ReviewJournal of cancer research and clinical oncology2023
Cyclins and cyclin-dependent kinases: from biology to tumorigenesis and therapeutic opportunities.
Review in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 50 citations in OpenAlex.
- CNN3 promotes vascular smooth muscle cells proliferation and migration to deteriorate atherosclerosis by β-catenin signaling pathway.Atherosclerosis plus · 2026Article
- The Role of Transcriptional and Atypical Cyclin-Dependent Protein Kinases in Melanoma.Cancers · 2026Review
- Review
- The Association of p27 With Prostate Cancer Outcomes: A Secondary Analysis of NRG/RTOG 8610 and 9202.Advances in radiation oncology · 2026Article
- Tumor necrosis factor α-induced endoplasmic reticulum stress promotes airway smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Article
- CDK2-Mediated Phosphorylation ofResearch (Washington, D.C.) · 2026Article
- Article
- Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with StrongJournal of medicinal chemistry · 2025Article
- Investigating miR-16-5p: The Tumor Suppressor That Influences Cell Cycle Genes in Colorectal Cancer.Journal of biomedical physics & engineering · 2025Article
- From cell cycle control to cancer therapy: exploring the role of CDK1 and CDK2 in tumorigenesis.Medical oncology (Northwood, London, England) · 2025Review
- MicroRNA‑21: A potential therapeutic target in lung cancer (Review).International journal of oncology · 2025Review
- Mechanism of Myh3 gene regulation of intramuscular fat content in Beijing black pigs via the MAPK signaling pathway.BMC genomics · 2025Article
- Botanical sources, biopharmaceutical profile, anticancer effects with mechanistic insight, toxicological and clinical evidence of prunetin: a literature review.Medical oncology (Northwood, London, England) · 2025Review
- Dinaciclib Interrupts Cell Cycle and Induces Apoptosis in Oral Squamous Cell Carcinoma: Mechanistic Insights and Therapeutic Potential.International journal of molecular sciences · 2025Article
- Recent advances on anticancer activity of benzodiazine heterocycles through kinase inhibition.RSC advances · 2025Review
- CDK2 inhibition sensitizes anthracycline-induced immunogenic cell death and enhances the efficacy of anti-PD-1 therapy.Frontiers in immunology · 2025Article
- The potential role of miR-155 in the tumorigenesis of cervical cancer.Frontiers in cell and developmental biology · 2025Review
- Anti-cancer effect of sodium pentaborate in combination with cisplatin on lung cancer cell lines.Molecular biology reports · 2024Article
- Cyclin-Dependent Kinase Inhibitors in the Rare Subtypes of Melanoma Therapy.Molecules (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discussion on cell proliferation cannot be continued without taking a look at the cell cycle regulatory machinery. Cyclin-dependent kinases (CDKs), cyclins, and CDK inhibitors (CKIs) are valuable members of this system and their equilibrium guarantees the proper progression of the cell cycle. As expected, any dysregulation in the expression or function of these components can provide a platform for excessive cell proliferation leading to tumorigenesis. The high frequency of CDK abnormalities in human cancers, together with their druggable structure has raised the possibility that perhaps designing a series of inhibitors targeting CDKs might be advantageous for restricting the survival of tumor cells; however, their application has faced a serious concern, since these groups of serine-threonine kinases possess non-canonical functions as well. In the present review, we aimed to take a look at the biology of CDKs and then magnify their contribution to tumorigenesis. Then, by arguing the bright and dark aspects of CDK inhibition in the treatment of human cancers, we intend to reach a consensus on the application of these inhibitors in clinical settings.
Indexed as
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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.