ReviewMobile DNA2026
Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.
Review in Mobile DNA, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Transposable elements (TEs) constitute nearly half of the human genome and profoundly influence hematopoietic stem cell (HSC) biology. In this review, we synthesize current evidence demonstrating that TEs exert dual and context-dependent roles in HSCs during steady-state hematopoiesis, stress responses, aging, and leukemogenesis. Under basal conditions, tightly controlled TE activity can be beneficial for HSC biology, through the induction of intrinsic type I interferon signaling and a fine-tuned control of gene expression. However, dysregulated TE activation upon stresses and aging can undermine HSC self-renewal, impair genomic integrity, and drive age-associated hematopoietic decline. TEs also play a dual role in leukemogenesis. Derepression of transcription factor motifs within TEs can activate oncogenic programs, while TE-derived nucleic acids can simultaneously elicit antiviral and DNA damage responses that trigger anti-tumoral p53- or interferon-dependent growth arrest or apoptosis. The balance between these pro- and anti-tumoral effects remains an open question, likely shaped by cellular context, TE subtypes, and the magnitude of TE expression. Finally, we discuss the potential to therapeutically modulate TE activity. Understanding TE dynamics in HSCs offers new opportunities for mechanistic insight and clinical innovation in myeloid malignancies.
Identifiers
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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.