Evidence map›Paper›PMID 23880963›Full record

ArticleEpigenetics2013

Analysis of the genomic response of human prostate cancer cells to histone deacetylase inhibitors.

Madeleine S Q Kortenhorst, Michel D Wissing, Ronald Rodríguez, Sushant K Kachhap, Judith J M Jans, Petra Van der Groep, Henk M W Verheul, Anuj Gupta, Paul O Aiyetan, Elsken van der Wall and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  15. Histone Deacetylase Inhibitors as Anticancer Drugs.International journal of molecular sciences · 2017
    Review
  16. Expression of HIV-1 matrix protein p17 and association with B-cell lymphoma in HIV-1 transgenic mice.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

13 authors at 5 institutions in 4 countries.

Madeleine S Q KortenhorstDepartment of Gynecology; Catharina Hospital Eindhoven; Eindhoven, The Netherlands; Prostate Cancer Program; Sidney Kimmel Comprehensive Cancer Center; Johns Hopkins University School of Medicine; Baltimore, MD USA; These authors contributed equally to this work.
Michel D Wissing
Ronald Rodríguez
Sushant K Kachhap
Judith J M Jans
Petra Van der Groep
Henk M W Verheul
Anuj Gupta
Paul O Aiyetan
Elsken van der Wall
Michael A Carducci
Paul J Van Diest
Luigi Marchionni
Johns Hopkins University · USJohns Hopkins Medicine · USUniversity Medical Center Utrecht · NLAmsterdam UMC Location VUmc · NLUniversity of Baltimore · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
NCI NIH HHS 5P30CA006973NCI NIH HHS P50 CA058236NCI NIH HHS P50CA058236
6 · The paper itself

Abstract

Histone deacetylases (HDACs) have emerged as important targets for cancer treatment. HDAC-inhibitors (HDACis) are well tolerated in patients and have been approved for the treatment of patients with cutaneous T-cell lymphoma (CTCL). To improve the clinical benefit of HDACis in solid tumors, combination strategies with HDACis could be employed. In this study, we applied Analysis of Functional Annotation (AFA) to provide a comprehensive list of genes and pathways affected upon HDACi-treatment in prostate cancer cells. This approach provides an unbiased and objective approach to high throughput data mining. By performing AFA on gene expression data from prostate cancer cell lines DU-145 (an HDACi-sensitive cell line) and PC3 (a relatively HDACi-resistant cell line) treated with HDACis valproic acid or vorinostat, we identified biological processes that are affected by HDACis and are therefore potential treatment targets for combination therapy. Our analysis revealed that HDAC-inhibition resulted among others in upregulation of major histocompatibility complex (MHC) genes and deregulation of the mitotic spindle checkpoint by downregulation of genes involved in mitosis. These findings were confirmed by AFA on publicly available data sets from HDACi-treated prostate cancer cells. In total, we analyzed 375 microarrays with HDACi treated and non-treated (control) prostate cancer cells. All results from this extensive analysis are provided as an online research source (available at the journal's website and at http://luigimarchionni.org/HDACIs.html). By publishing this data, we aim to enhance our understanding of the cellular changes after HDAC-inhibition, and to identify novel potential combination strategies with HDACis for the treatment of prostate cancer patients.

Indexed as

Cell Line, TumorGene Expression ProfilingGene Expression Regulation, NeoplasticGenome, HumanHistone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsMajor Histocompatibility ComplexMaleMicroarray AnalysisM Phase Cell Cycle CheckpointsProstatic NeoplasmsSignal TransductionValproic AcidVorinostatHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsValproic AcidVorinostatanalysis of functional annotationgene expression analysisHDACismajor histocompatibility complexmitotic spindle checkpointprostate cancervalproic acidvorinostat

Identifiers

PMID23880963
PMCPMC3883768
OpenAlexW2040867535

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.