ReviewNature reviews. Cancer2015
Replication stress and cancer.
Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 646 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
646 citing papers in PubMed.
- Folding a broken genome: the versatile roles of cohesin in genome maintenance.Nature reviews. Genetics · 2026Review
- Article
- Replication stress in cancer: origins, consequences and therapeutic opportunities.Nature reviews. Cancer · 2026Review
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Replication Stress Tolerance in Adult T-Cell Leukemia.Biomolecules · 2026Review
- Cumulative microscopy reveals cellular states in fibroblasts from patients with genetic disorders.EMBO reports · 2026Article
- Histone H4 lysine 20 tri-methylation safeguards breast cancer lineage fidelity and unfolded protein response.Nature communications · 2026Article
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Ionizing Radiation and Ultraviolet Light Irradiation-Associated DNA Damage Increasing Genomic Instability Risk.Cancer science · 2026Review
- Targeting epigenetic regulators induces transcription-replication conflicts to overcome ATR inhibitor resistance.Nucleic acids research · 2026Article
- FANCA-dependent FEN1 recruitment suppresses transcription-replication conflicts and PARPi sensitivity.Molecular cell · 2026Article
- RAD51 in Breast Cancer: From Vulnerability to Resistance.World journal of oncology · 2026Review
- Mechanisms of MCM2-7 helicase activation and initial DNA melting at near base-pair resolution.Nature communications · 2026Article
- ATZ-1 promotes DNA replication efficiency to maintain normal meiotic function.FEBS open bio · 2026Article
- Adaptive Regulation of dNTP Homeostasis Confers Osimertinib Resistance in EGFR-Mutant Non-Small Cell Lung Carcinoma.Cancer research · 2026Article
- Interaction of NDRG1 and TGM2 Modulates DNA Replication and Repair.Molecular cancer research : MCR · 2026Article
- Structure Elucidation and Initial Characterization of a N-glucuronide Metabolite (M1) of Tuvusertib.European journal of drug metabolism and pharmacokinetics · 2026Article
- Partial Depletion of SART1 Selectively Induces Mitotic Defects and Cell Death in Cancer Cells.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Exploring Stem Cell Based Senotherapeutic Strategies for Targeting Cellular Senescence in Brain Aging.Stem cell reviews and reports · 2026Review
- DNA replication stress and translational repression converge to drive CDK1- and caspase-dependent apoptosis in Ewing sarcoma.Oncogene · 2026Article
586 more citing papers are in PubMed but not listed here.
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
Abstract
Genome instability is a hallmark of cancer, and DNA replication is the most vulnerable cellular process that can lead to it. Any condition leading to high levels of DNA damage will result in replication stress, which is a source of genome instability and a feature of pre-cancerous and cancerous cells. Therefore, understanding the molecular basis of replication stress is crucial to the understanding of tumorigenesis. Although a negative aspect of replication stress is its prominent role in tumorigenesis, a positive aspect is that it provides a potential target for cancer therapy. In this Review, we discuss the link between persistent replication stress and tumorigenesis, with the goal of shedding light on the mechanisms underlying the initiation of an oncogenic process, which should open up new possibilities for cancer diagnostics and treatment.
Indexed as
Identifiers
25907220What 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.