ReviewCommunications biology2025
The need for speed: drivers and consequences of accelerated replication forks.
Review in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Adaptive Replication Fork Acceleration by CDK1-Cyclin B1 Sustains Genome Duplication despite Impaired Origin Firing.bioRxiv : the preprint server for biology · 2026Article
- Tumor cell cycle regulation: integrated perspective of stage characteristics, regulatory networks, and signaling pathway intervention strategies.Molecular biomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The modulation of DNA replication dynamics has emerged as a key area of study in understanding genome stability and its perturbations in various physiological and pathological contexts. Replication fork rate is influenced by a variety of factors, including DNA repair pathways, origin firing, chromatin organization, transcription, and oncogenic signaling. This review highlights recent findings on the molecular mechanisms driving replication fork acceleration, focusing on scenarios such as PARP inhibition, oncogene activation, depletion of replication factors, and defects in Okazaki fragment processing. We discuss how reduced origin firing, R-loop resolution, and metabolic changes contribute to fork rate modulation, as well as the involvement of innate immune signaling, particularly through pathways such as cGAS-STING and ISG15. Special attention is given to consequences of accelerated replication forks for genome stability and their role in disease progression, particularly cancer. By unraveling the molecular mechanisms of fork acceleration, this Mini Review underscores its critical role in shaping genome integrity and cellular homeostasis, providing insights into future research directions and therapeutic strategies.
Indexed as
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.