ReviewFrontiers in oncology2014
Size Does Matter: Why Polyploid Tumor Cells are Critical Drug Targets in the War on Cancer.
Review in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
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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.
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Who cites it
127 citing papers in PubMed.
- Atypical fusion among non-malignant cells: Unveiling the link between post-fusion-induced genome chaos and cancer initiation.Cancer cell international · 2026Article
- Ploidy-Dependent Response to Anticancer Drugs of Human Embryonic Stem Cells.Cell proliferation · 2026Article
- Clinical Implications of Polyploid Giant Cancer Cells in Solid Tumors: Biology, Diagnosis, and Therapeutic Considerations.Cancers · 2026Review
- Autophagy is essential for survival and function of polyploid giant cancer cells under therapeutic stress.Cancer letters · 2026Article
- Simultaneous CRISPR/Cas9-induced double-strand breaks are lethal in models of pancreatic cancer.The Journal of clinical investigation · 2026Article
- Polyploid and Chromosomal Copy Number Gain Cells in Metastatic Colon Cancer: Exploratory Genotype-Phenotype Correlations.Cancers · 2026Article
- Mapping the Progression of Therapy-Induced Senescence to Therapy Tolerance: An Evolutionarily Conserved Mechanism for Optimizing Cancer Treatment with Senotherapeutics.ACS pharmacology & translational science · 2025Article
- Decoding cancer dormancy: integrative genomic, phenotypic and live-cell imaging analysis to reveal the hidden cancer cell reservoir.Molecular cancer · 2025Review
- In situ phenotypic and karyotypic co-detection of aneuploid TCs and TECs in cytological specimens with abnormal cervical screening results.BMC cancer · 2025Article
- Article
- Polyploidy of MDA-MB-231 cells drives increased extravasation with enhanced cell-matrix adhesion.APL bioengineering · 2025Article
- Amitotic Cell Division, Malignancy, and Resistance to Anticancer Agents: A Tribute to Drs. Walen and Rajaraman.Cancers · 2024Article
- Towards Digital Quantification of Ploidy from Pan-Cancer Digital Pathology Slides using Deep Learning.bioRxiv : the preprint server for biology · 2024Article
- Metabolic reprogramming of poly(morpho)nuclear giant cells determines glioblastoma recovery from doxorubicin-induced stress.Journal of translational medicine · 2024Article
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- Changing the Landscape of Solid Tumor Therapy from Apoptosis-Promoting to Apoptosis-Inhibiting Strategies.Current issues in molecular biology · 2024Review
- Preclinical Evaluation of JAB-2485, a Potent AURKA Inhibitor with High Selectivity and Favorable Pharmacokinetic Properties.ACS omega · 2024Article
- The microtubule targeting agent ST-401 triggers cell death in interphase and prevents the formation of polyploid giant cancer cells.Journal of translational medicine · 2024Article
- Polyploidy and mTOR signaling: a possible molecular link.Cell communication and signaling : CCS · 2024Review
- Tumor acidosis-induced DNA damage response and tetraploidy enhance sensitivity to ATM and ATR inhibitors.EMBO reports · 2024Article
67 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor evolution presents a formidable obstacle that currently prevents the development of truly curative treatments for cancer. In this perspective, we advocate for the hypothesis that tumor cells with significantly elevated genomic content (polyploid tumor cells) facilitate rapid tumor evolution and the acquisition of therapy resistance in multiple incurable cancers. We appeal to studies conducted in yeast, cancer models, and cancer patients, which all converge on the hypothesis that polyploidy enables large phenotypic leaps, providing access to many different therapy-resistant phenotypes. We develop a flow-cytometry based method for quantifying the prevalence of polyploid tumor cells, and show the frequency of these cells in patient tumors may be higher than is generally appreciated. We then present recent studies identifying promising new therapeutic strategies that could be used to specifically target polyploid tumor cells in cancer patients. We argue that these therapeutic approaches should be incorporated into new treatment strategies aimed at blocking tumor evolution by killing the highly evolvable, therapy-resistant polyploid cell subpopulations, thus helping to maintain patient tumors in a drug sensitive state.
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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.