ReviewGenes2023
Therapeutic Targeting of DNA Replication Stress in Cancer.
Review in Genes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 37 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Review
- Chemotherapy-induced oxidative injury in pediatric acute lymphoblastic leukemia: The role of N-acetylcysteine (Review).Biomedical reports · 2026Review
- XPF mediates 3' flap processing for FEN1-independent Okazaki fragment maturation.Nucleic acids research · 2026Article
- The Mechanism of Gut Microbiota in Breast Cancer Based on the Bulk Transcriptome, Mendelian Randomization Analysis and Single Cell RNA Sequencing.MicrobiologyOpen · 2026Article
- DNA methyltransferase inhibitors in oncology: clinical progress, limitations and future directions.Epigenomics · 2026Review
- Ruthenium(II)-Arene Complexes: Biomolecular Binding, Thermodynamic Insights, and Selective Cytotoxicity.ACS omega · 2026Article
- Synthetic lethality and DNA damage response targeting in cancer stem cells: a comprehensive review.Discover oncology · 2026Review
- Glycolysis-related MiRNA signature predicts prognosis, recurrence risk, and therapeutic responses in hepatocellular carcinoma.Scientific reports · 2025Article
- Translational Aspects of DNA Damage Repair in Optimizing Cancer Chemotherapy.Advanced genetics (Hoboken, N.J.) · 2025Review
- XPF mediates 3' flap processing for FEN1-independent Okazaki fragment maturation.bioRxiv : the preprint server for biology · 2025Article
- Occurrence, Properties, Applications and Analytics of Cytosine and Its Derivatives.Molecules (Basel, Switzerland) · 2025Review
- Deciphering the prognostic signature of nonsmall cell lung cancer using cisplatin resistance and circulating tumor cell-related gene analysis.3 Biotech · 2025Article
- DNA repair and the contribution to chemotherapy resistance.Genome medicine · 2025Review
- The Quantum Paradox in Pharmaceutical Science: Understanding Without Comprehending-A Centennial Reflection.International journal of molecular sciences · 2025Review
- Computational inference of co-regulatory modules from transcription factors, MicroRNAs, and their targets using CanMod2.Scientific reports · 2025Article
- Targeting PCNA/PARP1 axis inhibits the malignant progression of hepatocellular carcinoma.Frontiers in pharmacology · 2025Article
- GETgene-AI: a framework for prioritizing actionable cancer drug targets.Frontiers in systems biology · 2025Article
- TMOD2 and DOCK4 as Novel Gut Microbiota-Associated Biomarkers for Colorectal Adenoma: Integrated Transcriptomic Analysis and Therapeutic Target Identification.Mediators of inflammation · 2025Article
- Targeting MDM2, RAS, and PCNA for cancer targeted therapy: pan-cancer approaches vs. cancer-specific strategies.Frontiers in pharmacology · 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This article reviews the currently used therapeutic strategies to target DNA replication stress for cancer treatment in the clinic, highlighting their effectiveness and limitations due to toxicity and drug resistance. Cancer cells experience enhanced spontaneous DNA damage due to compromised DNA replication machinery, elevated levels of reactive oxygen species, loss of tumor suppressor genes, and/or constitutive activation of oncogenes. Consequently, these cells are addicted to DNA damage response signaling pathways and repair machinery to maintain genome stability and support survival and proliferation. Chemotherapeutic drugs exploit this genetic instability by inducing additional DNA damage to overwhelm the repair system in cancer cells. However, the clinical use of DNA-damaging agents is limited by their toxicity and drug resistance often arises. To address these issues, the article discusses a potential strategy to target the cancer-associated isoform of proliferating cell nuclear antigen (caPCNA), which plays a central role in the DNA replication and damage response network. Small molecule and peptide agents that specifically target caPCNA can selectively target cancer cells without significant toxicity to normal cells or experimental animals.
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.