Duplication of chromosome arms 9q and 11q: Evidence for a novel, 14q32 translocation–independent pathogenetic pathway in multiple myeloma

✍ Scribed by Peter Liebisch; Daniel Scheck; Seiichi Alvise Erné; Alexander Wellmann; Christiane Wendl; Sibylle Janczik; Sonja Kolmus; Alexander Kröber; Hermann Einsele; Christian Straka; Hartmut Goldschmidt; Axel Benner; Stephan Stilgenbauer; Hartmut Döhner

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 66 KB
• Volume: 42
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/gcc.20098

✦ Synopsis

Abstract

14q32 translocations [t(14q)] represent critical but not universal events in multiple myeloma (MM). Gains of chromosome arms 1q, 9q, and 11q (+1q, +9q, and +11q) have recently been identified as frequent aberrations in this disease, but their pathogenetic significance remains unclear. We studied a series of 108 MM patients using fluorescence in situ hybridization and DNA probes mapping to chromosome bands 1q21, 9q34, 11q25, 13q14, and 14q32. Three subsets of tumors were defined: (1) MM+/+ (detection of +9q and +11q; 43.5% of cases), (2) MM+/− (+9q or +11q; 21.3%), and (3) MM−/− (neither +9q nor +11q; 35.2%). The incidence of t(14q) was significantly different in these subgroups: 23% in MM+/+, 56% in MM+/−, and 89% in MM−/−. Deletion of 13q (13q−) also was significantly less frequent in MM+/+ (23%) than in MM+/− and MM−/− (36% and 63%, respectively). The nonrandom distribution of chromosomal aberrations in the present series of MM tumors points to a novel, 14q32 translocation–independent pathogenetic pathway in plasma cell neoplasms. © 2005 Wiley‐Liss, Inc.