Evidence map›Paper›PMID 26986722›Full record

ArticlePloS one2016

Cisplatin Resistant Spheroids Model Clinically Relevant Survival Mechanisms in Ovarian Tumors.

Winyoo Chowanadisai, Shanta M Messerli, Daniel H Miller, Jamie E Medina, Joshua W Hamilton, Mark A Messerli, Alexander S Brodsky

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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  20. Upregulation of FAM3B Promotes Cisplatin Resistance in Gastric Cancer by Inducing Epithelial-Mesenchymal Transition.Medical science monitor : international medical journal of experimental and clinical research · 2020
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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 4 institutions in 1 country.

Winyoo ChowanadisaiDepartment of Nutritional Sciences, Oklahoma State University, Stillwater, Oklahoma, United States of America, 74078.
Shanta M MesserliMarine Biological Laboratory, Woods Hole, Massachusetts, United States of America, 02543.
Daniel H MillerDepartment of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, 02139.
Jamie E MedinaMarine Biological Laboratory, Woods Hole, Massachusetts, United States of America, 02543.
Joshua W HamiltonMarine Biological Laboratory, Woods Hole, Massachusetts, United States of America, 02543.
Mark A MesserliMarine Biological Laboratory, Woods Hole, Massachusetts, United States of America, 02543.
Alexander S BrodskyDepartment of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, 02139.
Marine Biological Laboratory · USBrown University · USMassachusetts Institute of Technology · USSouth Dakota State University · US

Funding

VOLTAMMETRIC DETECTION OF METAL IONSP41RR001395 · NCRR · MARINE BIOLOGICAL LABORATORY · PI SMITH, PETER JS · 1985 to 2010
$12.7M
NCRR NIH HHS P41 RR001395NCRR NIH HHS P41 RR001395-27S1
6 · The paper itself

Abstract

The majority of ovarian tumors eventually recur in a drug resistant form. Using cisplatin sensitive and resistant cell lines assembled into 3D spheroids we profiled gene expression and identified candidate mechanisms and biological pathways associated with cisplatin resistance. OVCAR-8 human ovarian carcinoma cells were exposed to sub-lethal concentrations of cisplatin to create a matched cisplatin-resistant cell line, OVCAR-8R. Genome-wide gene expression profiling of sensitive and resistant ovarian cancer spheroids identified 3,331 significantly differentially expressed probesets coding for 3,139 distinct protein-coding genes (Fc >2, FDR < 0.05) (S2 Table). Despite significant expression changes in some transporters including MDR1, cisplatin resistance was not associated with differences in intracellular cisplatin concentration. Cisplatin resistant cells were significantly enriched for a mesenchymal gene expression signature. OVCAR-8R resistance derived gene sets were significantly more biased to patients with shorter survival. From the most differentially expressed genes, we derived a 17-gene expression signature that identifies ovarian cancer patients with shorter overall survival in three independent datasets. We propose that the use of cisplatin resistant cell lines in 3D spheroid models is a viable approach to gain insight into resistance mechanisms relevant to ovarian tumors in patients. Our data support the emerging concept that ovarian cancers can acquire drug resistance through an epithelial-to-mesenchymal transition.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsCell Line, TumorCell SurvivalCisplatinFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansNeoplasm Recurrence, LocalOvarian NeoplasmsOvarySpheroids, CellularTumor Cells, CulturedAntineoplastic AgentsCisplatin

Identifiers

PMID26986722
PMCPMC4795743
OpenAlexW2318533023

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.