Abstract
Chromosome changes accompanying differentiation and tumorigenesis in azacytidine- (azaC) and insulin-induced preadipocytes of the Chinese hamster embryo fibroblast cell line CHEF/18 are described. Karyotype analysis of 47 clones, subclones, and tumor-derived cells has shown that trisomy for chromosome 3q (mar 1) is characteristic of azaC preadipocytes but not of insulin preadipocytes. AzaC preadipocytes were consistently tumorigenic as well as trisomic for chromosome 3q, whereas most insulin preadipocytes were nontumorigenic and diploid. Only the few insulin preadipocytes that were tumorigenic were also trisomic for chromosome 3q. Among the tumor-derived cell lines recovered from azaC preadipocytes injected into nude mice, four had no additional chromosome changes except trisomy for 3q, as detected by karyotype analysis. Thus trisomy for 3q may be a sufficient chromosome change to induce tumor-forming ability in these cells. The rearrangements of chromosome 3 seen in this and other work pinpoint the trisomic region between the centromere and 3q5.
Similar content being viewed by others
Literature cited
Harrison, J.J., Anisowicz, A., Gadi, I.K., Raffeld, M., and Sager, R. (1983).Proc. Natl. Acad. Sci. U.S.A. 80:6606–6610.
Sager, R., and Kovac, P.E. (1978).Somat. Cell Genet. 4:375–392.
Sager, R., and Kovac, P.E. (1979).Somat. Cell Genet. 5:491–502.
Kitchin, R.M., and Sager, R. (1980).Somat. Cell Genet. 6:75–87.
Kitchin, R.M., and Sager, R. (1980).Somat. Cell Genet. 6:615–630.
Smith, B.L., and Sager, R. (1982).Cancer Res. 42:389–392.
Sager, R., and Kovac, P.E. (1982).Proc. Natl. Acad. Sci. U.S.A. 79:480–484.
Constantinides, P.G., Taylor, S.M., and Jones, P.A. (1918).Dev. Biol. 66:57–71.
Taylor, S.M., and Jones, P.A. (1979).Cell 17:771–779.
Kitchin, R.M., Gadi, I.K., Smith, B.L., and Sager, R. (1982).Somat. Cell Genet. 8:677–689.
Kakati, S., and Sinha, A. (1972).Genetics 72:357–362.
Stubblefield, E. (1974). InThe Cell Nucleus, Vol. 2, (ed.) Busch, E. (Academic Press, New York), pp. 149–162.
ISCN: An International System for Human Cytogenetics Nomenclature (1978).Cytogenet. Cell Genet. 21:309–404.
Deaven, L.L., Cram, L.S., Wells, R.S., and Kraemer, P.M. (1981). InGenes, Chromosomes and Neoplasia, (eds.) Arrighi, F.E., Rao, P.N., and Stubblefield, E. (Raven Press, New York), pp. 419–449.
Sager, R., Bennett, F., and Smith, B.L. (1982).Cold Spring Harbor Symp. Quant. Biol. 9:231–241.
Cram, S.L., Bartholdi, M.F., Ray, A.F., Travis, G.L., and Kraemer, P.M. (1983).Cancer Res. 43:4828–4837.
Spira, J., Wiener, F., Babonits, M., Miller, J., and Klein, G. (1981).Int. J. Cancer 28:785–798.
Klein, G. (1981).Nature 294:313–318.
Klein, G. (1983).Cell 32:311–315.
Jones, P.A., and Taylor, S.M. (1981).Nucleic Acids Res. 9:2933–2946.
Razin, A., and Friedman, J. (1981). InProgress in Nucleic Acids Research and Molecular Biology, (ed.) Cohn, W.E., (Academic Press, New York), pp. 33–52.
Feinberg, A.P., and Vogelstein, B. (1983).Nature 301:89–92.
Bloch-Shtacher, N., and Sachs, L. (1977).J. Cell. Physiol. 93:205–212.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Gadi, I.K., Harrison, J.J. & Sager, R. Genetic analysis of tumerigenesis: XVI. Chromosome changes in azacytidine- and insulin-induced tumorigenesis. Somat Cell Mol Genet 10, 521–529 (1984). https://doi.org/10.1007/BF01534856
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1007/BF01534856