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Juxtaposition of N-myc and Ig kappa through a reciprocal t(6;12) translocation in a mouse plasmacytoma

Author:
  • H Axelson
  • Y Wang
  • S Silva
  • M G Mattei
  • G Klein
Publishing year: 1994-10
Language: English
Pages: 85-90
Publication/Series: Genes, Chromosomes and Cancer
Volume: 11
Issue: 2
Document type: Journal article
Publisher: John Wiley & Sons

Abstract english

Nearly all mouse plasmacytomas (MPCs) carry an Ig/myc translocation. Any one of the three Ig loci may participate, while the myc contribution has been limited to c-myc, excluding other members of the myc gene family. The same is true for the other two known Ig/myc translocation-carrying tumors, Burkitt's lymphoma and rat immunocytoma. It is believed that the Ig/myc juxtaposition plays a decisive, rate limiting role in the genesis of the three tumors, acting through the constitutive activation of myc that makes it refractory to normal regulation. Here we describe the molecular analysis of a unique t(6;12)(CI;B) translocation that we previously identified in an exceptional MPC that expressed N-myc but not c-myc. We now show that the translocation led to the juxtaposition of N-myc and Ig kappa. This is the first case of an Ig/myc-carrying tumor that involves N-myc rather than c-myc. These findings suggest that the translocation may already have occurred at the pro- or pre-B cell stage at which N-myc is open for transcription. According to this interpretation, constitutive activation of N-myc would suppress the expression of c-myc, but would not interfere with the differentiation of the pro-B cell into a fully mature plasma cell. Its tumorigenic influence would become manifest only at the time when the cell would normally be programmed to leave the cycling compartment, in connection with its terminal differentiation.

Keywords

  • Animals
  • Base Sequence
  • Chromosome Mapping
  • Cloning, Molecular
  • DNA Probes
  • Genes, myc
  • Immunoglobulin kappa-Chains
  • Mice
  • Molecular Sequence Data
  • Plasmacytoma
  • RNA Probes
  • Translocation, Genetic

Other

Published
  • ISSN: 1045-2257
Håkan Axelson
E-mail: hakan [dot] axelson [at] med [dot] lu [dot] se

Professor

Division of Translational Cancer Research

+46 46 222 64 34

MV 404 A31A2

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