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Lack of tumor suppression but induced loss of copies of indigenous chromosome 10 in vitro following microcell-mediated transfer of a deleted human der(9)t(X,9) chromosome to Syrian hamster BHK-191-5C cells
Linkoping Univ, Fac Hlth Sci, Dept Biomed & Surg, Div Cell Biol,Lab Canc Genet, S-58185 Linkoping, Sweden.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Clinical Chemistry.
1999 (English)In: Cytogenetics and Cell Genetics, ISSN 0301-0171, Vol. 87, no 1-2, 11-18 p.Article in journal (Refereed) Published
Abstract [en]

We have previously shown that microcell-mediated transfer of a der(9)t(X,9) chromosome, containing an almost complete human chromosome (HSA) 9 derived from the human fibroblast strain GM0705, into the Syrian hamster (Mesocricetus auratus) cell line BHK-191-5C suppressed the anchorage independence and tumorigenicity of the hybrids. Transfer of a normal HSA X did not have any effect on these phenotypes. Although the recipient cell line contained a 1:1 ratio of near-diploid and near-tetraploid cells, all hybrids retaining the der(9) chromosome were near-tetraploid, in contrast to hybrids retaining a normal X chromosome. In the present study, we have generated microcell hybrids by transferring another der(9)t(X,9) chromosome derived from the human fibroblast strain GM01429. This derivative chromosome contained a deletion on the short arm of HSA 9 and was also missing the distal part of the long arm of HSA 9 due to the involvement in a reciprocal (constitutive) translocation of this chromosome with HSA X. Cytogenetic analysis showed that all hybrid clones were near-tetraploid, confirming our previous finding. We also observed that the introduction of the deleted der(9) chromosome forced the hybrids to lose Syrian hamster chromosome 10. A soft agar test and nude mice assay indicated that none of the hybrids was suppressed for either anchorage independent growth or tumor formation. These data suggest that there is an antagonistic relationship between growth-promoting genes and antiproliferative genes. The observed dosage effects of both growth-promoting and growth-suppressing genes indicate that cellular growth may be a quantitative trait. Copyright (C) 1999 S. Karger AG, Basel.

Place, publisher, year, edition, pages
1999. Vol. 87, no 1-2, 11-18 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-49902OAI: diva2:270798
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2011-01-14

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