig Institute for Cancer Research , Olivia Newton John Cancer and Wellness Centre, Austin Health, Melbourne, Australia .
Lars TögelLudwig Institute for Cancer Research , Olivia Newton John Cancer and Wellness Centre, Austin Health, Melbourne, Australia .
John M MariadasonLudwig Institute for Cancer Research , Olivia Newton John Cancer and Wellness Centre, Austin Health, Melbourne, Australia .
Olivia Newton-John Cancer Wellness & Research Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

significanceClass I and II histone deacetylase inhibitors (HDACis) are approved for the treatment of cutaneous T-cell lymphoma and are undergoing clinical trials as single agents, and in combination, for other hematological and solid tumors. Understanding their mechanisms of action is essential for their more effective clinical use, and broadening their clinical potential. RECENT ADVANCES: HDACi induce extensive transcriptional changes in tumor cells by activating and repressing similar numbers of genes. These transcriptional changes mediate, at least in part, HDACi-mediated growth inhibition, apoptosis, and differentiation. Here, we highlight two fundamental mechanisms by which HDACi regulate gene expression—histone and transcription factor acetylation. We also review the transcriptional responses invoked by HDACi, and compare these effects within and across tumor types. CRITICAL ISSUES: The mechanistic basis for how HDACi activate, and in particular repress gene expression, is not well understood. In addition, whether subsets of genes are reproducibly regulated by these agents both within and across tumor types has not been systematically addressed. A detailed understanding of the transcriptional changes elicited by HDACi in various tumor types, and the mechanistic basis for these effects, may provide insights into the specificity of these drugs for transformed cells and specific tumor types. FUTURE DIRECTIONS: Understanding the mechanisms by which HDACi regulate gene expression and an appreciation of their transcriptional targets could facilitate the ongoing clinical development of these emerging therapeutics. In particular, this knowledge could inform the design of rational drug combinations involving HDACi, and facilitate the identification of mechanism-based biomarkers of response.

Indexed as

AcetylationAnimalsCell DifferentiationCell Line, TumorGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansHistone Deacetylase Inhibitors

Identifiers

PMID24512308
PMCPMC4492771
OpenAlexW1617320644

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.