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Implication of Chromosome 11 in the Suppression of Neoplastic Expression in Human Cell Hybrids¹

Department of Microbiology and Molecular Genetics, University of California, Irvine, California 92717 [E. S. S., E. J. S.], and Division of Hematology-Oncology, Children's Hospital of Los Angeles, Los Angeles, California 90027 [W. F. B.]

Cytogenetic analyses of intraspecies human HeLa x fibroblast hybrid cell populations have provided tentative evidence for the correlation of loss of a single copy of chromosomes 11 and 14 with reexpression of tumorigenicity. In this study paired combinations of nontumorigenic and tumorigenic segregant HeLa x fibroblast hybrid cells from two independent fusion events were examined for the presence or absence of normal chromosomes 11 and 14. In human hybrid cell lines the parental origin of chromosomes can be distinguished on the basis of restriction fragment length polymorphisms. Genes for c-Ha-ras, insulin, and apolipoprotein A-1 on chromosome 11 and a polymorphic locus AW101 on chromosome 14 were used as Southern hybridization probes. Analysis of DNA from the parental fibroblast and HeLa cell lines and their nontumorigenic and tumorigenic hybrids showed the loss of a fibroblast chromosome 11 in four of the tumorigenic segregants and a HeLa chromosome 11 in a fifth hybrid cell line. This latter segregant has, interestingly, also lost a copy of chromosome 14 of fibroblast origin. There was no obvious correlation of loss of a copy of normal chromosome 14 and reexpression of tumorigenicity in any of the other hybrid cell populations.

Our conclusion from these observations is that gene(s) that map to normal chromosome 11 might be involved in control of tumorigenic expression in these human hybrid cells.

¹ Supported by NIH Grant CA-19401, and Grant 1475 from the Council for Tobacco Research.

² To whom requests for reprints should be addressed.

Received 3/ 5/86. Revised 6/11/86. Revised 8/25/86. Accepted 9/ 3/86.