Evidence map›Paper›PMID 28769043›Full record

ArticleScientific reports2017

Common biological phenotypes characterize the acquisition of platinum-resistance in epithelial ovarian cancer cells.

Maura Sonego, Ilenia Pellizzari, Alessandra Dall'Acqua, Eliana Pivetta, Ilaria Lorenzon, Sara Benevol, Riccardo Bomben, Paola Spessotto, Roberto Sorio, Valter Gattei and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

31 citing papers in PubMed, 43 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

13 authors at 2 institutions in 2 countries.

Maura SonegoDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Ilenia PellizzariDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Alessandra Dall'AcquaDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Eliana PivettaDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Ilaria LorenzonDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Sara BenevolDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Riccardo BombenExperimental OncoHematology, National Cancer Institute, 33081, Aviano, Italy.
Paola SpessottoDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Roberto SorioMedical Oncology C CRO Aviano, IRCCS, National Cancer Institute, 33081, Aviano, Italy.
Valter GatteiExperimental OncoHematology, National Cancer Institute, 33081, Aviano, Italy.
Barbara BellettiDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.ORCID 0000-0003-2249-0285
Monica SchiappacassiDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy.
Gustavo BaldassarreDivision of Molecular Oncology, National Cancer Institute, 33081, Aviano, Italy. gbaldassarre@cro.it.ORCID 0000-0002-9750-8825
National Cancer Institute · UACentro di Riferimento Oncologico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Standard of care for Epithelial Ovarian Cancer (EOC) patients relies on platinum-based therapy. However, acquired resistance to platinum occurs frequently and predicts poor prognosis. To understand the mechanisms underlying acquired platinum-resistance, we have generated and characterized three platinum-resistant isogenic EOC cell lines. Resistant cells showed 3-to 5- folds increase in platinum IC50. Cross-resistance to other chemotherapeutic agents commonly used in the treatment of EOC patients was variable and dependent on the cell line utilized. Gene expression profiling (GEP) of coding and non-coding RNAs failed to identify a common signature that could collectively explain the mechanism of resistance. However, we observed that all resistant cell lines displayed a decreased level of DNA platination and a faster repair of damaged DNA. Furthermore, all platinum resistant cell lines displayed a change in their morphology and a higher ability to grown on mesothelium. Overall, we have established and characterized three new models of platinum-resistant EOC cell lines that could be exploited to further dissect the molecular mechanisms underlying acquired resistance to platinum. Our work also suggests that GEP studies alone, at least when performed under basal culture condition, do not represent the optimal way to identify molecular alterations linked to DNA repair pathway defects.

Indexed as

PhenotypeAntineoplastic AgentsCarcinoma, Ovarian EpithelialCell AdhesionCell CycleCell Line, TumorCell SurvivalCisplatinDrug Resistance, NeoplasmFemaleGene Expression ProfilingHumansPlatinumSignal TransductionTumor Cells, CulturedAntineoplastic AgentsCisplatinPlatinum

Identifiers

PMID28769043
PMCPMC5540908
OpenAlexW2739732018

What OpenQuestion holds

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LicenceCC BY
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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.