ReviewCellular and molecular life sciences : CMLS2014
Updating the mechanisms of common fragile site instability: how to reconcile the different views?
Review in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 59 citations in OpenAlex.
- Ubiquitin's code: UPS orchestrating DNA repair and genomic stability under genotoxic stress.Molecular and cellular biochemistry · 2026Review
- Participants in Transcription-Replication Conflict and Their Role in Formation and Resolution of R-Loops.International journal of molecular sciences · 2025Review
- Molecular Mechanisms and Clinical Divergences in HPV-Positive Cervical vs. Oropharyngeal Cancers: A Critical Narrative Review.BMC medicine · 2025Review
- Loss of G1-phase CDK-inhibition biases instability between genomic regions by unevenly reducing activity among replication origins.iScience · 2025Article
- ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancer.Nature communications · 2025Article
- Article
- Transcription-associated DNA DSBs activate p53 during hiPSC-based neurogenesis.Scientific reports · 2022Article
- Epigenomic signatures associated with spontaneous and replication stress-induced DNA double strand breaks.Frontiers in genetics · 2022Article
- Recurrent integration of human papillomavirus genomes at transcriptional regulatory hubs.NPJ genomic medicine · 2021Article
- R-Loops and Its Chro-Mates: The Strange Case of Dr. Jekyll and Mr. Hyde.International journal of molecular sciences · 2021Review
- CENP-A chromatin prevents replication stress at centromeres to avoid structural aneuploidy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Sites of chromosomal instability in the context of nuclear architecture and function.Cellular and molecular life sciences : CMLS · 2021Review
- High-resolution mapping of mitotic DNA synthesis regions and common fragile sites in the human genome through direct sequencing.Cell research · 2020Article
- Common Fragile Sites Are Characterized by Faulty Condensin Loading after Replication Stress.Cell reports · 2020Article
- Review
- Spontaneous DNA-RNA hybrids: differential impacts throughout the cell cycle.Cell cycle (Georgetown, Tex.) · 2020Review
- Transcription-mediated organization of the replication initiation program across large genes sets common fragile sites genome-wide.Nature communications · 2019Article
- Genome-wide mapping of 8-oxo-7,8-dihydro-2'-deoxyguanosine reveals accumulation of oxidatively-generated damage at DNA replication origins within transcribed long genes of mammalian cells.Nucleic acids research · 2019Article
- Review
- The Protective Role of Dormant Origins in Response to Replicative Stress.International journal of molecular sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are large chromosomal regions long identified by conventional cytogenetics as sequences prone to breakage in cells subjected to replication stress. The interest in CFSs came from their key role in the formation of DNA damage, resulting in chromosomal rearrangements. The instability of CFSs was notably correlated with the appearance of genome instability in precancerous lesions and during tumor progression. Identification of the molecular mechanisms responsible for their instability therefore represents a major challenge. A number of data show that breaks result from mitotic entry before replication completion but the mechanisms responsible for such delayed replication of CFSs and relaxed checkpoint surveillance are still debated. In addition, clues to the molecular events leading to breakage just start to emerge. We present here the results of recent reports addressing these questions.
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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.