Suppression of transformed phenotypes in intraspecific somatic cell hybrid clones between the c-myc activating mouse plasmacytoma line and normal cells.

The role of normal-cell-derived chromosome 15 in suppressing transformed phenotypes was studied in intraspecific hybrid clones between the c-myc oncogene activating BALB/c mouse plasmacytoma (S194) cells and normal spleen cells or fibroblasts from CBA/H-T6 mice. All the hybrid clones between S194 and normal spleen cells grew very rapidly in suspension and formed colonies in soft agar. In contrast, the hybrid clones between S194 and normal fibroblasts grew slowly in an attached form. They were divided into 2 groups on the basis of their morphology and growth properties: most clones showed flat type morphology, and no colony formation was seen in soft agar, while some clones grew in a piled-up fashion and formed colonies in soft agar. The hybrid clones between S194 and normal spleen cells lost some normal-cell-derived chromosomes but retained most tumor-derived marker chromosomes including the t(12;15) chromosome which carried the activated c-myc oncogene. On the other hand, hybrid clones between S194 cells and normal fibroblasts retained almost all chromosomes from both parental cells. With respect to retention of normal-cell-derived chromosome 15, both the flat and piled-up type clones retained 2 copies each of the t(14;15) and T6 marker chromosomes, the normal counterparts of the t(12;15) chromosomes. Our results suggest that the transformed phenotypes of the hybrid clones between S194 cells and normal fibroblasts are negatively modulated by normal-cell-derived chromosomes but not by normal-cell-derived chromosome 15 alone.