Evidence map›Paper›PMID 24925363›Full record

ReviewHuman & experimental toxicology2015

In vivo radioadaptive response: a review of studies relevant to radiation-induced cancer risk.

M Nenoi, B Wang, G Vares

Abstract readReview
In one paragraph

Review in Human & experimental toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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.

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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. DNA repair in tumor radioresistance: insights from fruit flies genetics.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
  6. Article
  7. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  8. Adaptive Response in Rat Retinal Cell Cultures Irradiated with γ-rays.International journal of molecular sciences · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Ionizing Radiation and Translation Control: A Link to Radiation Hormesis?International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  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

3 authors.

M NenoiResearch Center for Radiation Protection, National Institute of Radiological Sciences, Inage-ku, Chiba, Japan m_nenoi@nirs.go.jp.
B WangResearch Center for Radiation Protection, National Institute of Radiological Sciences, Inage-ku, Chiba, Japan.
G VaresResearch Center for Radiation Protection, National Institute of Radiological Sciences, Inage-ku, Chiba, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radioadaptive response (RAR) describes phenomena where small conditioning doses of ionizing radiation (IR) reduce detrimental effects of subsequent higher IR doses. Current radiation protection regulations do not include RAR because of the large variability in expression among individuals and uncertainties of the mechanism. However, RAR should be regarded as an indispensable factor for estimation and control of individual IR sensitivity. In this article, RAR studies relevant to individual cancer risk are reviewed. Using various stains of mice, carcinogenic RAR has been demonstrated. Consistently much in vivo evidence for RAR with end points of DNA and chromosome damage is reported. Most in vivo RAR studies revealed efficient induction of RAR by chronic or repeated low-dose priming irradiation. Chronic IR-induced RAR was observed also in human individuals after environmental, occupational, and nuclear accident radiation exposure. These observations may be associated with an intrinsically distinct feature of in vivo experimental systems that mainly consist of nonproliferating mature cells. Alternatively, induction of RAR by gap junction-mediated bystander effects suggests that multicellular systems comprising densely communicating cells may be capable of responding to long-lasting low-dose-rate priming irradiation. Regulation by endocrine factors is also a plausible mechanism for RAR at an individual level. Emerging evidence suggests that glucocorticoids, known as stress hormones, participate in in vivo RAR induction following long-term low-dose-rate exposure to IR.

Indexed as

Neoplasms, Radiation-InducedRadiation ToleranceAdaptation, PhysiologicalAnimalsBystander EffectHumansRiskendocrine regulationintercellular signal transductionlow-dose-rate radiationprotective bystander effectRadioadaptive response

Identifiers

PMID24925363
PMCPMC4442823

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Registered trials

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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.