Further cytogenetic characterization of multiple myeloma confirms that 14q32 translocations are a very rare event in hyperdiploid cases

被引:80
作者
Smadja, NV
Leroux, D
Soulier, J
Dumont, S
Arnould, C
Taviaux, S
Taillemite, JL
Bastard, C
机构
[1] Hop St Antoine, Lab Rech & Cytogenet Hematol, F-75571 Paris, France
[2] Ctr Hosp Univ, Onco Hematol Genet Lab, Grenoble, France
[3] Hop St Louis, Hematol Lab, Paris, France
[4] Ctr Henri Becquerel, Genet Lab & EMI 9906, Rouen, France
关键词
D O I
10.1002/gcc.10275
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Translocations involving the immunoglobulin heavy-chain genes are frequent in multiple myeloma (MM), which can be separated into two groups according to the chromosome number pattern. 14q32 translocations 14q32t are more frequent in hypodiploid than in hyperdiploid karyotypes. However, conventional cytogenetics (CC) misses cryptic translocations, especially t(4;14)(p16;q32). Furthermore, recent interphase fluorescence in situ hybridization (FISH) studies found 14q32t in as many as 75% of MM cases. To identify in which CC group we failed to detect translocations, we designed a study by use of FISH with a dual-color IGH probe on previously R-banded metaphase cells, allowing the detection of both 14q32t and overall chromosomal abnormalities, in a new series of 55 MM with abnormal karyotypes: 4/29 hyperdiploid (14%) and 19/26 hypodiploid (73%) cases had a 14q32t. The t(4;14) was found in 2 hyperdiploid (7%) and 10 hypodiploid (39%) cases. We therefore confirm that 14q32t are much more frequent in hypodiploid than in hyperdiploid MM (P < 0.0001) and that cryptic t(4;14)(p16;q32) is strongly associated with hypodiploid karyotypes (P < 0.01). Through the use of this reliable assay, only 42% of MM had 14q32t. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:234 / 239
页数:6
相关论文
共 24 条
[1]   Oncogenesis of multiple myeloma: 14q32 and 13q chromosomal abnormalities are not randomly distributed, but correlate with natural history, immunological features, and clinical presentation [J].
Avet-Loiseau, H ;
Facon, T ;
Grosbois, B ;
Magrangeas, F ;
Rapp, MJ ;
Harousseau, JL ;
Minvielle, S ;
Bataille, R .
BLOOD, 2002, 99 (06) :2185-2191
[2]  
Avet-Loiseau H, 1998, CANCER RES, V58, P5640
[3]  
Avet-Loiseau H, 1999, GENE CHROMOSOME CANC, V24, P9, DOI 10.1002/(SICI)1098-2264(199901)24:1<9::AID-GCC2>3.0.CO
[4]  
2-K
[5]   Promiscuous translocations into immunoglobulin heavy chain switch regions in multiple myeloma [J].
Bergsagel, PL ;
Chesi, M ;
Nardini, E ;
Brents, LA ;
Kirby, SL ;
Kuehl, WM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (24) :13931-13936
[6]   Frequent translocation t(4;14)(p16.3;q32.3) in multiple myeloma is associated with increased expression and activating mutations of fibroblast growth factor receptor 3 [J].
Chesi, M ;
Nardini, E ;
Brents, LA ;
Schrock, E ;
Ried, T ;
Kuehl, WM ;
Bergsagel, PL .
NATURE GENETICS, 1997, 16 (03) :260-264
[7]   Frequent dysregulation of the c-maf proto-oncogene at 16q23 by translocation to an Ig locus in multiple myeloma [J].
Chesi, M ;
Bergsagel, PL ;
Shonukan, OO ;
Martelli, ML ;
Brents, LA ;
Chen, T ;
Schröck, E ;
Ried, T ;
Kuehl, VM .
BLOOD, 1998, 91 (12) :4457-4463
[8]  
DURIE BGM, 1975, CANCER, V36, P842, DOI 10.1002/1097-0142(197509)36:3<842::AID-CNCR2820360303>3.0.CO
[9]  
2-U
[10]   Detection of t(4;14)(p16.3;q32) chromosomal translocation in multiple myeloma by double-color fluorescent in situ hybridization [J].
Finelli, P ;
Fabris, S ;
Zagano, S ;
Baldini, L ;
Intini, D ;
Nobili, L ;
Lombardi, L ;
Maiolo, AT ;
Neri, A .
BLOOD, 1999, 94 (02) :724-732