ReviewExperimental cell research2014
Replication stress and cancer: it takes two to tango.
Review in Experimental cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 134 citations in OpenAlex.
- Germline polymorphisms in genes maintaining the replication fork predict the efficacy of oxaliplatin and irinotecan in patients with metastatic colorectal cancer.British journal of cancer · 2022Trial
- An updated view on lagging strand DNA replication: implications for the replication stress response.Cell cycle (Georgetown, Tex.) · 2026Article
- RepliSage: a stochastic graph-based framework for 3D chromatin modeling across the cell cycle.Nucleic acids research · 2026Article
- Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization.Current issues in molecular biology · 2026Review
- MYC as a key target for melanoma therapy.Frontiers in cell and developmental biology · 2026Review
- A prognostic signature for hormone receptor-positive, human epidermal growth factor receptor 2-negative breast cancer.Scientific reports · 2025Article
- DNA polymerase α/primase extraction from chromatin by VCP/p97 restricts ATR activation during unperturbed DNA replication.Nature communications · 2025Article
- Targeting Ataxia Telangiectasia-Mutated and Rad3-Related for Anaplastic Thyroid Cancer.Cancers · 2025Article
- For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.Annual review of virology · 2023Review
- Novel Cellular Functions of ATR for Therapeutic Targeting: Embryogenesis to Tumorigenesis.International journal of molecular sciences · 2023Review
- Dynamic de novo heterochromatin assembly and disassembly at replication forks ensures fork stability.Nature cell biology · 2023Article
- Article
- MYC and therapy resistance in cancer: risks and opportunities.Molecular oncology · 2022Review
- ATR and CDK4/6 inhibition target the growth of methotrexate-resistant choriocarcinoma.Oncogene · 2022Article
- R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1.International journal of molecular sciences · 2022Review
- Cell cycle control in cancer.Nature reviews. Molecular cell biology · 2022Review
- Targeting the DNA Damage Response for Cancer Therapy by Inhibiting the Kinase Wee1.Frontiers in oncology · 2022Review
- Review
- USP7 and VCPCell reports · 2021Article
- PIF1 helicase promotes break-induced replication in mammalian cells.The EMBO journal · 2021Article
22 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Problems arising during DNA replication require the activation of the ATR-CHK1 pathway to ensure the stabilization and repair of the forks, and to prevent the entry into mitosis with unreplicated genomes. Whereas the pathway is essential at the cellular level, limiting its activity is particularly detrimental for some cancer cells. Here we review the links between replication stress (RS) and cancer, which provide a rationale for the use of ATR and Chk1 inhibitors in chemotherapy. First, we describe how the activation of oncogene-induced RS promotes genome rearrangements and chromosome instability, both of which could potentially fuel carcinogenesis. Next, we review the various pathways that contribute to the suppression of RS, and how mutations in these components lead to increased cancer incidence and/or accelerated ageing. Finally, we summarize the evidence showing that tumors with high levels of RS are dependent on a proficient RS-response, and therefore vulnerable to ATR or Chk1 inhibitors.
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.