## Abstract The expression of the transformed phenotype was studied in segregants from a hybrid cell line resulting from the fusion of SV40‐transformed BHK21 Syrian hamster cells (thioguanine resistant) and 3T3 mouse cells (bromodeoxyuridine resistant). Since the hamster cell parent was sensitive t
Susceptibility of primate-mouse hybrid cells to SV40
✍ Scribed by Barbara B. Knowles; Giuseppe Barbanti-Brodano; Hilary Koprowski
- Publisher
- John Wiley and Sons
- Year
- 1971
- Tongue
- English
- Weight
- 518 KB
- Volume
- 78
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Primate‐mouse hybrid cells were challenged with SV40 DNA and monitored for their ability to produce virus. All of the hybrid cells had lost at least half of their primate chromosomes at the time of challenge. Only SV40 T‐antigen‐positive hybrid cells derived from an SV40‐transformed human parental cell produced SV40. This finding suggests that the chromosome(s) necessary for SV40 replication are easily lost on fusion of mouse and primate cells unless the parental cells are already SV40‐transformed.
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A transplantable tumor of inbred mice was obtained by inoculating BALBIc mice subcutaneously with S V40-transformed mouse kidney (mKS-A) cells. Tumors were produced by mKS-A cells in the 7lst cell culture passage, but not by cells in the 26th passage. The tumor line has been serially passed in BALBI
## Abstract Gene amplification contributes to carcinogenesis by enhancing proto‐oncogene activity and causing chromosomal instability. The ease of detecting amplified tumor‐virus sequences has encouraged use of this system as a surrogate for studying the molecular events involved in endogenous gene