Key Points
Jumping translocations of 1q12 (JT1q12) provide a mechanism for the deletion of 17p in cytogenetically defined high-risk myeloma. Sequential JT1q12s introduce unexpected copy number gains and losses in receptor chromosomes during subclonal evolution.
Adjuvant chemotherapy appears to be effective to control both local- and distant-recurrences in stage I UCS; adding radiotherapy to chemotherapy may be effective to control local-recurrence when the tumor exhibits multiple risk factors.
Key Points
High-risk copy number gains of 1q21 originate in part by the hypomethylation of 1q12 pericentromeric heterochromatin. Novel CNAs can result from juxtaposition of chromosomal regions to hypomethylated 1q12.
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