ArticleNature genetics2026
No evidence of immunosurveillance in mutation-hotspot-driven clonal hematopoiesis.
Article in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Clinical progression of clonal hematopoiesis is determined by a combination of mutation timing, fitness, and clonal structure.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The theory of immunosurveillance posits that T cells eliminate clones harboring nonself-antigens generated by somatic mutations. Although a role of immunosurveillance in cancer is supported by evidence, whether it affects precancerous expansions has not been well established. Here we studied the association between MHC-variant binding and risk of clonal hematopoiesis (CH), a blood precancer state, predicting MHC binding affinity toward CH hotspot variants in 380,000 UK Biobank participants and examining the relationship between predicted binding to each variant and its expansion risk. Despite the study being powered to detect subtle differences in selective pressure, we did not find associations between predicted binding and CH prevalence for any of the examined variants. In CH-affected individuals, we identified no relationship between predicted variant binding and clone size. Overall, we found no evidence that the MHC genotype affects which variants expand in CH, suggesting a limited role for immunosurveillance in shaping clonal expansions in the blood.
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