PROMISCUOUS TRANSLOCATIONS OF CHROMOSOME ARM 17Q IN HUMAN NEUROBLASTOMAS

Deletions of chromosome arm 1p and amplification of the MYCN oncogene are well-recognized genetic changes in neuroblastoma cells, Technical difficulties in cytogenetic analysis of this tumour have hampered the recognition of other recurring abnormalities, but recent use of molecu lar cytogenetic techniques has indicated significant involvement of ch romosome arm 17q. In primary tumours and in cell lines, a recurrent un balanced translocation t(lp;17q) has been identified by fluorescence i n situ hybridization. We confirm the occurrence of this translocation in primary rumours and, in addition, we describe seven new structural rearrangements all of which result in gain of 17q in tumour cells. The se rearrangements involved chromosome arms 9p, 10q, I Ip, 14q, and 16q . Triplication of the 17q arm was seen in one case. The 17q breakpoint was most commonly q21. All these 17q changes were found in near-diplo id rumours. We have also reviewed the literature for neuroblastoma kar yotypes involving 17q abnormalities; taken in conjunction with our fin dings this indicates a remarkable promiscuity of translocation partner s, with more than 20 different chromosome regions involved in 17q tran slocations. (C) 1997 Wiley-Liss, Inc.