Delineation of a minimal region of deletion at 6q16.3 in follicular lymphoma and construction of a bacterial artificial chromosome contig spanning a 6-megabase region of 6q16-q21

被引:21
作者
Henderson, LJ
Okamoto, I
Lestou, VS
Ludkovski, O
Robichaud, M
Chhanabhai, M
Gascoyne, RD
Klasa, RJ
Connors, JM
Marra, MA
Horsman, DE
Lam, WL
机构
[1] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada
[2] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada
关键词
D O I
10.1002/gcc.20013
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Regional deletions of 6q are frequent karyotypic alterations in malignant lymphoma and are associated with an adverse clinical outcome. One such region of recurrent deletion is 6q16-q21; however, the specific genes affected have not been identified. Our objective in this study was to identify cases with deletion of 6q16-q21 in follicular lymphoma and to define a minimal region of deletion. A physical map of 6q16.2-q21 was constructed using map information from both sequence-based and bacterial artificial chromosome (BAC) fingerprint-based maps. Forty-three BAC clones spanning a 6-Mb region of 6q16.2-q21 were identified and obtained from the RP-11 library. Selected BACs were fluorescence-labeled and hybridized to a series of 34 follicular lymphomas with a regional 6q deletion detected by G banding. Twenty-four cases with deletion of the 6q16.3 region were detected. A minimal deletion of 2.3 Mb was defined. Our study has identified a limited region of deletion of 6q16.3 that may implicate four known genes in follicular lymphoma and possibly in other cancers. A BAC contig spanning a 6-Mb region has been anchored to the 6q16.2-q21 region. This map represents a useful resource for gene identification in this region, not only in lymphoma but also in other neoplasms with 6q alterations. (C) 2004 Wiley-Liss, Inc.
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页码:60 / 65
页数:6
相关论文
共 33 条
[1]  
Abe T, 1999, GENE CHROMOSOME CANC, V25, P60, DOI 10.1002/(SICI)1098-2264(199905)25:1<60::AID-GCC9>3.0.CO
[2]  
2-Y
[3]   Deletion of 6q27 in chronic lymphocytic leukemia and multiple myeloma detected by fluorescence in situ hybridization [J].
Amiel, A ;
Mulchanov, I ;
Elis, A ;
Gaber, E ;
Manor, Y ;
Fejgin, M ;
Lishner, M .
CANCER GENETICS AND CYTOGENETICS, 1999, 112 (01) :53-56
[4]  
Cigudosa JC, 1999, GENE CHROMOSOME CANC, V25, P123, DOI 10.1002/(SICI)1098-2264(199906)25:2<123::AID-GCC8>3.0.CO
[5]  
2-4
[6]   Deletion of the SIM1 gene (6q 16.2) in a patient with a Prader-Willi-like phenotype [J].
Faivre, L ;
Cormier-Daire, V ;
Lapierre, JM ;
Colleaux, L ;
Jacquemont, S ;
Geneviève, D ;
Saunier, P ;
Munnich, A ;
Turleau, C ;
Romana, S ;
Prieur, M ;
De Blois, MC ;
Vekemans, M .
JOURNAL OF MEDICAL GENETICS, 2002, 39 (08) :594-596
[7]   Role of the Bloom's syndrome helicase in maintenance of genome stability [J].
Hickson, ID ;
Davies, SL ;
Li, JL ;
Levitt, NC ;
Mohaghegh, P ;
North, PS ;
Wu, L .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2001, 29 :201-204
[8]  
Holder JL, 2000, HUM MOL GENET, V9, P101
[9]   Analysis of secondary chromosomal alterations in 165 cases of follicular lymphoma with t(14;18) [J].
Horsman, DE ;
Connors, JM ;
Pantzar, T ;
Gascoyne, RD .
GENES CHROMOSOMES & CANCER, 2001, 30 (04) :375-382
[10]  
ISCN, 1995, INT SYST HUM CYT NOM