ReviewOncogene2010
Harnessing the complexity of DNA-damage response pathways to improve cancer treatment outcomes.
Review in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 139 citations in OpenAlex.
- CHK1 targets spleen tyrosine kinase (L) for proteolysis in hepatocellular carcinoma.The Journal of clinical investigation · 2012Trial
- Identification of Tumor- and Immunosuppression-Driven Glioblastoma Subtypes Characterized by Clinical Prognosis and Therapeutic Targets.Current issues in molecular biology · 2026Article
- Article
- An Evaluation of the Potential Radiosensitization Effect of Spherical Gold Nanoparticles to Induce Cellular Damage Using Different Radiation Qualities.Molecules (Basel, Switzerland) · 2025Article
- Deubiquitinating enzyme USP28 inhibitor AZ1 alone and in combination with cisplatin for the treatment of non-small cell lung cancer.Apoptosis : an international journal on programmed cell death · 2024Article
- Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies.Signal transduction and targeted therapy · 2023Review
- JSI-124 Induces Cell Cycle Arrest and Regulates the Apoptosis in Glioblastoma Cells.Biomedicines · 2023Article
- New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.International journal of molecular sciences · 2023Review
- Cell Survival, Death, and Proliferation in Senescent and Cancer Cells: the Role of (Poly)phenols.Advances in nutrition (Bethesda, Md.) · 2023Review
- Review
- SPAG5, the upstream protein of Wnt and the target of curcumin, inhibits hepatocellular carcinoma.Oncology reports · 2023Article
- Review
- Pyruvate Facilitates FACT-Mediated γH2AX Loading to Chromatin and Promotes the Radiation Resistance of Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Review
- Review
- Dehydrocrenatidine extracted fromOncology reports · 2021Article
- Antimicrobial peptide 17BIPHE2 inhibits the proliferation of lung cancer cellsOncology letters · 2021Article
- DNA-Binding Anticancer Drugs: One Target, Two Actions.Molecules (Basel, Switzerland) · 2021Review
- AKR1B10 confers resistance to radiotherapy via FFA/TLR4/NF-κB axis in nasopharyngeal carcinoma.International journal of biological sciences · 2021Article
- ZNF300 promotes chemoresistance and aggressive behaviour in non-small-cell lung cancer.Cell proliferation · 2020Article
18 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
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA-damage response (DDR) pathways consist of interconnected components that respond to DNA damage to allow repair and promote cell survival. The DNA repair pathways and downstream cellular responses have diverged in cancer cells compared with normal cells because of genetic alterations that underlie drug resistance, disabled repair and resistance to apoptosis. Consequently, abrogating DDR pathways represents an important mechanism for enhancing the therapeutic index of DNA-damaging anticancer agents. In this review, we discuss the DDR pathways that determine antitumor effects of DNA-damaging agents with a specific focus on treatment outcomes in tumors carrying a defective p53 pathway. Finely tuned survival and death pathways govern the cellular responses downstream of the cytotoxic insults inherent in anticancer treatment. The significance and relative contributions of cellular responses including apoptosis, mitotic catastrophe and senescence are discussed in relation to the web of molecular interactions that affect such outcomes. We propose that promising combinations of DNA-damaging anticancer treatments with DDR-pathway inhibition would be further enhanced by activating downstream apoptotic pathways. The proposed rationale ensures that actual cell death is the preferred outcome of cancer treatment instead of other responses, including reversible cell cycle arrest, autophagy or senescence. Finally, to better measure the contribution of different cellular responses to anticancer treatments, multiplex in vivo assessments of therapy-induced response pathways such as cell death, senescence and mitotic catastrophe is desirable rather than the current reliance on the measurement of a single response pathway such as apoptosis.
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.