Evidence map›Paper›PMID 21949898›Full record

ArticleOxidative medicine and cellular longevity2011

Generation of reactive oxygen species during apoptosis induced by DNA-damaging agents and/or histone deacetylase inhibitors.

Barbora Brodská, Aleš Holoubek

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2011. 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
2.9field-weighted citation impact, top 10% 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, 70 citations in OpenAlex.

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  13. p53-Mediated PI3K/AKT/mTOR Pathway Played a Role in PtoxOxidative medicine and cellular longevity · 2019
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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

2 authors at 1 institution in 1 country.

Barbora BrodskáInstitute of Hematology and Blood Transfusion, U Nemocnice 1, 12820 Prague 2, Czech Republic. brodska@uhkt.cz
Aleš Holoubek
Institute of Haematology and Blood Transfusion · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species play an important role in the process of apoptosis in many cell types. In this paper, we analyzed the role of ROS in DNA-damaging agents (actinomycin D or decitabine), which induced apoptosis of leukemia cell line CML-T1 and normal peripheral blood lymphocytes (PBL). The possibility of synergism with histone deacetylase inhibitors butyrate or SAHA is also reported. We found that in cancer cell line, ROS production significantly contributed to apoptosis triggering, while in normal lymphocytes treated by cytostatic or cytotoxic drugs, necrosis as well as apoptosis occurred and large heterogeneity of ROS production was measured. Combined treatment with histone deacetylase inhibitor did not potentiate actinomycin D action, whereas combination of decitabine and SAHA brought synergistic ROS generation and apoptotic features in CML cell line. Appropriate decrease of cell viability indicated promising therapeutic potential of this combination in CML, but side effects on normal PBL should be taken into attention.

Indexed as

Antineoplastic AgentsApoptosisAzacitidineButyratesCaspase 3Cell Line, TumorCytostatic AgentsDactinomycinDecitabineDNA DamageDrug SynergismHistone Deacetylase InhibitorsHumansHydroxamic AcidsPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesAntineoplastic AgentsAzacitidineButyratesCaspase 3Cytostatic AgentsDactinomycinDecitabineHistone Deacetylase InhibitorsHydroxamic AcidsPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesVorinostat

Identifiers

PMID21949898
PMCPMC3178180
OpenAlexW2062499931

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.