Evidence map›Paper›PMID 31796056›Full record

ArticleClinical epigenetics2019

Cisplatin treatment of testicular cancer patients introduces long-term changes in the epigenome.

Cecilie Bucher-Johannessen, Christian M Page, Trine B Haugen, Marcin W Wojewodzic, Sophie D Fosså, Tom Grotmol, Hege S Haugnes, Trine B Rounge

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  10. Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress.American journal of physiology. Heart and circulatory physiology · 2022
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  16. Targeting protein tyrosine kinase 6 in cancer.Biochimica et biophysica acta. Reviews on cancer · 2020
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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

8 authors at 5 institutions in 1 country.

Cecilie Bucher-JohannessenDepartment of Research, Cancer Registry of Norway, Oslo, Norway.
Christian M PageOslo Centre for Biostatistics and Epidemiology, Section for Research Support, Oslo University Hospital, Oslo, Norway.
Trine B HaugenFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway.ORCID 0000-0003-2677-2722
Marcin W WojewodzicDepartment of Research, Cancer Registry of Norway, Oslo, Norway.
Sophie D FossåDepartment of Research, Cancer Registry of Norway, Oslo, Norway.
Tom GrotmolDepartment of Research, Cancer Registry of Norway, Oslo, Norway.
Hege S HaugnesDepartment of Oncology, University Hospital of North Norway, Tromsø, Norway.
Trine B RoungeDepartment of Research, Cancer Registry of Norway, Oslo, Norway. Trine.rounge@kreftregisteret.no.
Cancer Registry of Norway · NOOslo University Hospital · NOOsloMet – Oslo Metropolitan University · NOUniversity Hospital of North Norway · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCisplatin-based chemotherapy (CBCT) is part of standard treatment of several cancers. In testicular cancer (TC) survivors, an increased risk of developing metabolic syndrome (MetS) is observed. In this epigenome-wide association study, we investigated if CBCT relates to epigenetic changes (DNA methylation) and if epigenetic changes render individuals susceptible for developing MetS later in life. We analyzed methylation profiles, using the MethylationEPIC BeadChip, in samples collected ~ 16 years after treatment from 279 Norwegian TC survivors with known MetS status. Among the CBCT treated (n = 176) and non-treated (n = 103), 61 and 34 developed MetS, respectively. We used two linear regression models to identify if (i) CBCT results in epigenetic changes and (ii) epigenetic changes play a role in development of MetS. Then we investigated if these changes in (i) and (ii) links to genes, functional networks, and pathways related to MetS symptoms.

resultsWe identified 35 sites that were differentially methylated when comparing CBCT treated and untreated TC survivors. The PTK6-RAS-MAPk pathway was significantly enriched with these sites and infers a gene network of 13 genes with CACNA1D (involved in insulin release) as a network hub. We found nominal MetS-associations and a functional gene network with ABCG1 and NCF2 as network hubs.

conclusionOur results suggest that CBCT has long-term effects on the epigenome. We could not directly link the CBCT effects to the risk of developing MetS. Nevertheless, since we identified differential methylation occurring in genes associated with conditions pertaining to MetS, we hypothesize that epigenomic changes may also play a role in the development of MetS in TC survivors. Further studies are needed to validate this hypothesis.

Indexed as

AdultAntineoplastic AgentsCancer SurvivorsCase-Control StudiesCisplatinDNA MethylationEpigenesis, GeneticGene Regulatory NetworksGenome-Wide Association StudyHumansLinear ModelsMaleMetabolic SyndromeMiddle AgedNorwaySequence Analysis, DNAAntineoplastic AgentsCisplatinCisplatin-based chemotherapyDNA methylationEpigeneticEpigenome-wide association studyLong-term effectsMetabolic syndromePlatinumTesticular cancer survivors

Identifiers

PMID31796056
PMCPMC6892132
OpenAlexW2991772250

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.