Evidence map›Paper›PMID 21602884›Full record

ArticleOncogene2011

Role of connexin43 and ATP in long-range bystander radiation damage and oncogenesis in vivo.

M Mancuso, E Pasquali, S Leonardi, S Rebessi, M Tanori, P Giardullo, F Borra, S Pazzaglia, C C Naus, V Di Majo and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Article
  3. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Integration ofCancers · 2021
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Upregulation of connexin43 contributes to PX-12-induced oxidative cell death.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Review
  17. Article
  18. Article
  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

11 authors at 3 institutions in 2 countries.

M MancusoLaboratory of Radiation Biology and Biomedicine, Agenzia Nazionale per le Nuove Tecnologie, l'Energia e lo Sviluppo Economico Sostenibile (ENEA) CR-Casaccia, Rome, Italy. mariateresa.mancuso@enea.it
E Pasquali
S Leonardi
S Rebessi
M Tanori
P Giardullo
F Borra
S Pazzaglia
C C Naus
V Di Majo
A Saran
National Agency for New Technologies, Energy and Sustainable Economic Development · ITMarconi University · ITUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation is a genotoxic agent and human carcinogen. Recent work has questioned long-held dogmas by showing that cancer-associated genetic alterations occur in cells and tissues not directly exposed to radiation, questioning the robustness of the current system of radiation risk assessment. In vitro, diverse mechanisms involving secreted soluble factors, gap junction intercellular communication (GJIC) and oxidative metabolism are proposed to mediate these indirect effects. In vivo, the mechanisms behind long-range 'bystander' responses remain largely unknown. Here, we investigate the role of GJIC in propagating radiation stress signals in vivo, and in mediating radiation-associated bystander tumorigenesis in mouse central nervous system using a mouse model in which intercellular communication is downregulated by targeted deletion of the connexin43 (Cx43) gene. We show that GJIC is critical for transmission of oncogenic radiation damage to the non-targeted cerebellum, and that a mechanism involving adenosine triphosphate release and upregulation of Cx43, the major GJIC constituent, regulates transduction of oncogenic damage to unirradiated tissues in vivo. Our data provide a novel hypothesis for transduction of distant bystander effects and suggest that the highly branched nervous system, similar to the vascular network, has an important role.

Indexed as

Adenosine TriphosphateAnimalsBystander EffectCell Transformation, NeoplasticCerebellar NeoplasmsCerebellumConnexin 43DNA DamageGap JunctionsMiceNeoplasms, Radiation-InducedRadiation DosageSequence DeletionSignal TransductionAdenosine TriphosphateConnexin 43GJA1 protein, mouse

Identifiers

PMID21602884
OpenAlexW1979427988

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.