Evidence map›Paper›PMID 35354948›Full record

ArticleBritish journal of cancer2022

Anti-cancer therapy is associated with long-term epigenomic changes in childhood cancer survivors.

Natassia Robinson, John Casement, Marc J Gunter, Inge Huybrechts, Antonio Agudo, Miguel Rodríguez Barranco, Fabian Eichelmann, Theron Johnson, Rudolf Kaaks, Valeria Pala and 11 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Repair of DNA double-strand breaks after low radiation doses in childhood cancer survivors and matched cancer-free individuals.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

21 authors at 14 institutions in 6 countries.

Natassia RobinsonNewcastle University Centre for Cancer, Biosciences Institute, Newcastle University, Newcastle upon Tyne, UK.
John CasementBioinformatic Support Unit, Newcastle University, Newcastle upon Tyne, UK.
Marc J GunterSection of Nutrition and Metabolism, IARC, Lyon, France.
Inge HuybrechtsSection of Nutrition and Metabolism, IARC, Lyon, France.ORCID http://orcid.org/0000-0003-3838-855X
Antonio AgudoUnit of Nutrition and Cancer, Catalan Institute of Oncology - ICO, Nutrition and Cancer Group, Bellvitge Biomedical Research Institute - IDIBELL, L'Hospitalet de Llobregat, Barcelona, 08908, Spain.
Miguel Rodríguez BarrancoAndalusian School of Public Health, ibs.GRANADA, CIBERESP, Granada, Spain.ORCID http://orcid.org/0000-0002-9972-9779
Fabian EichelmannGerman Institute of Human Nutrition Potsdam-Rehbrücke, Heidelberg, Germany.
Theron JohnsonGerman Cancer Research Center (DKFZ), Heidelberg, Germany.
Rudolf KaaksGerman Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0003-3751-3929
Valeria PalaFondazione IRCCS Istituto Nazionale dei Tumori di Milano, Milan, Italy.ORCID http://orcid.org/0000-0001-5438-970X
Salvatore PanicoDipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy.
Torkjel M SandangerHealth Faculty, UiT-the Arctic University of Norway, Tromsø, Norway.
Matthias B SchultzeGerman Institute of Human Nutrition Potsdam-Rehbrücke, Heidelberg, Germany.
Ruth C TravisCancer Epidemiology Unit, University of Oxford, Oxford, UK.
Rosario TuminoCancer Registry and Histopathology Department Azienda Sanitaria Provinciale (ASP), Ragusa, Italy.ORCID http://orcid.org/0000-0003-2666-414X
Paolo VineisMRC Centre for Environment and Health, Imperial College London, London, UK.
Elisabete WeiderpassInternational Agency for Research on Cancer, Lyon, France.ORCID http://orcid.org/0000-0003-2237-0128
Roderick SkinnerNewcastle University Centre for Cancer, Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK.
Linda SharpNewcastle University Centre for Cancer, Population Health Sciences Institute, Newcastle upon Tyne, UK.ORCID http://orcid.org/0000-0001-9515-1722
Jill A McKayDepartment of Applied Sciences, Northumbria University, Newcastle upon Tyne, UK.
Gordon StrathdeeNewcastle University Centre for Cancer, Biosciences Institute, Newcastle University, Newcastle upon Tyne, UK. Gordon.Strathdee@ncl.ac.uk.ORCID http://orcid.org/0000-0001-9681-8429
Newcastle University · GBCentre international de recherche sur le cancer · FRGerman Cancer Research Center · DEGerman Institute of Human Nutrition · DEAgenzia Regionale Sanitaria della Puglia · ITFederico II University Hospital · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITGreat North Children's Hospital · GBInstitut d'Investigació Biomédica de Bellvitge · ESInstituto de Investigación Biosanitaria de Granada · ESMRC Centre for Environment and HealthNorthumbria University · GBUiT The Arctic University of Norway · NOUniversity of Oxford · GB

Funding

Cancer Research UK 29017Medical Research Council MR/S019669/1World Health Organization 001
6 · The paper itself

Abstract

backgroundChildhood cancer survivors (CCS) exhibit significantly increased chronic diseases and premature death. Abnormalities in DNA methylation are associated with development of chronic diseases and reduced life expectancy. We investigated the hypothesis that anti-cancer treatments are associated with long-term DNA methylation changes that could be key drivers of adverse late health effects.

methodsGenome-wide DNA methylation was assessed using MethylationEPIC arrays in paired samples (before/after therapy) from 32 childhood cancer patients. Separately, methylation was determined in 32 samples from different adult CCS (mean 22-years post-diagnosis) and compared with cancer-free controls (n = 284).

resultsWidespread DNA methylation changes were identified post-treatment in childhood cancer patients, including 146 differentially methylated regions (DMRs), which were consistently altered in the 32 post-treatment samples. Analysis of adult CCS identified matching methylation changes at 107/146 of the DMRs, suggesting potential long-term retention of post-therapy changes. Adult survivors also exhibited epigenetic age acceleration, independent of DMR methylation. Furthermore, altered methylation at the DUSP6 DMR was significantly associated with early mortality, suggesting altered methylation may be prognostic for some late adverse health effects in CCS.

conclusionsThese novel methylation changes could serve as biomarkers for assessing normal cell toxicity in ongoing treatments and predicting long-term health outcomes in CCS.

Indexed as

Cancer SurvivorsNeoplasmsAdultChildDNA MethylationEpigenesis, GeneticEpigenomicsHumansSurvivors

Identifiers

PMID35354948
PMCPMC9296636
OpenAlexW4220752485

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.