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| 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
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| 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.
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| 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.
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| Contributor(s) |
Haferlach C, Bacher U, Kohlmann A, Schindela S, Alpermann T, Kern W, Schnittger S, Haferlach T |
| Citation(s) |
21422114 |
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| Submission date |
Mar 08, 2011 |
| Last update date |
Nov 27, 2018 |
| Contact name |
Hans-Ulrich Klein |
| E-mail(s) |
h.klein@uni-muenster.de
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| Organization name |
Columbia University Medical Center
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| Department |
Neurology
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| Lab |
Center for Translational and Computational Neuroimmunology
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| Street address |
622 W 168th St
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| City |
New York |
| State/province |
NY |
| ZIP/Postal code |
10032 |
| Country |
USA |
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| Platforms (1) |
| GPL6801 |
[GenomeWideSNP_6] Affymetrix Genome-Wide Human SNP 6.0 Array |
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| Samples (7)
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| Relations |
| BioProject |
PRJNA137897 |
| 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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