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Series GSE12668 Query DataSets for GSE12668
Status Public on Aug 24, 2009
Title Waldenstrom's Macroglobulinemia patients: expression and aCGH data
Organism Homo sapiens
Experiment type Expression profiling by array
Genome variation profiling by array
Summary Waldenström’s macroglobulinemia (WM) is a distinct clinicobiological entity defined as a B-cell neoplasm characterized by a lymphoplasmacytic infiltrate in the bone marrow and immunoglobulin M paraprotein production. Cytogenetic analysis is limited by the difficulty in obtaining tumor metaphases and the genetic basis of the disease remains poorly defined. We performed a comprehensive analysis in 42 WM patients by using high-resolution array-based comparative genomic hybridization with the Human Genome 244A microarray. Overall, 83% of samples have chromosomal abnormalities, with a median of three abnormalities per patient (range 0 to 27). The most common abnormality was 6q deletion (40%) and four non-overlapped minimal deleted regions (MDR) were identified. Gain of 6p was the second most common abnormality (17%) and its presence was always concomitant with 6q loss. An interstitial MDR was delineated at 13q14 including MIRN15A and MIRN16-1 in 10% of patients. Other recurrent deletions were 7q22, 8p, 11q22-q23, 11q23-q24 and 17p11-p13 (7% each). Copy gains were identified in chromosomes 18 (17%), 4 (12%), 3 (10%), 8q (10%) and Xq27.1-q28 (10%). To note, we reported biallelic deletions and/or inactivating mutations with uniparental disomy in TRAF3 and TNFAIP3, two negative regulators of the NF-kB signaling pathway. Furthermore, we confirmed the association between TRAF3 inactivation and increased transcriptional activity of NF-kB target genes. Mutational activation of the NF-kB pathway, which is normally activated by ligand-receptor interactions within the bone marrow microenvironment, highlight its biologic importance, and suggest a therapeutic role for inhibitors of NF-KB pathway activation in the treatment of Waldenström’s macroglobulinemia.
Keywords: gene expression profiling; array comparative genomic hybridization
 
Overall design Expression data: Samples GSM318148-GSM318169.
We included 22 samples from WM patients. Tumor clone population was selected by CD19+ or concomitant CD19+ and CD138+ sorting.

aCGH data: Samples GSM318356-GSM318397.
We included samples from 42 WM patients. Tumor DNA samples were selected by CD19+ or concomitant CD19+ and CD138+ sorting.
 
Contributor(s) Braggio E, Fonseca R
Citation(s) 19351844, 19362969
Submission date Sep 04, 2008
Last update date Aug 10, 2018
Contact name Esteban Braggio
E-mail(s) braggio.esteban@mayo.edu
Organization name Mayo Clinic Arizona
Street address 13400 E. Shea Blvd, MCCRB-300
City Scottsdale
State/province AZ
ZIP/Postal code 85259
Country USA
 
Platforms (2)
GPL96 [HG-U133A] Affymetrix Human Genome U133A Array
GPL4091 Agilent-014693 Human Genome CGH Microarray 244A (Feature number version)
Samples (64)
GSM318148 Waldenstrom's Macroglobulinemia sample MC1336_GEP
GSM318149 Waldenstrom's Macroglobulinemia sample MC1339_GEP
GSM318150 Waldenstrom's Macroglobulinemia sample MC1340_GEP
Relations
BioProject PRJNA112739

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE12668_RAW.tar 2.5 Gb (http)(custom) TAR (of CEL, TXT)
Processed data included within Sample table
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