Evidence map›Paper›PMID 11704832›Full record

ArticleOncogene2001

Inflammatory-type responses after exposure to ionizing radiation in vivo: a mechanism for radiation-induced bystander effects?

S A Lorimore, P J Coates, G E Scobie, G Milne, E G Wright

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 1 pooled it
15.2field-weighted citation impact, top 1% 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

129 citing papers in PubMed, 1 synthesis or guideline pooled it, 376 citations in OpenAlex.

  1. Pooled it
  2. The burden of cardiovascular disease in prostate cancer: prevalence, pathophysiology, and implications for integrated care.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Macrophages in Lung Repair and Fibrosis.Results and problems in cell differentiation · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

69 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

5 authors at 2 institutions in 1 country.

S A LorimoreDepartment of Molecular and Cellular Pathology, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, UK.
P J Coates
G E Scobie
G Milne
E G Wright
Ninewells Hospital · GBUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Haemopoietic tissues exposed to ionizing radiation are shown to exhibit increased macrophage activation, defined by ultrastructural characteristics and increased lysosomal and nitric oxide synthase enzyme activities. Macrophage activation post-irradiation was also associated with enhanced respiratory burst activities and an unexpected neutrophil infiltration. Examination of p53-null mice demonstrated that macrophage activation and neutrophil infiltration were not direct effects of irradiation, but were a consequence of the recognition and clearance of radiation-induced apoptotic cells. Increased phagocytic cell activity was maintained after apoptotic bodies had been removed. These findings demonstrate that, contrary to expectation, recognition and clearance of apoptotic cells after exposure to radiation produces both a persistent macrophage activation and an inflammatory-type response. We also demonstrate a complexity of macrophage activation following radiation that is genotype dependent, indicating that the in vivo macrophage responses to radiation damage are genetically modified processes. These short-term responses of macrophages to radiation-induced apoptosis and their genetic modification are likely to be important determinants of the longer-term consequences of radiation exposure. Furthermore, in addition to any effects attributable to immediate radiation-induced damage, our findings provide a mechanism for the production of damage via a 'bystander' effect which may contribute to radiation-induced genomic instability and leukaemogenesis.

Indexed as

AnimalsApoptosisbeta-GalactosidaseBone MarrowBystander EffectChemotaxis, LeukocyteDose-Response Relationship, RadiationEnzyme InductionGamma RaysGenes, p53Genetic Predisposition to DiseaseGenotypeInflammationLysosomesMacrophage ActivationMice3-nitrotyrosinebeta-GalactosidaseNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouseTumor Suppressor Protein p53Tyrosine

Identifiers

PMID11704832
OpenAlexW2068755461

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.