Evidence map›Paper›PMID 27898692›Full record

ArticlePloS one2016

Targeting CDKs with Roscovitine Increases Sensitivity to DNA Damaging Drugs of Human Osteosarcoma Cells.

Serena Vella, Elisa Tavanti, Claudia Maria Hattinger, Marilù Fanelli, Rogier Versteeg, Jan Koster, Piero Picci, Massimo Serra

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 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  11. Cisplatin Resistance in Osteosarcoma:Frontiers in oncology · 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

8 authors at 2 institutions in 2 countries.

Serena VellaLaboratory of Experimental Oncology, Orthopaedic Rizzoli Institute, Italy.
Elisa TavantiLaboratory of Experimental Oncology, Orthopaedic Rizzoli Institute, Italy.
Claudia Maria HattingerLaboratory of Experimental Oncology, Orthopaedic Rizzoli Institute, Italy.
Marilù FanelliLaboratory of Experimental Oncology, Orthopaedic Rizzoli Institute, Italy.
Rogier VersteegDepartment of Human Genetics, Academic Medical Center, University of Amsterdam, The Netherlands.
Jan KosterDepartment of Oncogenomics, Academic Medical Center, University of Amsterdam, The Netherlands.
Piero PicciLaboratory of Experimental Oncology, Orthopaedic Rizzoli Institute, Italy.
Massimo SerraLaboratory of Experimental Oncology, Orthopaedic Rizzoli Institute, Italy.ORCID http://orcid.org/0000-0003-0742-1177
Istituto Ortopedico Rizzoli · ITAmsterdam UMC Location University of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinase 2 (CDK2) has been reported to be essential for cell proliferation in several human tumours and it has been suggested as an appropriate target to be considered in order to enhance the efficacy of treatment regimens based on the use of DNA damaging drugs. We evaluated the clinical impact of CDK2 overexpression on a series of 21 high-grade osteosarcoma (OS) samples profiled by using cDNA microarrays. We also assessed the in vitro efficacy of the CDKs inhibitor roscovitine in a panel of drug-sensitive and drug-resistant human OS cell lines. OS tumour samples showed an inherent overexpression of CDK2, and high expression levels at diagnosis of this kinase appeared to negatively impact on clinical outcome. CDK2 expression also proved to be relevant for in vitro OS cells growth. These findings indicated CDK2 as a promising candidate therapeutic marker for OS and therefore we assessed the efficacy of the CDKs-inhibitor roscovitine in both drug-sensitive and -resistant OS cell lines. All cell lines resulted to be responsive to roscovitine, which was also able to increase the activity of cisplatin and doxorubicin, the two most active DNA damaging drugs used in OS chemotherapy. Our results indicated that combined treatment with conventional OS chemotherapeutic drugs and roscovitine may represent a new candidate intervention approach, which may be considered to enhance tumour cell sensitivity to DNA damaging drugs.

Indexed as

DNA DamageMolecular Targeted TherapyAntineoplastic AgentsApoptosisCell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase 2DoxorubicinDrug SynergismGene Expression Regulation, NeoplasticGene SilencingHumansOsteosarcomaPurinesRoscovitineAntineoplastic AgentsCyclin-Dependent Kinase 2DoxorubicinPurinesRoscovitine

Identifiers

PMID27898692
PMCPMC5127503
OpenAlexW2557559453

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.