ReviewAgeing research reviews2017
Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.
Review in Ageing research reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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.
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
38 citing papers in PubMed.
- Low protein-induced-FGF-21 signaling remodels adipose tissue on reduced markers of senescence during aging.GeroScience · 2026Article
- Inborn errors of immunity with DNA repair disorders: at the interface of immune deficiency, immune dysregulation, and malignancy.Frontiers in immunology · 2026Review
- Analyzing different aging theories in the context of the brain: DNA damage, inflammation, redox imbalance, and neurodevelopment intertwine.Biogerontology · 2025Review
- [A case of hepatitis-associated aplastic anemia complicated by hemophagocytic lymphohistiocytosis and literature review].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- YY1 is involved in homologous recombination inhibition at guanine quadruplex sites in human cells.Nucleic acids research · 2024Article
- Article
- Review
- Article
- Application of mesenchymal stem cells for anti-senescence and clinical challenges.Stem cell research & therapy · 2023Review
- Discovery of a new hereditary RECQ helicase disorder RECON syndrome positions the replication stress response and genome homeostasis as centrally important processes in aging and age-related disease.Ageing research reviews · 2023Review
- Premature aging in genetic diseases: what conclusions can be drawn for physiological aging.Frontiers in aging · 2023Review
- Breaking the aging epigenetic barrier.Frontiers in cell and developmental biology · 2022Review
- Exome Sequencing Reveals Novel Variants and Expands the Genetic Landscape for Congenital Microcephaly.Genes · 2021Article
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- Multidisciplinary management of endocrinopathies and treatment-related toxicities in patients with Bloom syndrome and cancer.Pediatric blood & cancer · 2021Article
- DNA damage-how and why we age?eLife · 2021Review
- Human RecQ Helicases in DNA Double-Strand Break Repair.Frontiers in cell and developmental biology · 2021Review
- Alteration of genetic recombination and double-strand break repair in human cells by progerin expression.DNA repair · 2020Article
- DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells.Experimental & molecular medicine · 2020Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Genomic instability is a hallmark of cancer and aging. Premature aging (progeroid) syndromes are often caused by mutations in genes whose function is to ensure genomic integrity. The RecQ family of DNA helicases is highly conserved and plays crucial roles as genome caretakers. In humans, mutations in three RecQ genes - BLM, WRN, and RECQL4 - give rise to Bloom's syndrome (BS), Werner syndrome (WS), and Rothmund-Thomson syndrome (RTS), respectively. WS is a prototypic premature aging disorder; however, the clinical features present in BS and RTS do not indicate accelerated aging. The BLM helicase has pivotal functions at the crossroads of DNA replication, recombination, and repair. BS cells exhibit a characteristic form of genomic instability that includes excessive homologous recombination. The excessive homologous recombination drives the development in BS of the many types of cancers that affect persons in the normal population. Replication delay and slower cell turnover rates have been proposed to explain many features of BS, such as short stature. More recently, aberrant transcriptional regulation of growth and survival genes has been proposed as a hypothesis to explain features of BS.
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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.