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Fig. 7 | Molecular Cytogenetics

Fig. 7

From: Is cancer progression caused by gradual or simultaneous acquisitions of new chromosomes?

Fig. 7

a, b Karyotype-arrays of five cells of hybridoma Hyb 94 (a) and hybridoma Hyb 1-5 (b). Both hybridomas are clonally heterogeneous with chromosomal clonalities ranging from 40 to 100%. For example, the individual chromosome numbers of the five hybridoma Hyb 94 cells analyzed range from 71 to 82 for a clonal average of 74 (Tables 1 and 3). Nevertheless, all five Hyb 94 karyotypes shared 28 of the 31 myeloma-specific marker chromosomes and two Hyb 94-specific marker chromosomes (Table 3). The karyotype array of Hyb 1-5 was also relatively heterogeneous. Nevertheless, all five Hyb 1-5 karyotypes shared 30 of the 31 myeloma-specific marker chromosomes with the parental myeloma. In addition they shared all normal murine chromosomes with the parental mouse B-cell and some also with the parental myeloma. The simplest explanation for the high clonal heterogeneity of Hyb 94 and Hyb 105 suggests that these clones are still evolving precursor clones that are losing non-stabilizing chromosomes

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