ArticleGenes, chromosomes & cancer2012
Spontaneous transformation of murine epithelial cells requires the early acquisition of specific chromosomal aneuploidies and genomic imbalances.
Article in Genes, chromosomes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
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- The Value of DNA Quantitative Cytology Test for the Screening of Endometrial Cancer.Cancer management and research · 2019Article
- Stochastic changes in gene expression promote chaotic dysregulation of homeostasis in clonal breast tumors.Communications biology · 2019Article
- Increased insulin-like growth factor 1 production by polyploid adipose stem cells promotes growth of breast cancer cells.BMC cancer · 2018Article
- SMYD5 Controls Heterochromatin and Chromosome Integrity during Embryonic Stem Cell Differentiation.Cancer research · 2017Article
- Norovirus Cell Tropism Is Determined by Combinatorial Action of a Viral Non-structural Protein and Host Cytokine.Cell host & microbe · 2017Article
- CRISPR/CAS9 Technologies.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Review
- Novel mouse model recapitulates genome and transcriptome alterations in human colorectal carcinomas.Genes, chromosomes & cancer · 2017Article
- Simulated space radiation-induced mutants in the mouse kidney display widespread genomic change.PloS one · 2017Article
- Development of a cell line from the American eel brain expressing endothelial cell properties.In vitro cellular & developmental biology. Animal · 2016Article
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- Widespread Non-Canonical Epigenetic Modifications in MMTV-NeuT Breast Cancer.Neoplasia (New York, N.Y.) · 2015Article
- The shock of being united and symphiliosis. Another lesson from plants?Cell cycle (Georgetown, Tex.) · 2014Article
- Aneuploidy, oncogene amplification and epithelial to mesenchymal transition define spontaneous transformation of murine epithelial cells.Carcinogenesis · 2013Article
- The pivotal role of IKKα in the development of spontaneous lung squamous cell carcinomas.Cancer cell · 2013Article
- Immunosurveillance against tetraploidization-induced colon tumorigenesis.Cell cycle (Georgetown, Tex.) · 2013Article
- Inflammation-mediated genetic and epigenetic alterations drive cancer development in the neighboring epithelium upon stromal abrogation of TGF-β signaling.PLoS genetics · 2013Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Human carcinomas are defined by recurrent chromosomal aneuploidies, which result in a tissue-specific distribution of genomic imbalances. In order to develop models for these genome mutations and to determine their role in tumorigenesis, we generated 45 spontaneously transformed murine cell lines from normal epithelial cells derived from bladder, cervix, colon, kidney, lung, and mammary gland. Phenotypic changes, chromosomal aberrations, centrosome number, and telomerase activity were assayed in control uncultured cells and in three subsequent stages of transformation. Supernumerary centrosomes, binucleate cells, and tetraploidy were observed as early as 48 hr after explantation. In addition, telomerase activity increased throughout progression. Live-cell imaging revealed that failure of cytokinesis, not cell fusion, promoted genome duplication. Spectral karyotyping demonstrated that aneuploidy preceded immortalization, consisting predominantly of whole chromosome losses (4, 9, 12, 13, 16, and Y) and gains (1, 10, 15, and 19). After transformation, focal amplifications of the oncogenes Myc and Mdm2 were frequently detected. Fifty percent of the transformed lines resulted in tumors on injection into immunocompromised mice. The phenotypic and genomic alterations observed in spontaneously transformed murine epithelial cells recapitulated the aberration pattern observed during human carcinogenesis. The dominant aberration of these cell lines was the presence of specific chromosomal aneuploidies. We propose that our newly derived cancer models will be useful tools to dissect the sequential steps of genome mutations during malignant transformation, and also to identify cancer-specific genes, signaling pathways, and the role of chromosomal instability in this process.
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