Suppression of the translocated myc gene and expression of intracisternal A‐particle genes in tumorigenic and non‐tumorigenic hybrids between murine myeloma and normal fibroblasts

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Abstract
We have studied the tumorigenlc potential of a series of Independent intraspecies hybrid clones derived from fusion of murine myeloma (BALB/c) and normal fibroblasts (C3H). All of these hybrids grew as adherent cells and thus resembled the fibroblast phenotype. As judged by chromosome enumeration, these hybrids appear to retain the full complement of their parental cells. Three out of 4 hybrids tested were able to form colonies in soft agar and to grow as tumors in either nude or (BALB/c ± C3H) F1 mice, albeit at a reduced rate. The 4th hybrid did not grow in agar, was non‐tumorigenic and may have had a 2:1 fibroblast to myeloma genomic equivalence ratio. In contrast to the parental myeloma cells, all the hybrids exhibited restricted growth rates in serum‐free medium. As in our previous sets of hybrids formed between myeloma and L‐cells, expression of the Ig genes was inhibited in the new hybrids and the derived tumors. The constitutive expression of the translocated myc gene in the myeloma parental cells was decreased in the hybrids and in all their derived tumors. In contrast, all of the hybrid cell lines and the tumors express high levels of the intracisternal A particle mRNAs. Our results show that the tumorigenic phenotype of myeloma cells is either fully or partially suppressed in myeloma ± fibroblast hybrids and that this may be due to the fact that expression of the translocated c‐myc is suppressed. We suggest that, in addition to the translocated myc gene, myeloma cells contain other activated oncogene(s), and that the latter are responsible for the residual tumorigenic potential of the myeloma × fibroblast hybrids.