Evidence map›Paper›PMID 41609026›Full record

ReviewHaematologica2026

Clonal hematopoiesis driver mutations: molecular mechanisms and clinical implications - inclusive fitness of pre-leukemic hematopoietic stem and progenitor cells through pro-inflammatory features of their progeny.

Tal Bacharach, Adrian Duek, Liran I Shlush

Abstract readReview
In one paragraph

Review in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

3 authors.

Tal BacharachDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot.
Adrian DuekHemato-Oncology Department, Samson Assuta Ashdod University Hospital, Ashdod, Israel; Ben Gurion University of the Negev, Beer-Sheba.
Liran I ShlushDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel; Hemato-Oncology Department, Samson Assuta Ashdod University Hospital, Ashdod. liranshlush3@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal hematopoiesis is driven by the age-associated expansion of hematopoietic stem and progenitor cells that harbor somatic driver mutations; however, the mechanisms underlying the long-term persistence of these cells remain incompletely understood. This review frames clonal hematopoiesis through the lens of inclusive fitness, proposing that mutant pre-leukemic hematopoietic stem and progenitor cells enhance their evolutionary success not only through intrinsic self-renewal advantages, but also via indirect effects mediated by their differentiated progeny. We synthesize evidence showing that mutant immune cells promote inflammatory microenvironments that selectively impair wild-type hematopoietic stem cells while reinforcing mutant self-renewal, establishing self-sustaining feedback loops that shape clonal dynamics and systemic disease risk.

Indexed as

Clonal HematopoiesisHematopoietic Stem CellsMutationAnimalsHumansInflammation

Identifiers

PMID41609026
PMCPMC13136797

What OpenQuestion holds

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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.