Evidence map›Paper›PMID 40384356›Full record

ReviewCancer science2025

Clonal Hematopoiesis and Solid Cancers.

Yen T M Nguyen, Manabu Fujisawa, Shumpei Ishikawa, Mamiko Sakata-Yanagimoto

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. 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

4 authors.

Yen T M NguyenDepartment of Hematology, University of Tsukuba Hospital, University of Tsukuba, Tsukuba, Japan.ORCID https://orcid.org/0000-0003-3118-3674
Manabu FujisawaDepartment of Hematology, Institute of Medicine, University of Tsukuba, Tsukuba, Japan.
Shumpei IshikawaDepartment of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Mamiko Sakata-YanagimotoDepartment of Hematology, University of Tsukuba Hospital, University of Tsukuba, Tsukuba, Japan.ORCID https://orcid.org/0000-0001-7310-8045

Funding

Japan Agency for Medical Research and Development JP23tk0124002Japan Society for the Promotion of Science JP21H02945Japan Society for the Promotion of Science JP24K19213Leukemia and Lymphoma Society of Canada 3442-25Moonshot Research and Development Program JP22zf0127009
6 · The paper itself

Abstract

Clonal hematopoiesis refers to the expansion of hematopoietic stem cells harboring somatic mutations, a phenomenon increasingly recognized in aging populations. This review highlights the emerging relationship between clonal hematopoiesis and solid cancers, focusing on the prevalence and impact of clonal hematopoiesis-associated mutations such as DNMT3A, TET2, ASXL1, and TP53 in tumorigenesis. Key risk factors for the co-occurrence of clonal hematopoiesis and solid cancers, including germline genetic factors, aging, and environmental factors, are also discussed. We explore how clonal hematopoiesis mutations shape the tumor microenvironments in solid cancers by modulating immunoregulation, inflammation, and angiogenesis, thereby contributing to tumor progression. These findings underscore the dual role of clonal hematopoiesis as both a marker of cancer risk and a potential driver of solid cancer progression. The clinical implications of clonal hematopoiesis are also considered, including the prognostic value, impact on treatment response, and potential as a therapeutic target. Future directions are outlined to advance our understanding of clonal hematopoiesis and to exploit its clinical potential for cancer management.

Indexed as

Clonal HematopoiesisNeoplasmsAnimalsCarcinogenesisDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AHematopoietic Stem CellsHumansMutationProto-Oncogene ProteinsRepressor ProteinsRisk FactorsTumor MicroenvironmentTumor Suppressor Protein p53ASXL1 protein, humanDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanProto-Oncogene ProteinsRepressor ProteinsTET2 protein, humanTumor Suppressor Protein p53agingclonal hematopoiesissolid cancersT‐cell lymphomasTET2 mutationstumor microenvironments

Identifiers

PMID40384356
PMCPMC12317386

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.