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GenomicsGenome-wide Analysis Reveals Conserved and Divergent Features of Notch1/RBPJ Binding in Human and Murine T Lymphoblastic Leukemia Cells
Notch1 regulates gene expression by associating with the DNA-binding factor RBPJ and is oncogenic in murine and human T cell progenitors. Using ChIP-Seq, we find that in human and murine T-LL genomes Notch1 binds preferentially to promoters, to RBPJ binding sites, and near imputed ZNF143, Ets and Ru...
ORGANISM(S): Mus musculus 
2011-07-06 | E-GEOD-29600 | biostudies-arrayexpress
GenomicsNOTCH1/RBPJ complexes drive target gene expression through dynamic interactions with super-enhancers
The main oncogenic driver in T-lymphoblastic leukemia (T-LL) is NOTCH1, which activates genes by forming chromatin-associated Notch transcription complexes. Gamma-secretase (GSI) inhibitor treatment prevents NOTCH1 nuclear localization, but most genes with NOTCH1 binding sites are insensitive to GSI...
ORGANISM(S): Homo sapiens 
2013-12-27 | E-GEOD-51800 | biostudies-arrayexpress
GenomicsEpstein-Barr Virus Exploits Intrinsic B-Lymphocyte Transcription Programs to Achieve Immortal Cell Growth
Epstein-Barr Virus Nuclear Antigen 2 (EBNA2) gene regulation through the cell RBPJ transcription factor (TF) is essential for conversion of resting B-lymphocytes (RBLs) into Lymphoblastoid Cell Lines (LCLs). ChIP-seq investigation of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5151 and RBPJ at 10...
ORGANISM(S): Homo sapiens 
2011-07-01 | E-GEOD-29498 | biostudies-arrayexpress
TranscriptomicsDiscovery of biomarkers predictive of GSI response in triple negative breast cancer and adenoid cystic carcinoma
Next generation sequencing was used to identify Notch mutations in a large collection of diverse solid tumors. NOTCH1 and NOTCH2 rearrangements leading to constitutive receptor activation were confined to triple negative breast cancers (TNBC, 6 of 66 tumors). TNBC cell lines with NOTCH1 rearrangemen...
ORGANISM(S): Homo sapiens 
2014-08-14 | E-GEOD-59810 | biostudies-arrayexpress
TranscriptomicsGene profiles induced by overexpression of wild-type and mutant Notch1 variants in MCF10A mammary epithelial cell line
Expression of a constitutively active Notch-1 intracellular domain (NICD) in MCF-10A cells was found to induce two distinct types of 3D structures: large, hyperproliferative structures and small, growth-arrested structures with reduced cell-to-matrix adhesion. These heterogeneous phenotypes reflect...
ORGANISM(S): Homo sapiens 
2010-03-23 | E-GEOD-20285 | biostudies-arrayexpress
Genomicsena-DATASET-MGH2-10-11-2015-05:01:11:768-248 - samples
Whole genome sequences of ACC primagrafts, Histone modification maps and transcription factor binding maps for ACC primagrafts and primary tumors. Processed ChIP-seq data is available on GEO under accession number GSE76465.
EGAD00001001662 | EGA
GenomicsGenetic and epigenetic characterization of adenoid cystic carcinoma
Translocation events are frequent in cancer and may create chimeric fusions or regulatory rearrangements that drive oncogene overexpression. Although regulatory rearrangements are increasingly recognized in hematopoietic and even solid tumors, the underlying mechanisms remain obscure. Here we identi...
EGAS00001001457 | EGA
GenomicsDAC for ACC Study
Data Access Committee EGAC00001000376
EGAC00001000376 | EGA
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
TranscriptomicsDifferentiation of NUT midline carcinoma by epigenomic reprogramming
Knockdown of the oncogene, BRD4-NUT, in a rare cancer, termed NUTmidline carcinoma (NMC), results in morphologic features consistent with squamous differentiation. Treatment with the HDAC-inhibitor, TSA, appears to cause the same phenotype. Here, we use gene expression profiling to compare the cha...
ORGANISM(S): Homo sapiens 
2011-07-01 | E-GEOD-18668 | biostudies-arrayexpress
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