Multiple phenotypic consequences of the Ig/Myc translocation in B-cell-derived tumors

✍ Scribed by Dr. George Klein

• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: English
• Weight: 648 KB
• Volume: 1
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/gcc.2870010103

✦ Synopsis

Reciprocal translocation between the MYCcarrying chromosome and one of the three Ig loci is a regular feature of certain B-cell-derived tumors in three species: Burkitt's lymphomas (BL) in humans, induced plasmacytomas in Balb/c mice (MPC), and the spontaneous immunocytomas (RIC) of the Louvain rat (for review, see Klein and Klein, 1985). I know of no other example in the cancer field where equally homologous oncogene activation events are associated with tumors of different species and of different natural histories that have their cell lineage derivation as the only common denominator. In this brief review, I discuss the possible reasons for the extraordinary penetrance of the Ig/Myc translocations, as reflected by their virtually uniform presence in the three tumors, to the exclusion of other B-cell-derived neoplasms. I argue that this is due to multiple phenotypic effects by which the translocations facilitate the uncontrolled growth of their carriers. T h e constitutive activation of the ZG-juxtaposed MYC gene prevents the translocation carrying cells from leaving the cycling compartment when they are programmed to become resting virgin or memory cells and have already switched some of their phenotypic markers in accordance with that program. In the case of the BL cell, the resulting phenotype can be referred to as a "resting cell that is not resting.'' I argue that cells of this phenotype are relatively unavailable for T-cell-mediated rejection. T h e nonimmunological and immunological consequences of the IGIMYC juxtaposition are discussed in this order.

NONIMMUNOLOGICAL CONSEQUENCES OF THE /G/MYC TRANSLOCATION