ReviewCell & bioscience2025
Multiple functions of the ALT favorite helicase, BLM.
Review in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- RecurIndex-derived molecular features associated with total pathological complete response in triple-negative breast cancer: An exploratory prospective cohort study with single-cell transcriptomic contextualization.Cancer biology & therapy · 2026Article
- Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026Review
- ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway.International journal of molecular sciences · 2026Article
- MDS/AML-associated DDX41 helicase facilitates homologous recombination repair by potentially resolving R-loops.Nucleic acids research · 2026Article
- Review
- SLX4IP acts in parallel to FANCM to limit BLM-dependent replication stress at ALT telomeres.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic somatic cells undergo continuous telomere shortening because of end-replication problems. Approximately 10%~15% of human cancers rely on alternative lengthening of telomeres (ALT) to overcome telomere shortening. ALT cells are characterized by persistent telomere DNA replication stress and rely on recombination-based DNA repair pathways for telomere elongation. The Bloom syndrome (BLM) helicase is a member of the RecQ family, which has been implicated as a key regulator of the ALT mechanism as it is required for either telomere length maintenance or telomere clustering in ALT-associated promyelocytic leukemia bodies (APBs). Here, we summarize recent evidence detailing the role of BLM in the activation and maintenance of ALT. We propose that the role of BLM-dependent recombination and its interacting proteins remains a crucial question for future research in dissecting the molecular mechanisms of ALT.
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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.