Evidence map›Paper›PMID 19126655›Full record

ArticleCarcinogenesis2009

Death receptor pathways mediate targeted and non-targeted effects of ionizing radiations in breast cancer cells.

Audrey Luce, Aurélie Courtin, Céline Levalois, Sandrine Altmeyer-Morel, Paul-Henri Romeo, Sylvie Chevillard, Jérôme Lebeau

Open access · hybridAbstract read
In one paragraph

Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 68 citations in OpenAlex.

  1. Modulation of HMGB1, PRF1, TRAIL, and M-CSF after TARGIT-IORT in breast-conserving surgery: defining a unique acute immune landscape.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  17. Association of genetic variants in apoptosis genes FAS and FASL with radiation-induced late toxicity after prostate cancer radiotherapy.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2014
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  18. Mechanisms of radiation toxicity in transformed and non-transformed cells.International journal of molecular sciences · 2013
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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

7 authors at 4 institutions in 1 country.

Audrey LuceCEA, DSV, iRCM, SREIT, Laboratoire de Cancérologie Expérimentale, Fontenay-aux-Roses, France.
Aurélie Courtin
Céline Levalois
Sandrine Altmeyer-Morel
Paul-Henri Romeo
Sylvie Chevillard
Jérôme Lebeau
CEA Paris-Saclay - Etablissement de Fontenay-aux-roses · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRDirection des énergies · FRInstitut de Radiobiologie Cellulaire et Moléculaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Delayed cell death by mitotic catastrophe is a frequent mode of solid tumor cell death after gamma-irradiation, a widely used treatment of cancer. Whereas the mechanisms that underlie the early gamma-irradiation-induced cell death are well documented, those that drive the delayed cell death are largely unknown. Here we show that the Fas, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and tumor necrosis factor (TNF)-alpha death receptor pathways mediate the delayed cell death observed after gamma-irradiation of breast cancer cells. Early after irradiation, we observe the increased expression of Fas, TRAIL-R and TNF-R that first sensitizes cells to apoptosis. Later, the increased expression of FasL, TRAIL and TNF-alpha permit the apoptosis engagement linked to mitotic catastrophe. Treatments with TNF-alpha, TRAIL or anti-Fas antibody, early after radiation exposure, induce apoptosis, whereas the neutralization of the three death receptors pathways impairs the delayed cell death. We also show for the first time that irradiated breast cancer cells excrete soluble forms of the three ligands that can induce the death of sensitive bystander cells. Overall, these results define the molecular basis of the delayed cell death of irradiated cancer cells and identify the death receptors pathways as crucial actors in apoptosis induced by targeted as well as non-targeted effects of ionizing radiation.

Indexed as

ApoptosisBreast NeoplasmsBystander EffectCell DeathCell Line, TumorFas Ligand ProteinFemaleGamma RaysHumansReceptors, Death DomainSignal TransductionTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor-alphaFas Ligand ProteinReceptors, Death DomainTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor-alpha

Identifiers

PMID19126655
PMCPMC2650794
OpenAlexW2097659667

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.