ArticleCell cycle (Georgetown, Tex.)2015
Chromosomal instability, tolerance of mitotic errors and multidrug resistance are promoted by tetraploidization in human cells.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04203095 (Dynamic Monitor of Serum Chromosomal Instability Detected by UCAD as a Surrogate Biomarker of Treatment Efficacy in PD1 Inhibitor Based Immunotherapy for Lung Cancer Patients), which is not on this map. Cited by 128 papers.
What it found
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Dynamic Monitor of Serum Chromosomal Instability Detected by UCAD as a Surrogate Biomarker of Treatment Efficacy in PD1 Inhibitor Based Immunotherapy for Lung Cancer Patients
Who cites it
128 citing papers in PubMed, 185 citations in OpenAlex.
- Whole genome duplication through mitotic slippage causes nuclear instability.The EMBO journal · 2026Article
- Power-law scaling of mitotic spindles with genome sizes across eukaryotes is driven by chromosome crowding.Nature cell biology · 2026Article
- Lamin B1-dependent regulation of human separase in mitosis.Nucleic acids research · 2026Article
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- The immediate cellular response to whole-genome doubling is conserved across polyploid contexts.bioRxiv : the preprint server for biology · 2026Article
- Ploidy shapes gemcitabine response through altered potency and delayed cell death.bioRxiv : the preprint server for biology · 2026Article
- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Somatic copy number variation as a prognostic marker for recurrence in never-smokers with early-stage lung adenocarcinoma.International journal of cancer · 2026Article
- Profiling cell proliferation after whole-genome duplication in human cells.Biology open · 2026Article
- Cell and Nuclear Size Is Associated with Chromosomal Instability and Tumorigenicity in Cancer Cells That Undergo Whole Genome Doubling.Cancer research · 2026Article
- Sister chromatid separation determines the proliferative properties upon whole-genome duplication via homologous chromosome arrangement.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Protein Kinase D2 Regulates GRASP65 Phosphorylation and Golgi Ribbon Unlinking During G2/M Transition.Cells · 2026Article
- The Impact of Golgi Organization on Cell Cycle and Cancer Development.Sub-cellular biochemistry · 2026Review
- Modeling and targeting general and chromosome-specific aneuploidy in cancer.Genes & development · 2025Review
- Transcriptomic and Cytogenetic Analysis of Oxaliplatin-Resistant Colorectal Adenocarcinoma HCT116 Cells to Identify Markers Associated with Platinum Resistance.International journal of molecular sciences · 2025Article
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- Advances in tumor subclone formation and mechanisms of growth and invasion.Journal of translational medicine · 2025Review
68 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Up to 80% of human cancers, in particular solid tumors, contain cells with abnormal chromosomal numbers, or aneuploidy, which is often linked with marked chromosomal instability. Whereas in some tumors the aneuploidy occurs by missegregation of one or a few chromosomes, aneuploidy can also arise during proliferation of inherently unstable tetraploid cells generated by whole genome doubling from diploid cells. Recent findings from cancer genome sequencing projects suggest that nearly 40% of tumors underwent whole genome doubling at some point of tumorigenesis, yet its contribution to cancer phenotypes and benefits for malignant growth remain unclear. Here, we investigated the consequences of a whole genome doubling in both cancerous and non-transformed p53 positive human cells. SNP array analysis and multicolor karyotyping revealed that induced whole-genome doubling led to variable aneuploidy. We found that chromosomal instability (CIN) is a frequent, but not a default outcome of whole genome doubling. The CIN phenotypes were accompanied by increased tolerance to mitotic errors that was mediated by suppression of the p53 signaling. Additionally, the expression of pro-apoptotic factors, such as iASPP and cIAP2, was downregulated. Furthermore, we found that whole genome doubling promotes resistance to a broad spectrum of chemotherapeutic drugs and stimulates anchorage-independent growth even in non-transformed p53-positive human cells. Taken together, whole genome doubling provides multifaceted benefits for malignant growth. Our findings provide new insight why genome-doubling promotes tumorigenesis and correlates with poor survival in cancer.
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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.