Molecular genetic investigations of human tumors have increased our understanding of the mechanistic relationship between chromosome abnormalities and cancer. In leukemias and lymphomas, for which extensive karyotypic analysis has been possible, specific translocations and inversions have been identified that result in the deregulation of protooncogenes or the creation of aberrant fusion genes (1 ,2 ). Similarly, certain sarcomas (e.g., Ewing and synovial sarcomas) are characterized by specific translocations (3 ,4 ). In many cases, these translocations represent the only chromosome alteration present in the tumor cells, consistent with the notion that such changes play a critical role in the pathogenesis of these neoplasms.
