ArticleOncogene2022
Oncogenic RAS sensitizes cells to drug-induced replication stress via transcriptional silencing of P53.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- E2F3 amplification primes bladder cancer cells for premature mitosis.Cancer gene therapy · 2026Article
- Poly ADP Ribose Polymerase Inhibitors Potentiate Proton Therapy End-of-Range Effects by Accelerating Replication Forks and Promoting Transcription Conflict.International journal of radiation oncology, biology, physics · 2026Article
- Identification of small GTPases as potential target proteins of the mycotoxin and renal carcinogen ochratoxin A.Archives of toxicology · 2026Article
- Predicting Clinical Prognosis and Treatment Response in Glioblastoma Based on Gene Replication Stress-Related Features.Current medicinal chemistry · 2026Article
- Mitotic DNA repair by TMEJ suppresses replication stress-induced nuclear envelope reassembly defect.Nature communications · 2025Article
- Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs.Biomolecules · 2025Review
- Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance.Molecular oncology · 2025Article
- RECQ4-MUS81 interaction contributes to telomere maintenance with implications to Rothmund-Thomson syndrome.Nature communications · 2025Article
- Chemotherapy-induced intestinal epithelial damage directly promotes galectin-9-driven modulation of T cell behavior.iScience · 2024Article
- Endogenous oncogenic KRAS expression increases cell proliferation and motility in near-diploid hTERT RPE-1 cells.The Journal of biological chemistry · 2024Article
- ERK pathway agonism for cancer therapy: evidence, insights, and a target discovery framework.NPJ precision oncology · 2024Review
- Key Proteins of Replication Stress Response and Cell Cycle Control as Cancer Therapy Targets.International journal of molecular sciences · 2024Review
- Rewiring glucose metabolism improves 5-FU efficacy in p53-deficient/KRASCommunications biology · 2022Article
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Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells often experience high basal levels of DNA replication stress (RS), for example due to hyperactivation of oncoproteins like MYC or RAS. Therefore, cancer cells are considered to be sensitive to drugs that exacerbate the level of RS or block the intra S-phase checkpoint. Consequently, RS-inducing drugs including ATR and CHK1 inhibitors are used or evaluated as anti-cancer therapies. However, drug resistance and lack of biomarkers predicting therapeutic efficacy limit efficient use. This raises the question what determines sensitivity of individual cancer cells to RS. Here, we report that oncogenic RAS does not only enhance the sensitivity to ATR/CHK1 inhibitors by directly causing RS. Instead, we observed that HRAS
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