PMID- 12800155
OWN - NLM
STAT- MEDLINE
DCOM- 20030812
LR  - 20041117
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 37
IP  - 4
DP  - 2003 Aug
TI  - Identification of candidate tumor-suppressor genes in 6q27 by combined deletion 
      mapping and electronic expression profiling in lymphoid neoplasms.
PG  - 421-6
AB  - Deletions in the long arm of chromosome 6 (6q) are among the most frequent 
      chromosome aberrations in lymphoid neoplasms. Recently, the region of minimal 
      deletion (RMD1) in 6q27 was narrowed down to 5-9 Mb. In the present study, we 
      aimed to define the distal border of the commonly lost region in 6q27 more 
      precisely and to identify and investigate tumor-suppressor genes (TSGs) from this 
      region. Twenty-nine cases, in which our previous fluorescence in situ 
      hybridization (FISH) screening that used a set of 36 YAC probes revealed loss in 
      6q25-27, were further investigated by means of FISH. In all cases, deletions of 
      6q27 extended from yeast artificial chromosome (YAC) 977e10 spanning the proximal 
      border of RMD1 to the most telomeric YAC 933f7 within the recently established 
      YAC-contig of this region. An interstitial homozygous deletion, flanked by the 
      telomeric probe TelVysion6q and YAC 971g12, was detected, which substantially 
      narrows down the RMD1. To identify candidate TSGs down-regulated in malignant 
      lymphomas from this region of homozygous loss, we performed electronic profiling 
      of expressed sequences mapped to this region. This analysis suggested the gene 
      PDCD2 originally thought to be involved in programmed cell death to be probably 
      down-regulated in malignant B-cell lymphomas compared to normal B lymphocytes. 
      Nevertheless, mutation analyses failed to identify mutations in the coding region 
      of PDCD2 in nine lymphomas with FISH-proved 6q27 deletions. Furthermore, 
      epigenetic studies in these nine and an additional 48 lymphomas did not show 
      altered methylation of the PDCD2 locus in these tumors. Possibly 
      haploinsufficiency is effectual in accelerating tumor progression.
CI  - Copyright 2003 Wiley-Liss, Inc.
FAU - Steinemann, Doris
AU  - Steinemann D
AD  - Institute of Cell and Molecular Pathology, Hannover Medical School, Hannover, 
      Germany. steinemann.doris@mh_hannover.de
FAU - Gesk, Stefan
AU  - Gesk S
FAU - Zhang, Yanming
AU  - Zhang Y
FAU - Harder, Lana
AU  - Harder L
FAU - Pilarsky, Christian
AU  - Pilarsky C
FAU - Hinzmann, Bernd
AU  - Hinzmann B
FAU - Martin-Subero, Jose Ignacio
AU  - Martin-Subero JI
FAU - Calasanz, Maria Jose
AU  - Calasanz MJ
FAU - Mungall, Andrew
AU  - Mungall A
FAU - Rosenthal, Andre
AU  - Rosenthal A
FAU - Siebert, Reiner
AU  - Siebert R
FAU - Schlegelberger, Brigitte
AU  - Schlegelberger B
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
SB  - IM
MH  - Cell Line, Transformed
MH  - Chromosome Mapping/*methods
MH  - Chromosomes, Human, Pair 6/*genetics
MH  - *Gene Deletion
MH  - Gene Expression Profiling/*methods
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - *Genes, Tumor Suppressor
MH  - Humans
MH  - Lymphoma, B-Cell/*genetics
MH  - Oligonucleotide Array Sequence Analysis/*methods
MH  - Tumor Cells, Cultured
EDAT- 2003/06/12 05:00
MHDA- 2003/08/13 05:00
CRDT- 2003/06/12 05:00
PHST- 2003/06/12 05:00 [pubmed]
PHST- 2003/08/13 05:00 [medline]
PHST- 2003/06/12 05:00 [entrez]
AID - 10.1002/gcc.10231 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2003 Aug;37(4):421-6. doi: 10.1002/gcc.10231.