Evidence map›Paper›PMID 39626264›Full record

ReviewThe Journal of experimental medicine2025

Genetic and environmental risks for clonal hematopoiesis and cancer.

Stephanie Franco, Lucy A Godley

Abstract readReview
In one paragraph

Review in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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

2 authors.

Stephanie FrancoDepartment of Medicine, Northwestern Medicine, Chicago, IL, USA.ORCID 0000-0002-9951-820X
Lucy A GodleyDepartment of Medicine, Northwestern Medicine, Chicago, IL, USA.ORCID 0000-0003-1914-9158

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic variants accumulate in all organs with age, with a positive selection of clonal populations that provide a fitness advantage during times of heightened cellular stress leading to clonal expansion. Easily measured within the hematopoietic compartment, clonal hematopoiesis (CH) is now recognized as a common process in which hematopoietic clones with somatic variants associated with hematopoietic neoplasms exist within the blood or bone marrow of individuals without evidence of malignancy. Most cases of CH involve a limited number of genes, most commonly DNMT3A, TET2, and ASXL1. CH confers risk for solid and hematopoietic malignancies as well as cardiovascular and numerous inflammatory diseases and offers opportunities for cancer prevention. Here, we explore the genetic and environmental factors that predispose individuals to CH with unique variant signatures and discuss how CH drives cancer progression with the goals of improving individual cancer risk stratification, identifying key intervention opportunities, and understanding how CH impacts therapeutic strategies and outcomes.

Indexed as

Clonal HematopoiesisNeoplasmsAnimalsDioxygenasesDNA-Binding ProteinsDNA Methyltransferase 3AGene-Environment InteractionGenetic Predisposition to DiseaseHematologic NeoplasmsHematopoiesisHumansRisk FactorsDioxygenasesDNA-Binding ProteinsDNA Methyltransferase 3ADNMT3A protein, humanTET2 protein, human

Identifiers

PMID39626264
PMCPMC11614460

What OpenQuestion holds

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Registered trials

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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.