Evidence map›Paper›PMID 28060758›Full record

ArticleOncotarget2017

Exosomes as mediators of platinum resistance in ovarian cancer.

Jennifer Crow, Safinur Atay, Samagya Banskota, Brittany Artale, Sarah Schmitt, Andrew K Godwin

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

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  17. Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024
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19 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

6 authors at 3 institutions in 1 country.

Jennifer CrowDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Safinur AtayDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Samagya BanskotaDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Brittany ArtaleBioengineering Graduate Program, University of Kansas, Lawrence, KS, USA.
Sarah SchmittDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Andrew K GodwinDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
University of Kansas Medical Center · USDuke University · USUniversity of Kansas · US

Funding

Transgenic & Gene-Targeting Shared ResourceP30CA168524 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOLE L NOLLEN · 2012 to 2026
$40.1M
Exploiting Biological Networks to Improve Clinical Treatment of Ovarian CancerR01CA140323 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GODWIN, ANDREW K. · 2010 to 2014
$2.1M
NCI NIH HHS P30 CA168524NCI NIH HHS R01 CA140323
6 · The paper itself

Abstract

Exosomes have been implicated in the cell-cell transfer of oncogenic proteins and genetic material. We speculated this may be one mechanism by which an intrinsically platinum-resistant population of epithelial ovarian cancer (EOC) cells imparts its influence on surrounding tumor cells. To explore this possibility we utilized a platinum-sensitive cell line, A2780 and exosomes derived from its resistant subclones, and an unselected, platinum-resistant EOC line, OVCAR10. A2780 cells demonstrate a ~2-fold increase in viability upon treatment with carboplatin when pre-exposed to exosomes from platinum-resistant cells as compared to controls. This coincided with increased epithelial to mesenchymal transition (EMT). DNA sequencing of EOC cell lines revealed previously unreported somatic mutations in the Mothers Against Decapentaplegic Homolog 4 (SMAD4) within platinum-resistant cells. A2780 cells engineered to exogenously express these SMAD4 mutations demonstrate up-regulation of EMT markers following carboplatin treatment, are more resistant to carboplatin, and release exosomes which impart a ~1.7-fold increase in resistance in naive A2780 recipient cells as compared to controls. These studies provide the first evidence that acquired SMAD4 mutations enhance the chemo-resistance profile of EOC and present a novel mechanism in which exchange of tumor-derived exosomes perpetuates an EMT phenotype, leading to the development of subpopulations of platinum-refractory cells.

Indexed as

Antineoplastic AgentsCarboplatinCarcinoma, Ovarian EpithelialCell Line, TumorDrug Resistance, NeoplasmExosomesFemaleHumansMutationNeoplasms, Glandular and EpithelialOvarian NeoplasmsSmad4 ProteinTransfectionAntineoplastic AgentsCarboplatinSmad4 ProteinSMAD4 protein, humanEMTexosomesovarian cancerplatinum-resistanceSMAD4

Identifiers

PMID28060758
PMCPMC5355315
OpenAlexW2562144787

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.