Evidence map›Paper›PMID 25304378›Full record

ArticleCancer letters2015

BRCA1, FANCD2 and Chk1 are potential molecular targets for the modulation of a radiation-induced DNA damage response in bystander cells.

Susanne Burdak-Rothkamm, Kai Rothkamm, Keeva McClelland, Shahnaz T Al Rashid, Kevin M Prise

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. Review
  6. Review
  7. Anti-tumor activities ofJournal of ginseng research · 2021
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  9. Article
  10. NFrontiers in oncology · 2019
    Article
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  13. Article
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  16. Microvesicles Contribute to the Bystander Effect of DNA Damage.International journal of molecular sciences · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Susanne Burdak-RothkammCentre for Cancer Research and Cell Biology, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK. Electronic address: s.burdakrothkamm@yahoo.co.uk.
Kai RothkammPublic Health England, Centre for Radiation, Chemical and Environmental Hazards, Chilton/Didcot OX11 0RQ, UK.
Keeva McClellandCentre for Cancer Research and Cell Biology, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK.
Shahnaz T Al RashidCentre for Cancer Research and Cell Biology, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK.
Kevin M PriseCentre for Cancer Research and Cell Biology, Queen's University Belfast, 97 Lisburn Road, Belfast BT9 7BL, UK.
Queen's University Belfast · GBPublic Health England · GB

Funding

Breast Cancer Now 2009MAYPR03ACancer Research UK C1513/A7047
6 · The paper itself

Abstract

Radiotherapy is an important treatment option for many human cancers. Current research is investigating the use of molecular targeted drugs in order to improve responses to radiotherapy in various cancers. The cellular response to irradiation is driven by both direct DNA damage in the targeted cell and intercellular signalling leading to a broad range of bystander effects. This study aims to elucidate radiation-induced DNA damage response signalling in bystander cells and to identify potential molecular targets to modulate the radiation induced bystander response in a therapeutic setting. Stalled replication forks in T98G bystander cells were visualised via bromodeoxyuridine (BrdU) nuclear foci detection at sites of single stranded DNA. γH2AX co-localised with these BrdU foci. BRCA1 and FANCD2 foci formed in T98G bystander cells. Using ATR mutant F02-98 hTERT and ATM deficient GM05849 fibroblasts it could be shown that ATR but not ATM was required for the recruitment of FANCD2 to sites of replication associated DNA damage in bystander cells whereas BRCA1 bystander foci were ATM-dependent. Phospho-Chk1 foci formation was observed in T98G bystander cells. Clonogenic survival assays showed moderate radiosensitisation of directly irradiated cells by the Chk1 inhibitor UCN-01 but increased radioresistance of bystander cells. This study identifies BRCA1, FANCD2 and Chk1 as potential targets for the modulation of radiation response in bystander cells. It adds to our understanding of the key molecular events propagating out-of-field effects of radiation and provides a rationale for the development of novel molecular targeted drugs for radiotherapy optimisation.

Indexed as

Ataxia Telangiectasia Mutated ProteinsBlotting, WesternBrain NeoplasmsBRCA1 ProteinBystander EffectCell ProliferationCheckpoint Kinase 1DNA DamageDNA RepairDNA ReplicationFanconi Anemia Complementation Group D2 ProteinFlow CytometryGliomaHumansImmunoenzyme TechniquesMutationAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanBRCA1 ProteinBRCA1 protein, humanCheckpoint Kinase 1CHEK1 protein, humanFANCD2 protein, humanFanconi Anemia Complementation Group D2 ProteinProtein KinasesBRCADNA damage responseFanconi anaemiaIonising radiationRadiation-induced bystander effect

Identifiers

PMID25304378
PMCPMC4259524
OpenAlexW2065422258

What OpenQuestion holds

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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.