Evidence map›Paper›PMID 37931207›Full record

ReviewBlood2023

Causes and consequences of clonal hematopoiesis.

Lachelle D Weeks, Benjamin L Ebert

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07675967 (Clonal Hematopoiesis Chemotherapy and Radiation Effects Study), which is not on this map. Cited by 121 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 1 pooled it
36.0field-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.

NCT07675967 recruitingnot on this mapstarted 2025, after this paper: background citation

Clonal Hematopoiesis Chemotherapy and Radiation Effects Study

TypeobservationalSponsorDana-Farber Cancer InstituteRan2025 to 2035Enrolled5,000ConditionsLung Cancer (Diagnosis), Osteochondroma, Spitz Nevus, Solid CancersArmsSamples
3 · Its place in the literature

Who cites it

121 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Clinical Impact and Dynamics of Clonal Hematopoiesis withJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Risk factors of clonal hematopoiesis of indeterminate potential.Clinical medicine (London, England) · 2026
    Article
  13. Genetic influences on haematopoiesis.Nature reviews. Genetics · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

61 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Lachelle D WeeksDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.ORCID 0000-0001-8726-6212
Benjamin L EbertDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.ORCID 0000-0003-0197-5451
Harvard University · USHoward Hughes Medical Institute · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
Targeting SYK Kinase in AMLP50CA206963 · NCI · DANA-FARBER CANCER INST · PI STEGMAIER, KIMBERLY · 2017 to 2021
$10.6M
Functional Genomic Dissection of Refractory AnemiaR01HL082945 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI EBERT, BENJAMIN LEVINE · 2005 to 2022
$6.8M
The role of clonal hematopoiesis in the development and therapy of myeloid malignanciesR35CA253125 · NCI · DANA-FARBER CANCER INST · PI EBERT, BENJAMIN LEVINE · 2020 to 2024
$4.9M
Howard Hughes Medical InstituteNCI NIH HHS P01 CA066996NCI NIH HHS P50 CA206963NCI NIH HHS R35 CA253125NHLBI NIH HHS R01 HL082945
6 · The paper itself

Abstract

abstractClonal hematopoiesis (CH) is described as the outsized contribution of expanded clones of hematopoietic stem and progenitor cells (HSPCs) to blood cell production. The prevalence of CH increases dramatically with age. CH can be caused by somatic mutations in individual genes or by gains and/or losses of larger chromosomal segments. CH is a premalignant state; the somatic mutations detected in CH are the initiating mutations for hematologic malignancies, and CH is a strong predictor of the development of blood cancers. Moreover, CH is associated with nonmalignant disorders and increased overall mortality. The somatic mutations that drive clonal expansion of HSPCs can alter the function of terminally differentiated blood cells, including the release of elevated levels of inflammatory cytokines. These cytokines may then contribute to a broad range of inflammatory disorders that increase in prevalence with age. Specific somatic mutations in the peripheral blood in coordination with blood count parameters can powerfully predict the development of hematologic malignancies and overall mortality in CH. In this review, we summarize the current understanding of CH nosology and origins. We provide an overview of available tools for risk stratification and discuss management strategies for patients with CH presenting to hematology clinics.

Indexed as

Hematologic NeoplasmsPrecancerous ConditionsClonal HematopoiesisCytokinesHematopoiesisHumansMutationCytokines

Identifiers

PMID37931207
PMCPMC10862247
OpenAlexW4388406603

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.