ReviewWorld journal of surgery2009
DNA damage response pathways in tumor suppression and cancer treatment.
Review in World journal of surgery, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 99 citations in OpenAlex.
- Multi-omics analysis and functional validation of CHEK1 as an independent prognostic biomarker in Pancreatic cancer.PloS one · 2026Article
- The mechanistic role of cardiac glycosides in DNA damage response and repair signaling.Cellular and molecular life sciences : CMLS · 2023Review
- Role of condensates in modulating DNA repair pathways and its implication for chemoresistance.The Journal of biological chemistry · 2023Review
- Molecular Targeted Therapies in Metastatic Prostate Cancer: Recent Advances and Future Challenges.Cancers · 2023Review
- A review of treatments targeting DNA-repair gene defects in metastatic castration resistant prostate cancer.Frontiers in oncology · 2023Review
- Anticancer potential of metformin: focusing on gastrointestinal cancers.Cancer chemotherapy and pharmacology · 2021Review
- PARP1 Upregulation in Recurrent Oral Cancer and Treatment Resistance.Frontiers in cell and developmental biology · 2021Article
- Prexasertib (LY2606368) reduces clonogenic survival by inducing apoptosis in primary patient-derived osteosarcoma cells and synergizes with cisplatin and talazoparib.International journal of cancer · 2020Article
- Article
- Phosphatase POPX2 interferes with cell cycle by interacting with Chk1.Cell cycle (Georgetown, Tex.) · 2020Article
- Article
- Review
- The dual PI3K/mTOR inhibitor BEZ235 restricts the growth of lung cancer tumors regardless of EGFR status, as a potent accompanist in combined therapeutic regimens.Journal of experimental & clinical cancer research : CR · 2019Article
- Targeting RNA-Polymerase I in Both Chemosensitive and Chemoresistant Populations in Epithelial Ovarian Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells.Environmental science and pollution research international · 2017Article
- Differential expression profile analysis of DNA damage repair genes in CD133Oncology letters · 2017Article
- "Back to a false normality": new intriguing mechanisms of resistance to PARP inhibitors.Oncotarget · 2017Review
- Short-term inhibition of TERT induces telomere length-independent cell cycle arrest and apoptotic response in EBV-immortalized and transformed B cells.Cell death & disease · 2016Article
- Pluripotent Stem Cells and DNA Damage Response to Ionizing Radiations.Radiation research · 2016Review
- Predictors and Modulators of Synthetic Lethality: An Update on PARP Inhibitors and Personalized Medicine.BioMed research international · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mammalian cells are frequently at risk of DNA damage from multiple sources. Accordingly, cells have evolved the DNA damage response (DDR) pathways to monitor the integrity of their genome. Conceptually, DDR pathways contain three major components (some with overlapping functions): sensors, signal transducers, and effectors. At the level of sensors, ATM (ataxia telangiectasia mutated) and ATR (ATM-Rad3-related) are proximal kinases that act as the core sensors of and are central to the entire DDR. These two kinases function to detect various forms of damaged DNA and trigger DNA damage response cascades. If cells harbor DDR defects and fail to repair the damaged DNA, it would cause genomic instability and, as a result, lead to cellular transformation. Indeed, deficiencies of DDR frequently occur in human cancers. Interestingly, this property of cancer also provides a great opportunity for cancer therapy. For example, by using a synthetic lethality model to search for the effective drugs, ChK1 inhibitors have been shown to selectively target the tumor cells with p53 mutations. In addition, the inhibitors of poly(ADP-ribose) polymerase (PARP-1) showed selectively killing effects on the cells with defects of homologous recombination (HR), particularly in the context of BRCA1/2 mutations. Since Brit1 is a key regulator in DDR and HR repair, we believe that we can develop a similar strategy to target cancers with Brit1 deficiency. Currently, we are conducting a high-throughput screening to identify novel compounds that specifically target the Brit1-deficient cancer which will lead to development of effective personalized drugs to cure cancer in clinic.
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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.