Karyotype, marker formation, and oncogenicity in mouse plasmacytomas

Two common chromosome markers in the 2 plasmacytomas previously examined by Giemsa banding were consistently present in the mouse plasmacytoma X-5563, a transplantable hypertetraploid tumor of spontaneous origin in C3H mice. The 2 markers were found in both induced and spontaneous tumors and in either BALB/c or C3H mice. The derived cell line had 17 fewer chromosomes than the X-5563 tumor and was oncogenic, and its modal karyotype was identical to that of the tumor transmitted by the inoculation of the cell line. The homogeneity of a slight karyotypic modification in a second tumor suggested a possible clonal origin of that tumor. The high frequency of centric fusions between homologues and the structure of certain markers suggests that homologue association may precede marker formation. We proposed a second mechanism of marker formation, selective regional elongation, to account for the larger number of markers with proximal or distal elongations without evidence of translocation and for the observed alterations in length and banding pattern of markers after growth in vitro. Comparison of MOPC-21, MOPC-315, and X-5563 tumors showed preferential involvement of certain chromosomes in marker formation, an inferred association of the 2 common markers with an early stage in the origin of the 3 plasmacytomas, and consistent loss of an X chromosome. Loss of oncogenicity in cell lines was associated with a number of karyotypic changes, but did not require the loss of the characteristic markers or additional copies of a specific normal chromosome.