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Duplication of chromosome arms 9q and 11q: Evidence for a novel, 14q32 translocation–independent pathogenetic pathway in multiple myeloma
Author(s) -
Liebisch Peter,
Scheck Daniel,
Erné Seiichi Alvise,
Wellmann Alexander,
Wendl Christiane,
Janczik Sibylle,
Kolmus Sonja,
Kröber Alexander,
Einsele Hermann,
Straka Christian,
Goldschmidt Hartmut,
Benner Axel,
Stilgenbauer Stephan,
Döhner Hartmut
Publication year - 2005
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.20098
Subject(s) - chromosomal translocation , chromosome , fluorescence in situ hybridization , multiple myeloma , gene duplication , biology , chromosome 13 , comparative genomic hybridization , cancer research , microbiology and biotechnology , pathology , genetics , gene , medicine , immunology
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.