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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1202-1210. Prepublished online as a Blood First Edition Paper on October 19, 2006; DOI 10.1182/blood-2006-07-034256. This Article Full Text (PDF) Supplemental Table All Versions of this Article: blood-2006-07-034256v1 109/3/1202    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Pfeifer, D. Articles by Veelken, H. Search for Related Content PubMed PubMed Citation Articles by Pfeifer, D. Articles by Veelken, H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 7, 2006 Accepted September 17, 2006 Genome-wide analysis of DNA copy number changes and LOH in CLL using high-density SNP arrays Dietmar Pfeifer, Milena Pantic, Ilona Skatulla, Justyna Rawluk, Clemens Kreutz, Uwe M Martens, Paul Fisch, Jens Timmer, and Hendrik Veelken* Freiburg University Medical Center, Germany University of Freiburg, Germany * Corresponding author; email: hendrik.veelken{at}uniklinik-freiburg.de. Recurrent genomic aberrations are important prognostic parameters in CLL. High-resolution 10k and 50k Affymetrix SNP arrays were evaluated as a diagnostic tool for CLL and revealed chromosomal imbalances in 65.6% and 81.5% of 70 consecutive cases, respectively. Among the prognostically important aberrations, the del13q14 was present in 36 (51.4%), trisomy 12 in nine (12.8%), del11q22 in nine (12.8%), and del17p13 in four cases (5.7%). A prominent clustering of breakpoints on both sides of the miR-15a/miR-16-1 genes indicated the presence of recombination hot spots in the 13q14 region. Patients with a mono-allelic del13q14 had slower lymphocyte growth kinetics (P=0.002) than patients with bi-allelic deletions. In four CLL cases with unmutated VH genes, a common minimal 3.5 Mb gain of 2p16 spanning the REL and BCL11A oncogenes was identified, implicating these genes in the pathogenesis of CLL. Twenty-four large (>10 Mb) copy-neutral regions with loss of heterozygosity were identified in 14 cases. These regions with loss of heterozygosity are not detectable by alternative methods and may harbor novel imprinted genes or loss-of-function alleles which may be important for the pathogenesis of CLL. Genomic profiling with SNP arrays is a convenient and efficient screening method for simultaneous genome-wide detection of chromosomal aberrations. 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