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TranscriptomicsTranscription profiling of human T-ALL cell cultures treated with Compound E, a gamma-secretase inhibitor or vehicle only (DMSO) for 24 h
The NOTCH1 signaling pathway directly links extracellular signals with transcriptional responses in the cell nucleus and plays a critical role during T-cell development and in the pathogenesis over 50% of human T-cell lymphoblastic leukemia (T-ALL) cases. However, little is known about the transcrip...
ORGANISM(S): Homo sapiens 
2008-06-14 | E-GEOD-5827 | biostudies-arrayexpress
TranscriptomicsTranscription profiling of human gamma-secretase inhibitor-sensitive and -resistant T-ALL cell lines
Gain-of-function mutations in NOTCH1 are common in T-cell lymphoblastic leukemias making this receptor a promising target for drugs such as gamma-secretase inhibitors, which block a proteolytic cleavage required for NOTCH1 activation. However, the enthusiasm for these therapies has been tempered by ...
ORGANISM(S): Homo sapiens 
2008-06-14 | E-GEOD-5682 | biostudies-arrayexpress
TranscriptomicsGlobal Gene Expression analysis of CUTLL1 cell lines after treatment with Perhexiline
We identify perhexiline, a small molecule inhibitor of mitochondrial carnitine palmitoyltransferase-1, as a HES1-signature antagonist drug with robust antileukemic activity against NOTCH1 induced leukemias in vitro and in vivo. RNA-Seq from CUTLL1 cell lines treated with Perhexiline or vehicle for 3...
ORGANISM(S): Homo sapiens 
2015-05-07 | E-GEOD-66014 | biostudies-arrayexpress
TranscriptomicsTranscription profiling of human T-ALL cell lines with NOTCH1 activating mutations following CompE treatment
ChIP-on-chip has emerged as a powerful tool to dissect the complex network of regulatory interactions between transcription factors and their targets. However, most ChIP-on-chip analysis methods use conservative approaches aimed to minimize false-positive transcription factor targets. We present a m...
ORGANISM(S): Homo sapiens 
2008-12-12 | E-GEOD-12868 | biostudies-arrayexpress
TranscriptomicsExpression data from Hes1 conditional knock-out NOTCH1-induced leukemias
To formally address the biological activity of Hes1 in vivo, we tested the interaction between oncogenic NOTCH1 and acute Hes1 loss in a retroviral-transduction bone marrow transplantation model of NOTCH-induced T-ALL Forced expression of activated NOTCH1 in this model typically results in full leuk...
ORGANISM(S): Mus musculus 
2015-05-07 | E-GEOD-65863 | biostudies-arrayexpress
TranscriptomicsReverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL
The TLX1 and TLX3 transcription factor oncogenes play an important role in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL)1,2. Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This Systems Bi...
ORGANISM(S): Mus musculus 
2011-11-08 | E-GEOD-33550 | biostudies-arrayexpress
TranscriptomicsTranscription profiling of human T-ALL samples to investigate synergistic interaction of gamma-secretase inhibitor therapy and glucocorticoids
Glucocorticoids are an essential component of the treatment of lymphoid malignancies and resistance to glucocorticoid therapy constitutes a prominent clinical problem in relapsed and refractory lymphoblastic leukemias. Constitutively active NOTCH signaling is involved in the pathogenesis of over 50%...
ORGANISM(S): Homo sapiens 
2009-01-13 | E-GEOD-7067 | biostudies-arrayexpress
TranscriptomicsTranscription profiling of mouse small intestine following treatment with dexamethosone and DBZ
Gamma-secretase inhibitors (GSIs), which block the activation of NOTCH receptors, are being tested in the treatment of T-cell acute lymphoblastic leukemia (T-ALL). Thus far, limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical application of these targe...
ORGANISM(S): Mus musculus 
2009-04-10 | E-GEOD-11184 | biostudies-arrayexpress
TranscriptomicsExpression data from CUTLL1 cells infected with shHES1
To formally address the biological activity of HES1 in vitro, we measured the transcriptional effect of HES1 inactivation infectiing CUTLL1 leukemia cell lines with shHES1 HES1 knockdown triggered apoptosis in human T-ALL lymphoblasts. We show that HES1 inactivation induces programmed cell death in ...
ORGANISM(S): Homo sapiens 
2015-05-07 | E-GEOD-65872 | biostudies-arrayexpress
TranscriptomicsExpression data from mouse T-cell lymphomas
Transgenic expression of TLX1 induces T-cell leukemias in mice. We used microarrays to identify the gene expression signatures associated with TLX1 tumors compared with different genetic models T acute lymphoblastic lymphoma. RNA extraction from T-cell tumors from mice with different T-cell lymphom...
ORGANISM(S): Mus musculus 
2010-10-19 | E-GEOD-19499 | biostudies-arrayexpress
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