ReviewClinical and experimental medicine2025
Targeting the Werner syndrome protein in microsatellite instability cancers: mechanisms and therapeutic potential.
Review in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- PARP Inhibitor Sensitivity in Tumors Harboring Non-BRCA Homologous Recombination Gene Alterations: Current Evidence Across Ovarian, Breast, Prostate, and Pancreatic Cancers.International journal of molecular sciences · 2026Review
- Targeting DNA repair mechanisms in cancer therapy: the role of small molecule DNA repair inhibitors.NAR cancer · 2025Review
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Microsatellite instability (MSI) is a key feature of cancers with defective DNA mismatch repair, including colorectal, gastric, endometrial, and ovarian cancers. Tumors with MSI depend on the Werner syndrome protein (WRN) for genomic stability, making WRN an attractive therapeutic target. WRN inhibitors exploit the concept of synthetic lethality, inducing selective DNA damage and cell death in MSI tumors while sparing microsatellite stability (MSS) tumor cells or normal cells. Preclinical studies have shown that the efficacy of WRN inhibitors is enhanced when combined with DNA damage response inhibitors or immunotherapy. This review delineates the molecular mechanisms underlying WRN dependency in MSI cancers and explores the therapeutic potential of WRN inhibition. WRN inhibitors represent a promising strategy in precision oncology, especially for MSI tumors, and have the potential to enhance patient outcomes, either as monotherapy or in combination with other treatments.
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Identifiers
What Socratic holds
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 Socratic graph.