ReviewInternational journal of molecular sciences2024
Key Proteins of Replication Stress Response and Cell Cycle Control as Cancer Therapy Targets.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 46 citations in OpenAlex.
- 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
- TET1 Inhibition Promotes Therapeutic Sensitivity in TP53-Mutant GBM by Influencing Genome Fragility and Altering TAMs Biology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PKMYT1 in Cancer: Beyond Cell Cycle Checkpoints to Context-Dependent Therapeutic Vulnerability.Genes, chromosomes & cancer · 2026Review
- Multifaceted regulatory role of proline‑ and glutamine-rich splicing factor in tumors (Review).Molecular medicine reports · 2026Review
- Benzofuran-Annulated Naphthalimides Trigger Replication Stress, DNA Damage, and p53-Dependent Cell Cycle Arrest.Pharmaceutics · 2026Article
- Replication origin firing capacity indicates ATR inhibitor sensitivity.Nature communications · 2026Article
- Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization.Current issues in molecular biology · 2026Review
- Emerging Protein Therapeutics as a Strategy for Cervical Cancer Treatment.Current pharmaceutical biotechnology · 2026Review
- Identification of DNA Replication Stress-Related Genes as Prognostic Biomarkers for Bladder Cancer.Combinatorial chemistry & high throughput screening · 2026Article
- Synthetic lethality in cancer therapy: Mechanisms, models and clinical translation for overcoming therapeutic resistance.Clinical and translational medicine · 2026Review
- Targeting Extrachromosomal DNA (ecDNA) in Cancer: A New Era of CHK1 Inhibition and Personalized Treatments.Current gene therapy · 2026Article
- Distinct Immune Landscape and Gene Expression Profiles in Breast Cancer: Young versus Non-Young Patients.Breast care (Basel, Switzerland) · 2025Article
- Identification of Fibrillarin and Cajal Bodies Under DNA Replication Stress Conditions in Root Meristem Cells ofInternational journal of molecular sciences · 2025Article
- AZD6738 Attenuates LPS-Induced Corneal Inflammation and Fibrosis by Modulating Macrophage Function and Polarization.Inflammation · 2025Article
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- Targeted delivery of the PKMYT1 inhibitor RP-6306 mediates PANoptosis in pancreatic cancer via mitotic catastrophe.Cell death & disease · 2025Article
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- Oncogenic stress response mechanisms as new therapeutic targets in cancer treatment: A review.Medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Replication stress (RS) is a characteristic state of cancer cells as they tend to exchange precision of replication for fast proliferation and increased genomic instability. To overcome the consequences of improper replication control, malignant cells frequently inactivate parts of their DNA damage response (DDR) pathways (the ATM-CHK2-p53 pathway), while relying on other pathways which help to maintain replication fork stability (ATR-CHK1). This creates a dependency on the remaining DDR pathways, vulnerability to further destabilization of replication and synthetic lethality of DDR inhibitors with common oncogenic alterations such as mutations of
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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.