Evidence map›Paper›PMID 21389785›Full record

ArticleCell cycle (Georgetown, Tex.)2011

A minimally invasive assay for individual assessment of the ATM/CHEK2/p53 pathway activity.

Sylwia Kabacik, Ana Ortega-Molina, Alejo Efeyan, Paul Finnon, Simon Bouffler, Manuel Serrano, Christophe Badie

Registry-linked trialOpen access · bronzeAbstract readComparative Study
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. 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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 19% 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.

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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. A woman with a pleural mesothelioma and an inheritedAnnals of translational medicine · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Sylwia KabacikBiological Effects Department, Centre for Radiation Chemical and Environmental Hazards, Health Protection Agency, Didcot, Oxfordshire, UK.
Ana Ortega-Molina
Alejo Efeyan
Paul Finnon
Simon Bouffler
Manuel Serrano
Christophe Badie
Centro de Investigación del Cáncer · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation induces DNA Double-Strand Breaks (DSBs) which activate the ATM/CHEK2/p53 pathway leading to cell cycle arrest and apoptosis through transcription of genes including CDKN1A (p21) and BBC3 (PUMA). This pathway prevents genomic instability and tumorigenesis as demonstrated in heritable syndromes [e.g. Ataxia Telangiectasia (AT); Li-Fraumeni syndrome (LFS)]. Here, a simple assay based on gene expression in peripheral blood to measure accurately ATM/CHEK2/p53 pathway activity is described. The expression of p21, Puma and Sesn2 was determined in blood from mice with different gene copy numbers of Atm, Trp53 (p53), Chek2 or Arf and in human blood and mitogen stimulated T-lymphocyte (MSTL) cultures from AT, AT carriers, LFS patients, and controls, both before and after ex vivo ionizing irradiation. Mouse Atm/Chek2/p53 activity was highly dependent on the copy number of each gene except Arf. In human MSTL, an AT case, AT carriers and LFS patients showed responses distinct from healthy donors. The relationship between gene copy number and transcriptional induction upon radiation was linear for p21 and Puma and correlated well with cancer incidence in p53 variant mice. This reliable blood test provides an assay to determine ATM/CHEK2/p53 pathway activity and demonstrates the feasibility of assessing the activity of this essential cancer protection pathway in simple assays. These findings may have implications for the individualized prediction of cancer susceptibility.

Indexed as

AnimalsApoptosis Regulatory ProteinsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p21Disease SusceptibilityDNA-Binding ProteinsGene DosageGene Expression ProfilingGene Expression RegulationHumansLi-Fraumeni SyndromeMiceNeoplasmsApoptosis Regulatory ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseBBC3 protein, humanCell Cycle ProteinsCheckpoint Kinase 2CHEK2 protein, humanChek2 protein, mouseCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsNuclear ProteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsSESN2 protein, humanSestrinsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID21389785
PMCPMC3100888
OpenAlexW2075285740

What OpenQuestion holds

Textmetadata
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.