Evidence map›Paper›PMID 19377507›Full record

ReviewNature reviews. Cancer2009

Radiation-induced bystander signalling in cancer therapy.

Kevin M Prise, Joe M O'Sullivan

Registry-linked trialAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02780375 (Feasibility Study Testing Multi-panel Coding and Non-coding Transcriptional Responses as an Indicator of Individualised Responses to Radiation Effects in Radiation Therapy Patients), which is not on this map. Cited by 350 papers.

0numbers the graph read from it
0cells of the map it votes in
350citing papers in PubMed
–field-weighted citation impact
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.

NCT02780375 completednot on this mapstarted 2016, after this paper: background citation

Feasibility Study Testing Multi-panel Coding and Non-coding Transcriptional Responses as an Indicator of Individualised Responses to Radiation Effects in Radiation Therapy Patients

TypeobservationalSponsorInstitute of Cancer Research, United KingdomRan2016 to 2018Enrolled20ConditionsCancerArmsBlood donation during radiotherapy
3 · Its place in the literature

Who cites it

350 citing papers in PubMed.

  1. Review
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  18. Review
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290 more citing papers are in PubMed but not listed here.

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.

Kevin M PriseCentre for Cancer Research & Cell Biology, Queen's University Belfast, Belfast, UK. k.prise@qub.ac.uk
Joe M O'Sullivan

Funding

PHOTOACTIVE AGENTSP01CA095227 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI HELD, KATHRYN DALE · 2004 to 2007
$5.0M
Cancer Research UK A7047Cancer Research UK C1513/A7047NCI NIH HHS 5 P01 CA095227-02NCI NIH HHS P01 CA095227
6 · The paper itself

Abstract

Our understanding of how radiation kills normal and tumour cells has been based on an intimate knowledge of the direct induction of DNA damage and its cellular consequences. What has become clear is that, as well as responses to direct DNA damage, cell-cell signalling -- known as the bystander effect -- mediated through gap junctions and inflammatory responses may have an important role in the response of cells and tissues to radiation exposure and also chemotherapy agents. This Review outlines the key aspects of radiation-induced intercellular signalling and assesses its relevance for existing and future radiation-based therapies.

Indexed as

AnimalsBystander EffectCell CommunicationDNA DamageGap JunctionsHumansNeoplasmsRadiotherapy, Intensity-ModulatedSignal Transduction

Identifiers

PMID19377507
PMCPMC2855954

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.