Recurrent involvement of the REL and BCL11A loci in classical Hodgkin lymphoma

被引:161
作者
Martín-Subero, JI
Gesk, S
Harder, L
Sonoki, T
Tucker, PW
Schlegelberger, B
Grote, W
Novo, FJ
Calasanz, MJ
Hansmann, ML
Dyer, MJS
Siebert, R
机构
[1] Univ Hosp Kiel, Inst Human Genet, D-24105 Kiel, Germany
[2] Univ Navarra, Dept Genet, E-31080 Pamplona, Spain
[3] Kumamoto Univ, Sch Med, Kumamoto 860, Japan
[4] Univ Texas, Inst Cellular & Mol Biol, Austin, TX 78712 USA
[5] Univ Frankfurt, Dept Pathol, D-6000 Frankfurt, Germany
[6] Univ Leicester, Dept Haematol, Leicester LE1 7RH, Leics, England
关键词
D O I
10.1182/blood.V99.4.1474
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Comparative genomic hybridization studies have shown gains in chromosome region 2p as the most common imbalance in classical Hodgkin lymphoma (cHL). The minimal region of gain contained 2 candidate oncogenes, REL and BCL11A. This study examined the involvement of REL and BCL11A loci in 44 primary cases of cHL by combined Immunophenotyping and interphase cytogenetics (FICTION). A median 2p13 copy number above the tetraploid range was detected in 24 (55%) cases. Adjustment for centromere 2 copy number indicated gains of 2p13 in 11 of 31 cHLs (35%) with 8 (26%) high-level amplifications. One cHL displayed selective amplification of the REL locus not affecting BCL11A; another case studied by FICTION and a cHL with cytogenetic 2p change Investigated by fluorescence In situ hybridization showed signal patterns suggesting breakpoints in the region spanned by the REL probe. These data Indicate that REL rather than BCL11A may be the target of the 2p13 alterations In cHL (C) 2002 by The American Society of Hematology.
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收藏
页码:1474 / 1477
页数:4
相关论文
共 27 条
[1]   Cytogenetics of Hodgkin's disease [J].
Atkin, NB .
CYTOGENETICS AND CELL GENETICS, 1998, 80 (1-4) :23-27
[2]   Molecular-cytogenetic comparison of mucosa-associated marginal zone B-cell lymphoma and large B-cell lymphoma arising in the gastro-intestinal tract [J].
Barth, TFE ;
Bentz, M ;
Leithäuser, F ;
Stilgenbauer, S ;
Siebert, R ;
Schlotter, M ;
Schlenk, RF ;
Döhner, H ;
Möller, P .
GENES CHROMOSOMES & CANCER, 2001, 31 (04) :316-325
[3]  
DeerbergWittram J, 1996, ANN ONCOL, V7, P49
[4]   Overexpression of I kappa B alpha without inhibition of NF-κB activity and mutations in the I kappa B alpha gene in Reed-Sternberg cells [J].
Emmerich, F ;
Meiser, M ;
Hummel, M ;
Demel, G ;
Foss, HD ;
Jundt, F ;
Mathas, S ;
Krappmann, D ;
Scheidereit, C ;
Stein, H ;
Dorken, B .
BLOOD, 1999, 94 (09) :3129-3134
[5]  
Falzetti D, 1999, HAEMATOLOGICA, V84, P298
[6]   The regulation and roles of Rel/NF-κB transcription factors during lymphocyte activation [J].
Gerondakis, S ;
Grumont, R ;
Rourke, I ;
Grossmann, M .
CURRENT OPINION IN IMMUNOLOGY, 1998, 10 (03) :353-359
[7]   The use of real-time quantitative polymerase chain reaction and comparative genomic hybridization to identify amplification of the REL gene in follicular lymphoma [J].
Goff, LK ;
Neat, MJ ;
Crawley, CR ;
Jones, L ;
Jones, E ;
Lister, TA ;
Gupta, RK .
BRITISH JOURNAL OF HAEMATOLOGY, 2000, 111 (02) :618-625
[8]   The World Health Organization classification of hematological malignancies report of the Clinical Advisory Committee Meeting, Airlie House, Virginia, November 1997 [J].
Harris, NL ;
Jaffe, ES ;
Diebold, J ;
Flandrin, G ;
Muller-Hermelink, HK ;
Vardiman, J ;
Lister, TA ;
Bloomfield, CD .
MODERN PATHOLOGY, 2000, 13 (02) :193-207
[9]  
Harris NL, 1999, MODERN PATHOL, V12, P159
[10]  
HARRIS NL, 1994, BLOOD, V84, P1361