ReviewCell death & disease2012
Mitosis-targeted anti-cancer therapies: where they stand.
Review in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 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
156 citing papers in PubMed.
- Cdk1-phosphorylated Nur77 accumulates at the centrosome during mitosis to regulate the Cep192-PLK1 signaling axis.Cell death & disease · 2026Article
- Genome-Wide CRISPR Screens Identify ABCG2-Mediated Drug Resistance to the Threonine Tyrosine Kinase (TTK) Inhibitor CFI-402257 in Breast Cancer.International journal of molecular sciences · 2026Article
- Article
- The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ.Nature communications · 2025Article
- Upstream open reading frame translation enhances immunogenic peptide presentation in mitotically arrested cancer cells.Nature communications · 2025Article
- Exploring Experimental and In Silico Approaches for Antibody-Drug Conjugates in Oncology Therapies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Targeting receptor for activated C kinase 1 with a small molecule induces mitotic catastrophe and suppresses lipid metabolic reprogramming in hepatocellular carcinoma.Clinical and translational medicine · 2025Article
- Inhibition of p38-MK2 pathway enhances the efficacy of microtubule inhibitors in breast cancer cells.eLife · 2025Article
- Functionalized Niosomes for Co-Delivery of Curcumin and Imatinib Mesylate to Treat Breast Cancer: In Vitro and In Vivo Investigations.AAPS PharmSciTech · 2025Article
- Inhibition of p38-MK2 pathway enhances the efficacy of microtubule inhibitors in breast cancer cells.bioRxiv : the preprint server for biology · 2025Article
- Structure-based identification of Jervine as a potent dual-targeting inhibitor of cell cycle kinases.Frontiers in pharmacology · 2025Article
- DeSUMOylating isopeptidase 1 participates in the faithful chromosome segregation and vincristine sensitivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Article
- Harnessing bacterial metabolites for enhanced cancer chemotherapy: unveiling unique therapeutic potentials.Archives of microbiology · 2024Review
- HURP binding to the vinca domain of β-tubulin accounts for cancer drug resistance.Nature communications · 2024Article
- DNA repair is efficient in irradiated M phase zygotes.The Journal of reproduction and development · 2024Article
- A Novel 2-Methoxyestradiol Derivative: Disrupting Mitosis Inhibiting Cell Motility and Inducing Apoptosis in HeLa Cells In Vitro.Pharmaceutics · 2024Article
- Weakened APC/C activity at mitotic exit drives cancer vulnerability to KIF18A inhibition.The EMBO journal · 2024Article
- Dual TTK/PLK1 inhibition has potent anticancer activity in TNBC as monotherapy and in combination.Frontiers in oncology · 2024Article
- Synthesis and evaluation of tirbanibulin derivatives: a detailed exploration of the structure-activity relationship for anticancer activity.RSC advances · 2023Article
96 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The strategy of clinically targeting cancerous cells at their most vulnerable state during mitosis has instigated numerous studies into the mitotic cell death (MCD) pathway. As the hallmark of cancer revolves around cell-cycle deregulation, it is not surprising that antimitotic therapies are effective against the abnormal proliferation of transformed cells. Moreover, these antimitotic drugs are also highly selective and sensitive. Despite the robust rate of discovery and the development of mitosis-selective inhibitors, the unpredictable complexities of the human body's response to these drugs still herald the biggest challenge towards clinical success. Undoubtedly, the need to bridge the gap between promising preclinical trials and effective translational bedside treatment prompts further investigations towards mapping out the mechanistic pathways of MCD, understanding how these drugs work as medicine in the body and more comprehensive target validations. In this review, current antimitotic agents are summarized with particular emphasis on the evaluation of their clinical efficacy as well as their limitations. In addition, we discuss the basis behind the lack of activity of these inhibitors in human trials and the potential and future directions of mitotic anticancer strategies.
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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.