Evidence map›Paper›PMID 31234549›Full record

ArticleInternational journal of molecular sciences2019

Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines.

Jan J Bandolik, Alexandra Hamacher, Christian Schrenk, Robin Weishaupt, Matthias U Kassack

Open access · goldAbstract readComparative Study
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

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  6. Entinostat Enhances the Efficacy of Chemotherapy in Small Cell Lung Cancer Through S-phase Arrest and Decreased Base Excision Repair.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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  18. New Acetophenones and Chromenes from the Leaves ofMolecules (Basel, Switzerland) · 2021
    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

5 authors at 1 institution in 1 country.

Jan J BandolikInstitute for Pharmaceutical and Medicinal Chemistry, University of Duesseldorf, 40225 Duesseldorf, Germany. jan.bandolik@hhu.de.ORCID 0000-0003-4282-0229
Alexandra HamacherInstitute for Pharmaceutical and Medicinal Chemistry, University of Duesseldorf, 40225 Duesseldorf, Germany. alexandra.hamacher@hhu.de.
Christian SchrenkInstitute for Pharmaceutical and Medicinal Chemistry, University of Duesseldorf, 40225 Duesseldorf, Germany. schrenc@hhu.de.
Robin WeishauptInstitute for Computer Science, Computational Complexity and Cryptology, University of Duesseldorf, 40225 Duesseldorf, Germany. robin.weishaupt@hhu.de.
Matthias U KassackInstitute for Pharmaceutical and Medicinal Chemistry, University of Duesseldorf, 40225 Duesseldorf, Germany. matthias.kassack@uni-duesseldorf.de.
Heinrich Heine University Düsseldorf · DE

Funding

Deutsche Forschungsgemeinschaft INST 208/690-1
6 · The paper itself

Abstract

High grade serous ovarian cancer (HGSOC) is the most common and aggressive ovarian cancer subtype with the worst clinical outcome due to intrinsic or acquired drug resistance. Standard treatment involves platinum compounds. Cancer development and chemoresistance is often associated with an increase in histone deacetylase (HDAC) activity. The purpose of this study was to examine the potential of HDAC inhibitors (HDACi) to increase platinum potency in HGSOC. Four HGSOC cell lines with different cisplatin sensitivity were treated with combinations of cisplatin and entinostat (class I HDACi), panobinostat (pan-HDACi), or nexturastat A (class IIb HDACi), respectively. Inhibition of class I HDACs by entinostat turned out superior in increasing cisplatin potency than pan-HDAC inhibition in cell viability assays (MTT), apoptosis induction (subG1), and caspase 3/7 activation. Entinostat was synergistic with cisplatin in all cell lines in MTT and caspase activation assays. MTT assays gave combination indices (CI values) < 0.9 indicating synergism. The effect of HDAC inhibitors could be attributed to the upregulation of pro-apoptotic genes (

Indexed as

Antineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBenzamidesCell Line, TumorCell SurvivalCisplatinCystadenocarcinoma, SerousDrug SynergismFemaleHistone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsOvarian NeoplasmsPanobinostat4-((1-butyl-3-phenylureido)methyl)-N-hydroxybenzamideAntineoplastic AgentsBenzamidesCisplatinentinostatHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsPanobinostatPhenylurea CompoundsPyridinesantitumor platinum agentscaspase activitycisplatincombination treatmententinostathigh grade serous ovarian cancer (HGSOC)histone deacetylase inhibitorsnexturastat Apanobinostat

Identifiers

PMID31234549
PMCPMC6627993
OpenAlexW2950953612

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.