ArticleNature cancer2024
Small-molecule inhibition of kinesin KIF18A reveals a mitotic vulnerability enriched in chromosomally unstable cancers.
Article in Nature cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 55 citations in OpenAlex.
- KIF18A inhibitor prevents chromosomally unstable osteosarcoma growth by activating spindle assembly checkpoint.Cancer biology & therapy · 2026Article
- KIF18A knockdown enhances oxidative phosphorylation, suggesting a metabolic basis for antiviral activity against influenza A virus.Genes & genomics · 2026Article
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Kinesins in Cancer Drug Resistance: Mechanisms, Therapeutic Targeting, and Translational Potential.Cancers · 2026Review
- Spindle Assembly Checkpoint Competency Determines Sensitivity to KIF18A Inhibition in Small Cell Lung Cancer.Cancer research communications · 2026Article
- Genomic landscape and tumor immune microenvironment of osteosarcoma: Bridging mechanistic insights to precision therapeutics.Bone reports · 2026Review
- A bioinformatics analysis of KIF transcriptomic subtyping reveals prognostic heterogeneity and differential therapeutic responses in cervical cancer.Oncology letters · 2026Article
- Incorporation of Organosilicon Motifs in Natural and Synthetic Small Molecules for Anticancer Therapeutics: Current Perspectives and Future Opportunities in Drug Design.Molecules (Basel, Switzerland) · 2026Review
- Acidosis-associated gene signature defines novel subtypes and dual-target therapeutic candidates in breast cancer.Journal of translational medicine · 2026Article
- Switchable annulation paths to diverse N-bridged bicyclic scaffolds via ligand-directed dicarbonylation.Nature communications · 2026Article
- Molecular and Cell Biological Characterization of Patient-Derived Head and Neck Squamous Carcinoma Cell Lines.Cancer science · 2026Article
- Simultaneous CRISPR/Cas9-induced double-strand breaks are lethal in models of pancreatic cancer.The Journal of clinical investigation · 2026Article
- KIF18A Maintains Kinetochore-Microtubule Attachments in CIN Cells by Limiting Microtubule Polymerization.bioRxiv : the preprint server for biology · 2026Article
- Identification of a novel platelet-related prognostic model for hepatocellular carcinoma.Discover oncology · 2026Article
- Epigenetic Regulation of Chromosomal Instability by EZH2 Methyltransferase.Cancer discovery · 2026Article
- Emerging hallmarks and the rise of complexities and heterogeneity of tumor.Biochemistry and biophysics reports · 2025Review
- Article
- KIF18A promotes chromosome congression in cooperation with CENP-E downstream of CENP-C.Cell reports · 2025Article
- Centromere protein I facilitates breast cancer tumorigenesis and disease progression through modulation of Wnt/β-Catenin signaling.Cancer cell international · 2025Article
- Kinesin superfamily proteins in ovarian cancer: from molecular mechanisms to clinical applications.Medical oncology (Northwood, London, England) · 2025Review
Corrections and comments
- Commented on by
Authors and funding
29 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal instability (CIN) is a hallmark of cancer, caused by persistent errors in chromosome segregation during mitosis. Aggressive cancers like high-grade serous ovarian cancer (HGSOC) and triple-negative breast cancer (TNBC) have a high frequency of CIN and TP53 mutations. Here, we show that inhibitors of the KIF18A motor protein activate the mitotic checkpoint and selectively kill chromosomally unstable cancer cells. Sensitivity to KIF18A inhibition is enriched in TP53-mutant HGSOC and TNBC cell lines with CIN features, including in a subset of CCNE1-amplified, CDK4-CDK6-inhibitor-resistant and BRCA1-altered cell line models. Our KIF18A inhibitors have minimal detrimental effects on human bone marrow cells in culture, distinct from other anti-mitotic agents. In mice, inhibition of KIF18A leads to robust anti-cancer effects with tumor regression observed in human HGSOC and TNBC models at well-tolerated doses. Collectively, our results provide a rational therapeutic strategy for selective targeting of CIN cancers via KIF18A inhibition.
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.