ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2025
Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- Emerging roles of ATR beyond DNA damage repair: orchestrating transcriptional reprogramming during epithelial-to-mesenchymal transition.The Journal of clinical investigation · 2026Article
- Multi-omics dissection of R-loop dynamics in tumorigenesis: From transcription-replication conflict to therapeutic targets.Molecular therapy. Oncology · 2026Review
- The implications of TMSB4X in TIM3 hypermethylation and CD8Scientific reports · 2026Article
- RAD51C-XRCC3 complex regulates FANCM-mediated R-loop resolution to safeguard genome integrity.Science advances · 2026Article
- Spontaneous Mutations Occur More in Highly Transcribed Regions in Daphnia.Genome biology and evolution · 2026Article
- Identification of small GTPases as potential target proteins of the mycotoxin and renal carcinogen ochratoxin A.Archives of toxicology · 2026Article
- KCTD10 as a selective cancer dependency from transcription-replication conflicts (TRCs).Ageing and cancer research & treatment · 2026Article
- LUMINIDEPENDENS orchestrates global transcriptional repression inProceedings of the National Academy of Sciences of the United States of America · 2025Article
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
No grant is acknowledged in the PubMed record.
Abstract
Genome instability (GIN) is a cell pathology linked to cancer promotion and tumor evolution. Transcription is an essential cellular process but also a potential source of DNA damage and GIN. Transcription-replication conflicts (TRCs) are a predominant source of GIN, and defective TRC resolution may seriously compromise genome integrity. Importantly, chromatin dynamics helps orchestrate the response to TRCs to preserve genome integrity. Multiple epigenetic deficiencies have been shown to cause transcription-induced replication stress, resulting in DNA breaks and mutations. Consistently, chromatin alterations are frequent in cancer and correlate with increased mutation burden at TRC sites in tumors. Here, we review our current knowledge of TRC processing, the consequences of its dysfunction, and its relevance in cancer. We focus on the interplay between the DNA damage response (DDR) and chromatin dynamics and discuss the clinical potential of targeting TRCs as anticancer strategies and drugging the associated epigenetic signatures.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.