Evidence map›Paper›PMID 15738394›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Identification and functional significance of genes regulated by structurally different histone deacetylase inhibitors.

Melissa J Peart, Gordon K Smyth, Ryan K van Laar, David D Bowtell, Victoria M Richon, Paul A Marks, Andrew J Holloway, Ricky W Johnstone

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 1 pooled it
16.3field-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

240 citing papers in PubMed, 1 synthesis or guideline pooled it, 541 citations in OpenAlex.

  1. Pooled it
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  7. Phase II multi-institutional trial of the histone deacetylase inhibitor romidepsin as monotherapy for patients with cutaneous T-cell lymphoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009
    Trial
  8. Article
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  10. The Spermidine Synthase Gene as a Reporter of Transcription Inhibition inInternational journal of molecular sciences · 2026
    Article
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  12. Article
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  19. Article
  20. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review

180 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

8 authors at 3 institutions in 2 countries.

Melissa J PeartThe Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne 3002, Victoria, Australia.
Gordon K Smyth
Ryan K van Laar
David D Bowtell
Victoria M Richon
Paul A Marks
Andrew J Holloway
Ricky W Johnstone
Peter MacCallum Cancer Centre · AUMemorial Sloan Kettering Cancer Center · USWalter and Eliza Hall Institute of Medical Research · AU

Funding

Wellcome Trust
6 · The paper itself

Abstract

Histone deacetylase inhibitors (HDACis) inhibit tumor cell growth and survival, possibly through their ability to regulate the expression of specific proliferative and/or apoptotic genes. However, the HDACi-regulated genes necessary and/or sufficient for their biological effects remain undefined. We demonstrate that the HDACis suberoylanilide hydroxamic acid (SAHA) and depsipeptide regulate a highly overlapping gene set with at least 22% of genes showing altered expression over a 16-h culture period. SAHA and depsipeptide coordinately regulated the expression of several genes within distinct apoptosis and cell cycle pathways. Multiple genes within the Myc, type beta TGF, cyclin/cyclin-dependent kinase, TNF, Bcl-2, and caspase pathways were regulated in a manner that favored induction of apoptosis and decreased cellular proliferation. APAF-1, a gene central to the intrinsic apoptotic pathway, was induced by SAHA and depsipeptide and shown to be important, but not essential, for HDACi-induced cell death. Overexpression of p16(INK4A) and arrest of cells in G(1) can suppress HDACi-mediated apoptosis. Although p16(INK4A) did not affect the genome-wide transcription changes mediated by SAHA, a small number of apoptotic genes, including BCLXL and B-MYB, were differentially regulated in a manner consistent with attenuated HDACi-mediated apoptosis in arrested cells. We demonstrate that different HDACi alter transcription of a large and common set of genes that control diverse molecular pathways important for cell survival and proliferation. The ability of HDACi to target multiple apoptotic and cell proliferation pathways may provide a competitive advantage over other chemotherapeutic agents because suppression/loss of a single pathway may not confer resistance to these agents.

Indexed as

Histone Deacetylase InhibitorsApoptosisApoptotic Protease-Activating Factor 1Cell ProliferationCells, CulturedDepsipeptidesEnzyme InhibitorsGene Expression ProfilingGene Expression RegulationHumansHydroxamic AcidsPolymerase Chain ReactionProteinsRNA, Small InterferingVorinostatAPAF1 protein, humanApoptotic Protease-Activating Factor 1DepsipeptidesEnzyme InhibitorsHistone Deacetylase InhibitorsHydroxamic AcidsProteinsRNA, Small InterferingVorinostat

Identifiers

PMID15738394
PMCPMC552783
OpenAlexW2024425375

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.