Presence of two cytogenetic forms of amplified dna

Evidence for a role in tumor growth in an intraspecific mouse hybrid cell line

Caroline B. Wigley, John Kenneth Cowell

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

An intraspecific mouse hybrid epithelial cell line, F5/B, is described in which the homogeneously staining region (HSR)-containing marker chromosome from one parent is absent in about half of the cells. It is replaced in these cells by double minutes (DM), an alternative form of amplified DNA, which is liable to loss because of its instability at mitosis. DM probably arise from the breakdown of the HSR during clonal growth of F5/B. Subclones were derived possessing one or another cytogenetic feature, and their cloning efficiency in vitro and tumorigenicity in syngeneic animals were compared. There were no differences in in vitro tumorigenicity, but in vivo DM-containing subclones were significantly less tumorigenic than HSR-containing subclones or the F5/B parent hybrid. In tumors that developed after long latent periods, cells had increased numbers of DM compared with the inoculated population, demonstrating a selective advantage in vivo for cells with a high DM content. These results indicate a role for the amplified DNA in tumor growth.

Original languageEnglish (US)
Pages (from-to)219-226
Number of pages8
JournalJournal of the National Cancer Institute
Volume73
Issue number1
DOIs
StatePublished - Jan 1 1984
Externally publishedYes

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Hybrid Cells
Cytogenetics
Cell Line
Staining and Labeling
Growth
Neoplasms
DNA
Genetic Markers
Mitosis
Organism Cloning
Epithelial Cells
Population
In Vitro Techniques

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

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abstract = "An intraspecific mouse hybrid epithelial cell line, F5/B, is described in which the homogeneously staining region (HSR)-containing marker chromosome from one parent is absent in about half of the cells. It is replaced in these cells by double minutes (DM), an alternative form of amplified DNA, which is liable to loss because of its instability at mitosis. DM probably arise from the breakdown of the HSR during clonal growth of F5/B. Subclones were derived possessing one or another cytogenetic feature, and their cloning efficiency in vitro and tumorigenicity in syngeneic animals were compared. There were no differences in in vitro tumorigenicity, but in vivo DM-containing subclones were significantly less tumorigenic than HSR-containing subclones or the F5/B parent hybrid. In tumors that developed after long latent periods, cells had increased numbers of DM compared with the inoculated population, demonstrating a selective advantage in vivo for cells with a high DM content. These results indicate a role for the amplified DNA in tumor growth.",
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