ArticleOncotarget2010
The requirement of p53 for maintaining chromosomal stability during tetraploidization.
Article in Oncotarget, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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Who cites it
30 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
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- Review
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
- Genomic and prognostic heterogeneity among RAS/BRAFMolecular oncology · 2021Article
- Somatic Sex: On the Origin of Neoplasms With Chromosome Counts in Uneven Ploidy Ranges.Frontiers in cell and developmental biology · 2021Article
- Characterizing genomic differences of human cancer stratified by the TP53 mutation status.Molecular genetics and genomics : MGG · 2018Article
- Survivin protects fused cancer cells from cell death.BMB reports · 2017Article
- Cancer cell-secreted IGF2 instigates fibroblasts and bone marrow-derived vascular progenitor cells to promote cancer progression.Nature communications · 2017Article
- Establishment of Proliferative Tetraploid Cells from Nontransformed Human Fibroblasts.Journal of visualized experiments : JoVE · 2017Article
- Disentangling the aneuploidy and senescence paradoxes: a study of triploid breast cancers non-responsive to neoadjuvant therapy.Histochemistry and cell biology · 2016Article
- Tetraploid cells produced by absence of substrate adhesion during cytokinesis are limited in their proliferation and enter senescence after DNA replication.Cell cycle (Georgetown, Tex.) · 2016Article
- Immunosuppressants in cancer prevention and therapy.Oncoimmunology · 2013Review
- Pan-cancer patterns of somatic copy number alteration.Nature genetics · 2013Article
- Elucidation of proliferative capability of mononuclear tetraploid cells, emerging spontaneously from diploid cells, using image cytometry and fluorescence in situ hybridization.Cell proliferation · 2013Article
- Establishment of proliferative tetraploid cells from normal human fibroblasts.Frontiers in oncology · 2013Article
- G-CSF prevents progression of diabetic nephropathy in rat.PloS one · 2013Article
- p53 expression controls prostate cancer sensitivity to chemotherapy and the MDM2 inhibitor Nutlin-3.Cell cycle (Georgetown, Tex.) · 2012Article
- p63 the guardian of human reproduction.Cell cycle (Georgetown, Tex.) · 2012Review
- Tissue-specific expression of p73 C-terminal isoforms in mice.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tetraploidization is believed to promote genome instability and tumorigenesis. Whether tetraploids per se are intrinsically unstable and transforming remain incompletely understood. In this report, tetraploidization was induced with cell fusion using mouse fibroblasts. Due to the unequal segregation of chromosomes during multipolar mitosis, the majority of cells were eliminated by p53-dependent mechanisms after tetraploidization. The rare tetraploid fibroblasts that were able to undergo bipolar mitosis remained chromosomally stable and nontransformed over many generations. Suppression of p53 functions during tetraploidization, either by RNA interference or by using p53-deficient mouse fibroblasts, produced cells that were chromosomally unstable. They were fast growing and displayed anchorage-independent growth in soft agar. In contrast, impairment of p53 functions after tetraploids were established was ineffective in triggering chromosomal instability and transformation. Collectively, these results are consistent with a model that during early stages of tetraploidization, the lack of p53 promotes the survival of chromosomally unstable sub-tetraploids, leading to transformation. Once tetraploids are established, however, p53 is not essential for maintaining chromosome stability.
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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.