Duelli, D. M., Hearn, S., Myers, M. P., Lazebnik, Y. (November 2005) A primate virus generates transformed human cells by fusion. J Cell Biol, 171 (3). pp. 493-503. ISSN 0021-9525 (Print)
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Abstract
A model that explains both the origin and sporadic nature of cancer argues that cancer cells are a chance result of events that cause genomic and epigenetic variability. The prevailing view is that these events are mutations that affect chromosome segregation or stability. However, genomic and epigenetic variability is also triggered by cell fusion, which is often caused by viruses. Yet, cells fused by viruses are considered harmless because they die. We provide evidence that a primate virus uses both viral and exosomal proteins involved in cell fusion to produce transformed proliferating human cells. Although normal cells indeed fail to proliferate after fusion, expression of an oncogene or a mutated tumor suppressor p53 in just one of the fusion partners is sufficient to produce heterogeneous progeny. We also show that this virus can produce viable oncogenically transformed cells by fusing cells that are otherwise destined to die. Therefore, we argue that viruses can contribute to carcinogenesis by fusing cells.
| Item Type: | Paper |
|---|---|
| Uncontrolled Keywords: | Animals Cell Fusion Cell Line Cell Survival Cell Transformation Neoplastic Cell Transformation Viral Genes p53 Humans Hybrid Cells Mason-Pfizer monkey virus genetics physiology Mutation Oncogenes |
| Subjects: | diseases & disorders > cancer Investigative techniques and equipment > cell fusion bioinformatics > genomics and proteomics > genetics & nucleic acid processing > epigenetics bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > epigenetics |
| CSHL Authors: | |
| Communities: | CSHL labs > Labeznik lab |
| Depositing User: | CSHL Librarian |
| Date: | 7 November 2005 |
| Date Deposited: | 13 Jan 2012 16:17 |
| Last Modified: | 03 May 2018 14:56 |
| PMCID: | PMC2171256 |
| Related URLs: | |
| URI: | https://repository.cshl.edu/id/eprint/22557 |
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