PMID- 18246537
OWN - NLM
STAT- MEDLINE
DCOM- 20080508
LR  - 20120605
IS  - 0008-543X (Print)
IS  - 0008-543X (Linking)
VI  - 112
IP  - 6
DP  - 2008 Mar 15
TI  - Molecular allelokaryotyping of early-stage, untreated chronic lymphocytic 
      leukemia.
PG  - 1296-305
LID - 10.1002/cncr.23270 [doi]
AB  - BACKGROUND: To the authors' knowledge, genetic abnormalities in early-stage 
      chronic lymphocytic leukemia (CLL) have not been examined fully. Single 
      nucleotide polymorphism (SNP) genomic array (SNP-chip) is a new tool that can 
      detect copy number changes and uniparental disomy (UPD) over the entire genome 
      with very high resolution. METHODS: The authors performed SNP-chip analysis on 56 
      samples from patients with early-stage, untreated CLL. To validate the SNP-chip 
      data, fluorescence in situ hybridization (FISH) analysis was performed at 
      selected sites. Expression levels of ZAP-70 and the mutational status of 
      immunoglobulin heavy-chain gene also were examined. RESULTS: SNP-chip analysis 
      easily detected nearly all changes that were identified by FISH, including 
      trisomy 12, deletion of TP53 (17p13), deletion of ATM (11q22), and deletion of 
      13q14. Only 10 of 56 CLL samples (18%) had no genomic abnormalities. Excluding 
      the 4 common abnormalities mentioned above, 25 CLL samples (45%) had a total of 
      45 copy number changes detected by SNP-chip analysis. Four samples had 6q 
      deletion at 6q21 that involved the AIM1 gene. UPD was detected in 4 samples; 2 
      samples involved whole chromosome 13 resulting in homozygous deletion of 
      micro-RNA-15a (miR-15a)/miR-16-1. CLL samples with deletion of 13q14 and trisomy 
      12 were mutually exclusive. CONCLUSIONS: Genetic abnormalities, including whole 
      chromosome 13 UPD, are very common events in early-stage CLL. SNP-chip analysis 
      can detect small genetic abnormalities in CLL and may be able to support or even 
      supplant FISH and cytogenetics.
CI  - Copyright (c) 2008 American Cancer Society.
FAU - Lehmann, Soren
AU  - Lehmann S
AD  - Department of Hematology/Oncology, Cedars-Sinai Medical Center, University of 
      California at Los Angeles School of Medicine, Los Angeles, California 90048, USA.
FAU - Ogawa, Seishi
AU  - Ogawa S
FAU - Raynaud, Sophie D
AU  - Raynaud SD
FAU - Sanada, Masashi
AU  - Sanada M
FAU - Nannya, Yasuhito
AU  - Nannya Y
FAU - Ticchioni, Michel
AU  - Ticchioni M
FAU - Bastard, Christian
AU  - Bastard C
FAU - Kawamata, Norihiko
AU  - Kawamata N
FAU - Koeffler, H Phillip
AU  - Koeffler HP
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer
JT  - Cancer
JID - 0374236
RN  - 0 (DNA Primers)
RN  - 0 (Immunoglobulin Heavy Chains)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.10.2 (ZAP-70 Protein-Tyrosine Kinase)
RN  - EC 2.7.10.2 (ZAP70 protein, human)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Alleles
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 13/genetics
MH  - Cohort Studies
MH  - DNA Primers/chemistry
MH  - Female
MH  - Flow Cytometry
MH  - *Genome, Human
MH  - Humans
MH  - Immunoglobulin Heavy Chains
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Leukemia, Lymphocytic, Chronic, B-Cell/*genetics
MH  - Male
MH  - Middle Aged
MH  - Mutation
MH  - Oligonucleotide Array Sequence Analysis
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - RNA, Messenger/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - ZAP-70 Protein-Tyrosine Kinase/genetics
EDAT- 2008/02/05 09:00
MHDA- 2008/05/09 09:00
CRDT- 2008/02/05 09:00
PHST- 2008/02/05 09:00 [pubmed]
PHST- 2008/05/09 09:00 [medline]
PHST- 2008/02/05 09:00 [entrez]
AID - 10.1002/cncr.23270 [doi]
PST - ppublish
SO  - Cancer. 2008 Mar 15;112(6):1296-305. doi: 10.1002/cncr.23270.