ReviewOncogene2012
Checkpoint control and cancer.
Review in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed.
- Synergistic Effects of DNA-PKcs Inhibition and Radiotherapy in Esophageal Squamous Cell Carcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Essential genetic mutations impair DNA damage repair and modulate tumor immune microenvironment in ccRCC.MedScience · 2026Review
- Enhanced Ciliogenesis of Human Bronchial Epithelial Cells by Simulated Microgravity.Life (Basel, Switzerland) · 2025Article
- Quinalizarin induces autophagy, apoptosis and mitotic catastrophe in cervical and prostate cancer cells.Scientific reports · 2025Article
- Regulatory influence of α-Pinene on MATN3 expression in hepatocellular carcinoma: Extending to pan-cancer analysis.PloS one · 2025Article
- A fast-acting lipid checkpoint in G1 prevents mitotic defects.Nature communications · 2024Article
- Knockdown of TFAP2E results in rapid GOncology letters · 2024Article
- Article
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy.Cell & bioscience · 2022Article
- Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway.Cell death and differentiation · 2022Article
- LRSAM1 E3 Ubiquitin Ligase Promotes Choriocarcinoma Progression and Metastasis via p53/p21 Signaling Impediment.BioMed research international · 2022Article
- miR-155, miR-21, and let-7a Expressions in MCF-10A and MCF-7 Cell Lines after Low to High Dose Irradiation.Cell journal · 2021Article
- The effects of T-DXd on the expression of HLA class I and chemokines CXCL9/10/11 in HER2-overexpressing gastric cancer cells.Scientific reports · 2021Article
- Balancing DNA repair to prevent ageing and cancer.Experimental cell research · 2021Review
- Toward Multitasking Pharmacological COX-Targeting Agents: Non-Steroidal Anti-Inflammatory Prodrugs with Antiproliferative Effects.Molecules (Basel, Switzerland) · 2021Article
- Single nucleotide polymorphisms in breast cancer susceptibility gene 1 are associated with susceptibility to lung cancer.Oncology letters · 2021Article
- The State-of-the-Art of Phase II/III Clinical Trials for Targeted Pancreatic Cancer Therapies.Journal of clinical medicine · 2021Review
- Cell cycle inertia underlies a bifurcation in cell fates after DNA damage.Science advances · 2021Article
- H4K20 monomethylation inhibition causes loss of genomic integrity in mouse preimplantation embryos.The Journal of reproduction and development · 2020Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-damaging therapies represent the most frequently used non-surgical anticancer strategies in the treatment of human tumors. These therapies can kill tumor cells, but at the same time they can be particularly damaging and mutagenic to healthy tissues. The efficacy of DNA-damaging treatments can be improved if tumor cell death is selectively enhanced, and the recent application of poly-(ADP-ribose) polymerase inhibitors in BRCA1/2-deficient tumors is a successful example of this. DNA damage is known to trigger cell-cycle arrest through activation of DNA-damage checkpoints. This arrest can be reversed once the damage has been repaired, but irreparable damage can promote apoptosis or senescence. Alternatively, cells can reenter the cell cycle before repair has been completed, giving rise to mutations. In this review we discuss the mechanisms involved in the activation and inactivation of DNA-damage checkpoints, and how the transition from arrest and cell-cycle re-entry is controlled. In addition, we discuss recent attempts to target the checkpoint in anticancer strategies.
Indexed as
Identifiers
21963855What 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.