|
| Status |
Public on Apr 28, 2017 |
| Title |
Epigenetic identity in AML is mostly dependent on disruption of non-promoter regulatory elements and reveals potentially antagonistic effects of mutations in epigenetic modifiers |
| Organism |
Homo sapiens |
| Experiment type |
Third-party reanalysis
Methylation profiling by high throughput sequencing
|
| Summary |
This SuperSeries is composed of the SubSeries listed below.
|
| |
|
| Overall design |
Refer to individual Series
|
| |
|
| Citation(s) |
28408400 |
| |
| Submission date |
Apr 28, 2017 |
| Last update date |
May 15, 2019 |
| Contact name |
Jacob Lowell Glass |
| Organization name |
Memorial Sloan Kettering Cancer Center
|
| Street address |
1275 York Avenue
|
| City |
New York |
| State/province |
NY |
| ZIP/Postal code |
10065 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
|
| Samples (126)
|
|
| This SuperSeries is composed of the following SubSeries: |
| GSE86952 |
Epigenetic identity in AML is mostly dependent on disruption of non-promoter regulatory elements and reveals potentially antagonistic effects of mutations in epigenetic modifiers [human] |
| GSE96744 |
Epigenetic identity in AML is mostly dependent on disruption of non-promoter regulatory elements and reveals potentially antagonistic effects of mutations in epigenetic modifiers [mouse] |
|
| Relations |
| BioProject |
PRJNA384795 |
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