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| Status |
Public on Sep 01, 2017 |
| Title |
Comparison of gene expression between control and Panobinostat treated Notch1-driven T-ALL |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
T-cell acute lymphoblastic leukaemia (T-ALL) is a disease characterized by the uncontrolled clonal proliferation of immature lymphoid cells. Despite improvement in remission rates using conventional chemotherapeutics, the prognosis for T-ALL remains poor due to disease relapse associated with intrinsic, or acquired tumor cell resistance to the initial therapies. Although T-ALL is a genetically heterogenous disease, mutations resulting in activation of the Notch-1 signaling pathway are present in over 50% of patients, thus defining Notch signaling as a central player in T-ALL onset and progression. Studies also defined an oncogenic c-MYC gene signature as a key characteristic of these T-ALL and connectivity map experiments implicated histone deacetylase inhibitors (HDACi) as potential modifiers of pathways de-regulated by Notch. Recently, studies have shown that panobinostat, an FDA-approved HDACi shows efficacy against human T-ALL cell lines in-vitro, but the molecular mechanism that underpin the therapeutic efficacy of panobinostat is poorly understood. To investigate this, we performed 3'mRNA-seq analysis on T-ALL cells treated for 2 hours with panobinostat in vitro.
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| Overall design |
3'mRNA-seq analysis on T-ALL cells treated for 2 hours with panobinostat in vitro
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| Contributor(s) |
Johnstone RW, Vervoort SJ |
| Citation missing |
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| |
| Submission date |
Aug 17, 2017 |
| Last update date |
May 15, 2019 |
| Contact name |
Stephin J Vervoort |
| E-mail(s) |
stephin.vervoort@petermac.org
|
| Organization name |
Peter MacCallum Cancer Centre
|
| Street address |
305 Grattan Street
|
| City |
Melbourne |
| ZIP/Postal code |
3000 |
| Country |
Australia |
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| Platforms (1) |
| GPL19057 |
Illumina NextSeq 500 (Mus musculus) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA398621 |
| SRA |
SRP115618 |
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