ReviewExpert opinion on therapeutic targets2010
Cyclin-dependent kinases (cdks) and the DNA damage response: rationale for cdk inhibitor-chemotherapy combinations as an anticancer strategy for solid tumors.
Review in Expert opinion on therapeutic targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 107 citations in OpenAlex.
- A Phase I Study of Dinaciclib in Combination With MK-2206 in Patients With Advanced Pancreatic Cancer.Clinical and translational science · 2020Trial
- Innovative strategies to overcome cancer drug resistance: from nanodelivery systems to targeted therapeutics.Discover oncology · 2026Review
- An Overview of the Mechanisms of HPV-Induced Cervical Cancer: The Role of Kinase Targets in Pathogenesis and Drug Resistance.Cancers · 2026Review
- Unraveling systemic responses to NQO1-activated IB-DNQ and Rucaparib single and dual agent therapy in triple-negative breast cancers.bioRxiv : the preprint server for biology · 2025Article
- CDK1 may promote breast cancer progression through AKT activation and immune modulation.Frontiers in oncology · 2025Article
- Targeting CDK1 and copper homeostasis in breast cancer via a nanopolymer drug delivery system.Cell biology and toxicology · 2024Article
- Exploiting spirooxindoles for dual DNA targeting/CDK2 inhibition and simultaneous mitigation of oxidative stress towards selective NSCLC therapy; synthesis, evaluation, and molecular modelling studies.RSC medicinal chemistry · 2024Article
- CDK-independent role of D-type cyclins in regulating DNA mismatch repair.Molecular cell · 2024Article
- CDK9-55 guides the anaphase-promoting complex/cyclosome (APC/C) in choosing the DNA repair pathway choice.Oncogene · 2024Article
- D-type cyclins regulate DNA mismatch repair in the G1 and S phases of the cell cycle, maintaining genome stability.bioRxiv : the preprint server for biology · 2024Article
- Bruceine D and Narclasine inhibit the proliferation of breast cancer cells and the prediction of potential drug targets.PloS one · 2024Article
- Advances with Lipid-Based Nanosystems for siRNA Delivery to Breast Cancers.Pharmaceuticals (Basel, Switzerland) · 2023Review
- CRISPR/Cas9 gene editing: a new approach for overcoming drug resistance in cancer.Cellular & molecular biology letters · 2022Review
- Radiotherapy resistance: identifying universal biomarkers for various human cancers.Journal of cancer research and clinical oncology · 2022Review
- Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response.International journal of molecular sciences · 2022Review
- Cell-penetrating peptides improve pharmacokinetics and pharmacodynamics of anticancer drugs.Tissue barriers · 2022Review
- The related miRNAs involved in doxorubicin resistance or sensitivity of various cancers: an update.Cancer chemotherapy and pharmacology · 2021Review
- Exploiting DNA Damage Repair in Precision Cancer Therapy: BRCA1 as a Prime Therapeutic Target.Cancers · 2021Review
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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 at 1 institution in 1 country.
Funding
Abstract
importance of the fieldThe eukaryotic cell division cycle is a tightly regulated series of events coordinated by the periodic activation of multiple cyclin-dependent kinases (cdks). Small-molecule cdk-inhibitory compounds have demonstrated preclinical synergism with DNA-damaging agents in solid tumor models. An improved understanding of how cdks regulate the DNA damage response now provides an opportunity for optimization of combinations of cdk inhibitors and DNA damaging chemotherapy agents that can be translated to clinical settings. AREAS COVERED IN THIS REVIEW: Here, we discuss novel work uncovering multiple roles for cdks in the DNA-damage-response network. First, they activate DNA damage checkpoint and repair pathways. Later their activity is turned off, resulting in cell cycle arrest, allowing time for DNA repair to occur. Recent clinical data on cdk inhibitor-DNA-damaging agent combinations are also discussed. WHAT THE READER WILL GAIN: Readers will learn about novel areas of cdk biology, the complexity of DNA damage signaling networks and clinical implications. TAKE HOME MESSAGE: New data demonstrate that cdks are 'master' regulators of DNA damage checkpoint and repair pathways. Cdk inhibition may therefore provide a means of potentiating the clinical activity of DNA-damaging chemotherapeutic agents for the treatment of cancer.
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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.