Evidence map›Paper›PMID 41690920›Full record

ArticleNature communications2026

Blood-based epigenetic instability linked to human aging and disease.

Salman Basrai, Ido Nofech-Mozes, Rajesh Detroja, Fernando L Scolari, Mehran Bakhtiari, Andrea Arruda, Tracy Murphy, Scott V Bratman, Steven M Chan, Mark D Minden and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Salman BasraiOntario Institute for Cancer Research, Toronto, ON, Canada.
Ido Nofech-MozesOntario Institute for Cancer Research, Toronto, ON, Canada.ORCID http://orcid.org/0000-0003-1973-5472
Rajesh DetrojaPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Fernando L ScolariPeter Munk Cardiac Centre, University Health Network, Toronto, ON, Canada.
Mehran BakhtiariPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Andrea ArrudaPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Tracy MurphyDivision of Medical Oncology and Hematology, Princess Margaret Cancer Centre, Toronto, ON, Canada.
Scott V BratmanPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Steven M ChanPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.ORCID http://orcid.org/0000-0002-4354-0731
Mark D MindenPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Jae Sook AhnChonnam National University Hwasun Hospital, Chonnam National University, Hwasun, Korea.
Dennis D H KimPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Robert KridelPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.ORCID http://orcid.org/0000-0003-0287-7124
Filio BilliaPeter Munk Cardiac Centre, University Health Network, Toronto, ON, Canada.ORCID http://orcid.org/0000-0002-2824-1215
Sagi AbelsonOntario Institute for Cancer Research, Toronto, ON, Canada. SAbelson@oicr.on.ca.ORCID http://orcid.org/0000-0003-1747-3819

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The abundance, dynamics, and context-dependent heterogeneity of DNA methylation, where a pattern considered abnormal in one cell type may be normal in another, complicate the identification of early methylation changes that drive or signal disease development. This complexity can obscure early markers of increased disease risk, making it challenging to detect and intervene in disease processes at their inception. Here, we report 31,744 CpG loci exhibiting highly consistent methylation profiles in the blood of young, healthy individuals. We assess alterations at these epigenetically stable loci in 8,886 individuals across 29 diverse cohorts, including those with hematological cancers (n = 3159), cardiovascular complications (n = 2788), and healthy controls (n = 2939). Our findings reveal methylation pattern disruption in myeloid and lymphoid malignancies, correlating with clonal burden dynamics and mutation frequency throughout leukemia treatment. In non-cancer cohorts, we observe that methylation levels at epigenetically stable loci become increasingly variable with age, a shift linked to higher cardiovascular disease risk and lower survival rates. This study highlights DNA methylation instability as a blood-based biomarker for both hematological cancer and cardiovascular disease and uncovers a mechanistic link between methylation dynamics and the expansion of maladaptive hematopoietic clones.

Indexed as

AgingCardiovascular DiseasesDNA MethylationEpigenesis, GeneticHematologic NeoplasmsAdultAgedCpG IslandsFemaleHumansMaleMiddle AgedYoung Adult

Identifiers

PMID41690920
PMCPMC13018287

What OpenQuestion holds

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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.