ReviewInternational journal of molecular sciences2025
Claspin and Cancer: Where Are We Now?
Review in International journal of molecular sciences, 2025. 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.
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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
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells arise from the cumulative acquisition of genetic and epigenetic alterations that affect vital cellular functions. Genomic instability results from deficiencies in protective mechanisms, such as cell cycle checkpoints, DNA replication control, or DNA repair. Claspin integrates a group of crucial proteins that maintain genome integrity. It participates in key cellular events such as DNA damage checkpoint activation, DNA replication, replication stress responses, DNA repair, epigenetic memory, and apoptosis. Given its crucial functions, a role for Claspin in cancer is not a surprise. Indeed, there is a considerable body of evidence linking Claspin deregulation with cancer. For instance, over-expression of Claspin and Tim promoted the survival of cancer cells by enabling adaptation to oncogene-induced replication stress. In addition, Claspin gene (
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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.