Evidence map›Paper›PMID 33986496›Full record

ReviewNature reviews. Genetics2021

Germline risk of clonal haematopoiesis.

Alexander J Silver, Alexander G Bick, Michael R Savona

Erratum issuedOpen access · hybridAbstract readReview
In one paragraph

Review in Nature reviews. Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Impact of Germline CHEK2 Pathogenic Variants on the Risk of Acute Myeloid Leukemia and Myelodysplastic Syndrome.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  5. Review
  6. Article
  7. Lexicon for Clonal Hematopoiesis in Liquid Biopsy.Clinical and translational science · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Alexander J SilverProgram in Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.ORCID http://orcid.org/0000-0001-8255-3140
Alexander G BickProgram in Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.ORCID http://orcid.org/0000-0001-5824-9595
Michael R SavonaProgram in Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA. michael.savona@vanderbilt.edu.ORCID http://orcid.org/0000-0003-3763-5504
Vanderbilt University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Medical Scientist Training ProgramT32GM152284 · NIGMS · VANDERBILT UNIVERSITY · PI Christopher S. Williams · 2024 to 2026
$4.8M
Targeting Clonal Hematopoiesis of Indeterminate Potential Using Human GeneticsDP5OD029586 · OD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BICK, ALEXANDER · 2020 to 2024
$2.3M
Harnessing EHR-linked Genomics Data to Study Clonal Hematopoiesis and its Evolution to Inflammatory PhenotypesF30DK127699 · NIDDK · VANDERBILT UNIVERSITY · PI SILVER, ALEXANDER JAMES · 2020 to 2023
$166k
NIDDK NIH HHS F30 DK127699NIGMS NIH HHS T32 GM007347NIGMS NIH HHS T32 GM152284NIH HHS DP5 OD029586
6 · The paper itself

Abstract

Clonal haematopoiesis (CH) is a common, age-related expansion of blood cells with somatic mutations that is associated with an increased risk of haematological malignancies, cardiovascular disease and all-cause mortality. CH may be caused by point mutations in genes associated with myeloid neoplasms, chromosomal copy number changes and loss of heterozygosity events. How inherited and environmental factors shape the incidence of CH is incompletely understood. Even though the several varieties of CH may have distinct phenotypic consequences, recent research points to an underlying genetic architecture that is highly overlapping. Moreover, there are numerous commonalities between the inherited variation associated with CH and that which has been linked to age-associated biomarkers and diseases. In this Review, we synthesize what is currently known about how inherited variation shapes the risk of CH and how this genetic architecture intersects with the biology of diseases that occur with ageing.

Indexed as

AgingClonal HematopoiesisMutationCardiovascular DiseasesGerm CellsHumans

Identifiers

PMID33986496
PMCPMC8117131
OpenAlexW3162309098

What OpenQuestion holds

Textmetadata
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.