A 3-cM commonly deleted region in 6q21 in leukemias and lymphomas delineated by fluorescence in situ hybridization

Citation
Ym. Zhang et al., A 3-cM commonly deleted region in 6q21 in leukemias and lymphomas delineated by fluorescence in situ hybridization, GENE CHROM, 27(1), 2000, pp. 52-58
Citations number
28
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
GENES CHROMOSOMES & CANCER
ISSN journal
10452257 → ACNP
Volume
27
Issue
1
Year of publication
2000
Pages
52 - 58
Database
ISI
SICI code
1045-2257(200001)27:1<52:A3CDRI>2.0.ZU;2-U
Abstract
Deletions of the long arm of chromosome 6 (6q) are frequent chromosome aber rations in non-Hodgkin lymphomas (NHLs) and acute lymphoblastic leukemias ( ALLs). It is presumed that one or more tumor suppressor genes are localized on 6q. By means of fluorescence in situ hybridization (FISH), we attempted to detect and delineate deletions of 6q in leukemias and lymphomas. We per formed FISH on 148 cases of lymphoma and acute leukemia using a panel of 36 YAC probes distributed from 6q12 to 6q27 and a centromeric probe of chromo some 6 as internal control. Deletions of 6q that included a 7-cM commonly d eleted region in 6q21 were detected in 59 patients who had B- and T-cell lo w-grade and high-grade NHL and ALL FISH with two YAC probes flanking this r egion was performed on an additional 97 cases of NHL and leukemia. Deletion s in 6q21 were detected in an additional 21 cases. In five cases of high-gr ade B- and T-cell NHL and ALL, the deletion breakpoints were located within the commonly deleted region. To define the deletion breakpoints exactly an d to narrow this region further, FISH was performed with six additional YAC probes that have been physically localized within this region. A 3-cM (4-5 Mb) commonly deleted region in 6q21 was delineated. Our study suggests tha t this commonly deleted region harbors a putative tumor suppressor gene inv olved in the pathogenesis of both low-grade and high-grade NHL and ALL. Gen es Chromosomes Cancer 27:52-58, 2000. (C) 2000 Wiley-Liss, Inc.