Promiscuous translocations of chromosome arm 17q in human neuroblastomas

Genes Chromosomes Cancer. 1997 Jul;19(3):143-9.


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 molecular cytogenetic techniques has indicated significant involvement of chromosome arm 17q. In primary tumours and in cell lines, a recurrent unbalanced translocation t(1p;17q) has been identified by fluorescence in situ hybridization. We confirm the occurrence of this translocation in primary tumours and, in addition, we describe seven new structural rearrangements all of which result in gain of 17q in tumour cells. These rearrangements involved chromosome arms 9p, 10q, 11p, 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-diploid tumours. We have also reviewed the literature for neuroblastoma karyotypes involving 17q abnormalities; taken in conjunction with our findings this indicates a remarkable promiscuity of translocation partners, with more than 20 different chromosome regions involved in 17q translocations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bone Marrow Neoplasms / genetics
  • Bone Marrow Neoplasms / pathology
  • Chromosome Aberrations
  • Chromosomes, Human, Pair 10 / genetics
  • Chromosomes, Human, Pair 11 / genetics
  • Chromosomes, Human, Pair 14 / genetics
  • Chromosomes, Human, Pair 16 / genetics
  • Chromosomes, Human, Pair 17 / genetics*
  • Chromosomes, Human, Pair 9 / genetics
  • Female
  • Humans
  • In Situ Hybridization, Fluorescence
  • Karyotyping
  • Male
  • Neuroblastoma / genetics*
  • Neuroblastoma / pathology
  • Translocation, Genetic*
  • Tumor Cells, Cultured