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Series GSE27832 Query DataSets for GSE27832
Status Public on Dec 16, 2011
Title CDKN1B encoding the cyclin-dependent kinase inhibitor 1B (p27) is located in the minimally deleted region of 12p abnormalities in myeloid malignancies and its low expression is a favorable prognostic marker in acute myeloid leukemia
Organism Homo sapiens
Experiment type Genome variation profiling by SNP array
Summary Alterations of the short arm of chromosome 12 (12p) occur in various hematological malignancies and ETV6 and CDKN1B, which are located on 12p, have been implicated as leukemogenic genes of interest. Design and Methods: We selected 7 patients with myeloid malignancies and small 12p deletions by FISH encompassing only the region centromeric of ETV6 and further evaluated them by SNP microarrays. Results: The minimal deleted region (MDR) contained nine genes only. These genes were subsequently analyzed by microarray expression profiling in an independent cohort of 781 cases mostly with different hematological malignancies or without any hematological malignancy: CREBL2, MANSC1, and CDKN1B were expressed in >25% of cases, while the other 6 genes were expressed in a minority of cases only. As CDKN1B is a cell cycle regulator and functions as a tumor suppressor gene, this gene was selected for further expression studies in 286 AML patients. In cases with low CDKN1B expression (expression level <1,160; 1st quartile), RUNX1-RUNX1T1 (11/83; 13.3%; vs. 5/203; 2.5%; p=0.001), PML-RARA rearrangements (11/83; 13.3%; vs. 4/203; 2.0%; p<0.001), 11q23/MLL rearrangements (6/83; 7.2%; vs. 4/203; 2.0%; p=0.038), and FLT3-TKD mutations (7/63; 11.1% vs. 6/167; 3.6%; p=0.047) were more frequently observed than in patients with intermediate/high expression (2nd-4th quartiles). Low CDKN1B expressers had longer median OS and EFS (not reached vs. 14.9 months; p=0.005 and 31.0 vs. 9.7 months; p=0.013, respectively) than intermediate/high expressers. Conclusions: CDKN1B is an interesting candidate gene as a potential biomarker for acute myeloid leukemia prognostication.
 
Overall design Affymetrix SNP arrays were performed according to the manufacturer's directions using DNA extracted from mononuclear cells after Ficoll density centrifugation from bone marrow or peripheral blood samples.
 
Contributor(s) Haferlach C, Bacher U, Kohlmann A, Schindela S, Alpermann T, Kern W, Schnittger S, Haferlach T
Citation(s) 21422114
Submission date Mar 08, 2011
Last update date Nov 27, 2018
Contact name Hans-Ulrich Klein
E-mail(s) h.klein@uni-muenster.de
Organization name Columbia University Medical Center
Department Neurology
Lab Center for Translational and Computational Neuroimmunology
Street address 622 W 168th St
City New York
State/province NY
ZIP/Postal code 10032
Country USA
 
Platforms (1)
GPL6801 [GenomeWideSNP_6] Affymetrix Genome-Wide Human SNP 6.0 Array
Samples (7)
GSM687172 MDS CMML-1
GSM687173 AML (1)
GSM687174 AML (2)
Relations
BioProject PRJNA137897

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
GSE27832_RAW.tar 461.1 Mb (http)(custom) TAR (of CEL, CNCHP)
Processed data included within Sample table
Processed data provided as supplementary file

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