ReviewGenes2016
Targeting DNA Replication Stress for Cancer Therapy.
Review in Genes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 93 citations in OpenAlex.
- A Phase II Study of Berzosertib in Combination with Carboplatin Compared with Docetaxel with Carboplatin in Metastatic Castration-Resistant Prostate Cancer.Cancer research communications · 2026Trial
- BAYESIAN EMPIRICAL LIKELIHOOD FOR ULTRA-HIGH DIMENSIONAL VARIABLE SELECTION WITH APPLICATION TO DRUG SENSITIVITY.The annals of applied statistics · 2026Article
- Targeting the DNA damage response prevents regrowth of colorectal peritoneal metastasis-derived organoids following treatment with mitomycin C.British journal of cancer · 2026Article
- Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization.Current issues in molecular biology · 2026Review
- Enhanced Anti-Leukemic Activity of Platinum Lamivudine Compared To Lamivudine Through Differential Gene Regulation and DNA Groove Binding.Cell biochemistry and biophysics · 2025Article
- A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells.Nature communications · 2025Article
- Article
- Case Report: Successful delivery following chemotherapy in a pregnant patient with metastatic SMARCB1-deficient renal medullary carcinoma.Frontiers in oncology · 2025Article
- Prognostic value and potential biological function ofJournal of thoracic disease · 2024Article
- Cancer Mutations Converge on a Collection of Protein Assemblies to Predict Resistance to Replication Stress.Cancer discovery · 2024Article
- Pancreatic Cancer:Cancers · 2023Review
- Studying the DNA damage response pathway in hematopoietic canine cancer cell lines, a necessary step for finding targets to generate new therapies to treat cancer in dogs.Frontiers in veterinary science · 2023Article
- SLU7: A New Hub of Gene Expression Regulation-From Epigenetics to Protein Stability in Health and Disease.International journal of molecular sciences · 2022Review
- Functional screening reveals HORMAD1-driven gene dependencies associated with translesion synthesis and replication stress tolerance.Oncogene · 2022Article
- Replication stress defines distinct molecular subtypes across cancers.Cancer research communications · 2022Article
- WEE1 inhibition augments CDC7 (DDK) inhibitor-induced cell death in Ewing sarcoma by forcing premature mitotic entry and mitotic catastrophe.Cancer research communications · 2022Article
- Perspective on the Use of DNA Repair Inhibitors as a Tool for Imaging and Radionuclide Therapy of Glioblastoma.Cancers · 2022Review
- Targeting Cell Cycle Checkpoint Kinases to Overcome Intrinsic Radioresistance in Brain Tumor Cells.Cancers · 2022Review
- Efficacy and safety of gemcitabine plus doxorubicin in patients with renal medullary carcinoma.Clinical genitourinary cancer · 2021Article
- Integrative meta-analysis of gene expression profiles identifies FEN1 and ENDOU as potential diagnostic biomarkers for cervical squamous cell carcinoma.Oncology letters · 2021Article
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 2 institutions in 1 country.
Funding
Abstract
The human cellular genome is under constant stress from extrinsic and intrinsic factors, which can lead to DNA damage and defective replication. In normal cells, DNA damage response (DDR) mediated by various checkpoints will either activate the DNA repair system or induce cellular apoptosis/senescence, therefore maintaining overall genomic integrity. Cancer cells, however, due to constitutive growth signaling and defective DDR, may exhibit "replication stress" -a phenomenon unique to cancer cells that is described as the perturbation of error-free DNA replication and slow-down of DNA synthesis. Although replication stress has been proven to induce genomic instability and tumorigenesis, recent studies have counterintuitively shown that enhancing replicative stress through further loosening of the remaining checkpoints in cancer cells to induce their catastrophic failure of proliferation may provide an alternative therapeutic approach. In this review, we discuss the rationale to enhance replicative stress in cancer cells, past approaches using traditional radiation and chemotherapy, and emerging approaches targeting the signaling cascades induced by DNA damage. We also summarize current clinical trials exploring these strategies and propose future research directions including the use of combination therapies, and the identification of potential new targets and biomarkers to track and predict treatment responses to targeting DNA replication stress.
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.