Evidence map›Paper›PMID 20526748›Full record

ArticleCellular & molecular biology letters2010

Switching p53-dependent growth arrest to apoptosis via the inhibition of DNA damage-activated kinases.

Pavla Hublarova, Kristina Greplova, Jitka Holcakova, Borivoj Vojtesek, Roman Hrstka

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 16 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

5 authors at 1 institution in 1 country.

Pavla HublarovaDepartment of Oncological and Experimental Pathology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
Kristina Greplova
Jitka Holcakova
Borivoj Vojtesek
Roman Hrstka
Masaryk Memorial Cancer Institute · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin and doxorubicin are widely used anticancer drugs that cause DNA damage, which activates the ATM-Chk2-p53 pathway in cancer cells. This activation leads to cell cycle block or apoptosis, depending on the nature of the DNA damage. In an attempt to enhance the effects of these agents, we inhibited ATM/ATR and Chk2, which are known upstream regulators of p53. The cancer cell lines A2780 and ARN8, bearing the wild-type p53 protein, were used to study changes in p53 activation and trans-activation. Our results suggest that the G(1)-checkpoint, normally activated by DNA damage, is functionally overcome by the action of kinase inhibitors that sensitize cells to apoptosis. Both inhibitors show these effects, albeit with variable intensity in different cell lines, which is promising for other studies and theoretically for use in clinical practice.

Indexed as

ApoptosisDNA DamageAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorCheckpoint Kinase 2CisplatinDNA-Binding ProteinsDown-RegulationDoxorubicinFlow CytometryHumansProtein Kinase InhibitorsProtein Serine-Threonine KinasesResting Phase, Cell CycleAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanCell Cycle ProteinsCheckpoint Kinase 2CHEK2 protein, humanCisplatinDNA-Binding ProteinsDoxorubicinProtein Kinase InhibitorsProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20526748
PMCPMC6275699
OpenAlexW2012160211

What OpenQuestion holds

Textmetadata
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.