Evidence map›Paper›PMID 28073598›Full record

ArticleGynecologic oncology2017

HDAC10 as a potential therapeutic target in ovarian cancer.

Muhtadi M Islam, Tapahsama Banerjee, Colin Z Packard, Shweta Kotian, Karuppaiyah Selvendiran, David E Cohn, Jeffrey D Parvin

Open access · greenAbstract read
In one paragraph

Article in Gynecologic oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
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

29 citing papers in PubMed, 59 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Muhtadi M IslamDepartment of Biomedical Informatics, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States.
Tapahsama BanerjeeDepartment of Biomedical Informatics, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States.
Colin Z PackardDepartment of Biomedical Informatics, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States.
Shweta KotianDepartment of Biomedical Informatics, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States.
Karuppaiyah SelvendiranDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States.
David E CohnDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States.
Jeffrey D ParvinDepartment of Biomedical Informatics, The Ohio State University Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, United States. Electronic address: Jeffrey.Parvin@osumc.edu.
The Ohio State University · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Informatics methods for identifying breast cancer control genes and proteinsR01CA141090 · NCI · OHIO STATE UNIVERSITY · PI CATALYUREK, UMIT V., HUANG, KUN · 2009 to 2013
$2.2M
NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA141090
6 · The paper itself

Abstract

objectiveWe analyzed histone deacetylase 10 (HDAC10) for function in the context of the DNA damage response in BRCA1-null ovarian cancer cells as well as evaluated the potential of general HDAC inhibitors in primary ovarian carcinoma cells. HDAC10 had previously been shown to be highly stimulatory to the process of homology directed repair in HeLa cells, and in this study we investigated whether HDAC10 could impact in vitro the response to anticancer therapies. We hypothesized that the loss of HDAC10 would sensitize cells to platinum therapy.

methodsWe combined informatics analysis of large DNA sequencing datasets from ovarian cancer tumors with tissue culture based assays of primary and established cell lines to test for sensitivity to platinum therapy if HDAC10 activity was inhibited or depleted.

resultsUsing The Cancer Genome Atlas (TCGA) dataset, we found that deep deletions in HDAC10 occurred in 5-10% of ovarian cancer tumors. From the TCGA data we found that low HDAC10 mRNA levels correlated with platinum sensitivity of the tumors. Cell proliferation and DNA damage assays in a BRCA1-null ovarian carcinoma cell line demonstrated reduced DNA repair capacity and sensitization of platinum therapy. Similarly, primary ovarian carcinoma cells demonstrated a sensitization to platinum therapies when treated with HDAC inhibitors.

conclusionsFrom the results of this study, we suggest that the inhibition of HDAC10 may potentiate the effects of platinum therapies in ovarian tumors.

Indexed as

Cell Line, TumorCisplatinFemaleHeLa CellsHistone Deacetylase InhibitorsHistone DeacetylasesHumansMolecular Targeted TherapyOvarian NeoplasmsRecombinational DNA RepairRNA, MessengerCisplatinHDAC10 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesRNA, MessengerCisplatinDNA repairHDAC10Ovarian cancer

Identifiers

PMID28073598
PMCPMC6020686
OpenAlexW2568385018

What OpenQuestion holds

Textmetadata
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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.