Evidence map›Paper›PMID 26944314›Full record

ReviewCancer letters2016

Radiogenomics: A systems biology approach to understanding genetic risk factors for radiotherapy toxicity?

Carsten Herskind, Christopher J Talbot, Sarah L Kerns, Marlon R Veldwijk, Barry S Rosenstein, Catharine M L West

Abstract readReview
In one paragraph

Review in Cancer letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
–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

41 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  4. Review
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  7. Article
  8. Review
  9. A radiogenomics study onBMC cancer · 2025
    Article
  10. Article
  11. Article
  12. Predicting the germline dependence of hematuria risk in prostate cancer radiotherapy patients.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
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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

6 authors.

Carsten HerskindDepartment of Radiation Oncology, Universitätsmedizin Mannheim, Medical Faculty Mannheim, Heidelberg University, Germany. Electronic address: carsten.herskind@medma.uni-heidelberg.de.
Christopher J TalbotDepartment of Genetics, University of Leicester, Leicester, UK.
Sarah L KernsDepartment of Radiation Oncology, Mount Sinai School of Medicine, New York, USA; Department of Radiation Oncology, University of Rochester Medical Center, Rochester, USA.
Marlon R VeldwijkDepartment of Radiation Oncology, Universitätsmedizin Mannheim, Medical Faculty Mannheim, Heidelberg University, Germany.
Barry S RosensteinDepartment of Radiation Oncology, Mount Sinai School of Medicine, New York, USA; Department of Radiation Oncology, New York University School of Medicine, USA; Department of Dermatology, Mount Sinai School of Medicine, New York, USA.
Catharine M L WestInstitute of Cancer Sciences, University of Manchester, Christie Hospital, Manchester, UK.

Funding

Risk Prediction for Development of Adverse Effects FOllowing Radiotherapy for Prostate CancerK07CA187546 · NCI · UNIVERSITY OF ROCHESTER · PI KERNS, SARAH L. · 2015 to 2019
$649k
Cancer Research UK 18504NCI NIH HHS K07 CA187546
6 · The paper itself

Abstract

Adverse reactions in normal tissue after radiotherapy (RT) limit the dose that can be given to tumour cells. Since 80% of individual variation in clinical response is estimated to be caused by patient-related factors, identifying these factors might allow prediction of patients with increased risk of developing severe reactions. While inactivation of cell renewal is considered a major cause of toxicity in early-reacting normal tissues, complex interactions involving multiple cell types, cytokines, and hypoxia seem important for late reactions. Here, we review 'omics' approaches such as screening of genetic polymorphisms or gene expression analysis, and assess the potential of epigenetic factors, posttranslational modification, signal transduction, and metabolism. Furthermore, functional assays have suggested possible associations with clinical risk of adverse reaction. Pathway analysis incorporating different 'omics' approaches may be more efficient in identifying critical pathways than pathway analysis based on single 'omics' data sets. Integrating these pathways with functional assays may be powerful in identifying multiple subgroups of RT patients characterised by different mechanisms. Thus 'omics' and functional approaches may synergise if they are integrated into radiogenomics 'systems biology' to facilitate the goal of individualised radiotherapy.

Indexed as

Polymorphism, Single NucleotideRadiation DosageSystems IntegrationGene Expression ProfilingGenetic MarkersGenetic Predisposition to DiseaseGenome-Wide Association StudyGenomicsHumansPhenotypeProteomicsRadiation ExposureRadiation InjuriesRadiotherapyRisk AssessmentRisk FactorsGenetic MarkersGene expression microarraysGenome-wide association studiesNormal-tissue reactionPredictive testsRadiotherapySingle-nucleotide polymorphisms

Identifiers

PMID26944314
PMCPMC5016239

What OpenQuestion holds

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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.