ReviewBritish journal of cancer2015
Hitting the brakes: targeting microtubule motors in cancer.
Review in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed.
- Molecular Dynamics Simulations Provide Further Insights into the Allosteric Regulation of the Kinesin-5 Motor Domain by Loop 5.Journal of chemical information and modeling · 2026Article
- Article
- KIF15 promotes the development and progression of chordoma via activating PI3K-AKT signalling pathway.Heliyon · 2024Article
- Article
- Microtubule-Targeting Agents: Disruption of the Cellular Cytoskeleton as a Backbone of Ovarian Cancer Therapy.Advances in experimental medicine and biology · 2024Review
- Synthesis and bioactive evaluation ofRSC medicinal chemistry · 2023Article
- Electro-detachment of kinesin motor domain from microtubule in silico.Computational and structural biotechnology journal · 2023Article
- Design, synthesis, and biological screening of a series of 4'-fluoro-benzotriazole-acrylonitrile derivatives as microtubule-destabilising agents (MDAs).Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Upregulation of KIF18B facilitates malignant phenotype of esophageal squamous cell carcinoma by activating CDCA8/mTORC1 pathway.Journal of clinical laboratory analysis · 2022Article
- Activation of STAT3 through combined SRC and EGFR signaling drives resistance to a mitotic kinesin inhibitor in glioblastoma.Cell reports · 2022Article
- Coordination of two kinesin superfamily motor proteins, KIF3A and KIF13A, is essential for pericellular matrix degradation by membrane-type 1 matrix metalloproteinase (MT1-MMP) in cancer cells.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- KIF13A-A Key Regulator of Recycling Endosome Dynamics.Frontiers in cell and developmental biology · 2022Review
- Review
- Pan-cancer analysis of pathway-based gene expression pattern at the individual level reveals biomarkers of clinical prognosis.Cell reports methods · 2021Article
- Mechanisms by Which Kinesin-5 Motors Perform Their Multiple Intracellular Functions.International journal of molecular sciences · 2021Review
- MiR-19a/miR-96-mediated low expression of KIF26A suppresses metastasis by regulating FAK pathway in gastric cancer.Oncogene · 2021Article
- Ixabepilone: Overview of Effectiveness, Safety, and Tolerability in Metastatic Breast Cancer.Frontiers in oncology · 2021Review
- Design, synthesis, and biological evaluation of novel 5,6,7-trimethoxy quinolines as potential anticancer agents and tubulin polymerization inhibitors.Iranian journal of basic medical sciences · 2020Article
- KIF11 and KIF15 mitotic kinesins are potential therapeutic vulnerabilities for malignant peripheral nerve sheath tumors.Neuro-oncology advances · 2020Article
- Antitumor Potential of the Isoflavonoids (+)- and (-)-2,3,9-Trimethoxypterocarpan: Mechanism-of-Action Studies.ACS medicinal chemistry letters · 2020Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Despite the growing number of therapies that target cancer-specific pathways, cytotoxic treatments remain important clinical tools. The rationale for targeting cell proliferation by chemotherapeutic agents stems from the assumption that tumours harbour a greater fraction of actively dividing cells than normal tissues. One such group of cytotoxic drugs impair microtubule polymers, which are cytoskeletal components of cells essential for many processes including mitosis. However, in addition to their antimitotic action, these agents cause debilitating and dose-limiting neurotoxicity because of the essential functions of microtubules in neurons. To overcome this limitation, drugs against mitosis-specific targets have been developed over the past decade, albeit with variable clinical success. Here we review the key lessons learnt from antimitotic therapies with a focus on inhibitors of microtubule motor proteins. Furthermore, based on the cancer genome data, we describe a number of motor proteins with tumour type-specific alterations, which warrant further investigation in the quest for cytotoxic targets with increased cancer specificity.
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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.