Evidence map›Paper›PMID 28671573›Full record

ReviewInternational journal of molecular sciences2017

Histone Deacetylase Inhibitors as Anticancer Drugs.

Tomas Eckschlager, Johana Plch, Marie Stiborova, Jan Hrabeta

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 636 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
636citing papers in PubMed, 1 pooled it
47.8field-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

636 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,159 citations in OpenAlex.

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  18. International journal of molecular sciences · 2026
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576 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 1 institution in 1 country.

Tomas EckschlagerDepartment of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84/1, Prague 5 CZ-150 06, Czech Republic. tomas.eckschlager@lfmtol.cuni.cz.
Johana PlchDepartment of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84/1, Prague 5 CZ-150 06, Czech Republic. plchova.johana@gmail.com.
Marie StiborovaDepartment of Biochemistry, Faculty of Science, Charles University, Albertov 2030/8, Prague 2 CZ-128 43, Czech Republic. stiborov@natur.cuni.cz.
Jan HrabetaDepartment of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University and University Hospital Motol, V Uvalu 84/1, Prague 5 CZ-150 06, Czech Republic. janhrabeta@gmail.com.
Charles University · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carcinogenesis cannot be explained only by genetic alterations, but also involves epigenetic processes. Modification of histones by acetylation plays a key role in epigenetic regulation of gene expression and is controlled by the balance between histone deacetylases (HDAC) and histone acetyltransferases (HAT). HDAC inhibitors induce cancer cell cycle arrest, differentiation and cell death, reduce angiogenesis and modulate immune response. Mechanisms of anticancer effects of HDAC inhibitors are not uniform; they may be different and depend on the cancer type, HDAC inhibitors, doses, etc. HDAC inhibitors seem to be promising anti-cancer drugs particularly in the combination with other anti-cancer drugs and/or radiotherapy. HDAC inhibitors vorinostat, romidepsin and belinostat have been approved for some T-cell lymphoma and panobinostat for multiple myeloma. Other HDAC inhibitors are in clinical trials for the treatment of hematological and solid malignancies. The results of such studies are promising but further larger studies are needed. Because of the reversibility of epigenetic changes during cancer development, the potency of epigenetic therapies seems to be of great importance. Here, we summarize the data on different classes of HDAC inhibitors, mechanisms of their actions and discuss novel results of preclinical and clinical studies, including the combination with other therapeutic modalities.

Indexed as

AcetylationAngiogenesis InhibitorsAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisAutophagyCell Cycle CheckpointsClinical Trials as TopicDrug Evaluation, PreclinicalEpigenesis, GeneticGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansImmunomodulationSignal TransductionAngiogenesis InhibitorsAntineoplastic AgentsHistone Deacetylase Inhibitorsanti-angiogenic effectapoptosisautophagycancercell cycle arrestdrug combinationshistone deacetylase inhibitorshistone deacetylases

Identifiers

PMID28671573
PMCPMC5535906
OpenAlexW2724336500

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.