ReviewTrends in cancer2020
Why Great Mitotic Inhibitors Make Poor Cancer Drugs.
Review in Trends in cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed.
- Reconstruction of septin higher-order nano-size structures in ovarian cancer cells uncover susceptibility to the septin-targeting small molecule UR214-9.bioRxiv : the preprint server for biology · 2026Article
- Synthesis and Development of 3-((2,4-Difluorophenyl)Amino)Propanoic Acid Derivatives as an Antiproliferative Medicinal Chemistry Scaffold Targeting Growth Factor Receptors.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Epigenetic Regulation of Chromosomal Instability by EZH2 Methyltransferase.Cancer discovery · 2026Article
- Biological clocks keep a watch on mitosis.Nature cell biology · 2026Review
- Advancing Cancer Immunotherapy: Chimeric Antigen Receptor (CAR)-T Cell Engineering through Novel Screening Methods.Biomolecules & therapeutics · 2026Review
- Anti-Cancer Activity ofMarine drugs · 2025Article
- The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ.Nature communications · 2025Article
- Temporal control of human DNA replication licensing by CDK4/6-RB signalling and chemical genetics.Nature communications · 2025Article
- Co-Encapsulation of Multiple Antineoplastic Agents in Liposomes by Exploring Microfluidics.International journal of molecular sciences · 2025Review
- The Persistent Power of the Taxane/Platin Chemotherapy.Cancers · 2025Review
- Targeting chromosomally unstable tumors with a selective KIF18A inhibitor.Nature communications · 2025Article
- The Second Selectivity of Taxanes to Malignant Cells --- Nuclear Envelope Malleability.Journal of Cancer · 2025Article
- Lessons learned from 20 years of preclinical testing in pediatric cancers.Pharmacology & therapeutics · 2024Review
- Uncovering Cell Cycle Dysregulations and Associated Mechanisms in Cancer and Neurodegenerative Disorders: A Glimpse of Hope for Repurposed Drugs.Molecular neurobiology · 2024Review
- Centrosome amplification primes ovarian cancer cells for apoptosis and potentiates the response to chemotherapy.PLoS biology · 2024Article
- PDZ-Binding Kinase, a Novel Regulator of Vascular Remodeling in Pulmonary Arterial Hypertension.Circulation · 2024Article
- Use of Drug Sensitisers to Improve Therapeutic Index in Cancer.Pharmaceutics · 2024Review
- Phenotypic targeting using magnetic nanoparticles for rapid characterization of cellular proliferation regulators.Science advances · 2024Article
- Repurposing screen identifies novel candidates for broad-spectrum coronavirus antivirals and druggable host targets.Antimicrobial agents and chemotherapy · 2024Article
- Glial cell-derived soluble factors increase the metastatic potential of pancreatic adenocarcinoma cells and induce epithelial-to-mesenchymal transition.Journal of cancer research and clinical oncology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Chemotherapy is central to oncology, perceived to operate only on prolific cancerous tissue. Yet, many non-neoplastic tissues are more prolific compared with typical tumors. Chemotherapies achieve sufficient therapeutic windows to exert antineoplastic activity because they are prodrugs that are bioactivated in cancer-specific environments. The advent of precision medicine has obscured this concept, favoring the development of high-potency kinase inhibitors. Inhibitors of essential mitotic kinases exemplify this paradigm shift, but intolerable on-target toxicities in more prolific normal tissues have led to repeated failures in the clinic. Proliferation rates alone cannot be used to achieve cancer specificity. Here, we discuss integrating the cancer specificity of prodrugs from classical chemotherapeutics and the potency of mitotic kinase inhibitors to generate a class of high-precision cancer therapeutics.
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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.