This SuperSeries is composed of the SubSeries listed below.
Integrative genomic characterization of oral squamous cell carcinoma identifies frequent somatic drivers.
Sex, Specimen part
View SamplesOral cavity squamous cell carcinoma (OSCC) is a disease with extensive morbidity and mortality and few useful molecular targets.
Integrative genomic characterization of oral squamous cell carcinoma identifies frequent somatic drivers.
Sex, Specimen part
View SamplesThe transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in human MCF7 cells using recombinant adenovirus vectors. A hybrid construct, 3Mutc, which is a variant of c-Myb harboring three v-Myb-derived DNA binding domain mutations was also analyzed. All the samples were compared to cells infected with a control adenovirus. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.
Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.
No sample metadata fields
View SamplesThe transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in primary human monocytes using recombinant adenovirus vectors. All the samples were compared to cells infected with a control adenovirus expressing only GFP. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.
Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.
No sample metadata fields
View SamplesRecombinant adenovirus vectors were used to express wild type or domain swap mutants of A-Myb and c-Myb transcription factors in MCF-7 cells or pimary lung epithelial cells or fibroblasts. The results show that Myb proteins have extreme context specificity and identify sub-domains responsible for the activation of specific sets of target genes.
Positive and negative determinants of target gene specificity in myb transcription factors.
No sample metadata fields
View SamplesWhile prion infections have been extensively characterized in the laboratory mouse, little is known regarding the molecular responses to prions in other rodents. To explore these responses and make comparisons, we generated a prion disease in the laboratory rat by successive passage of mouse RML prions. Here we describe the accumulation of prions and associated pathology in the rat and describe the transcriptional impact throughout prion disease. Comparative transcriptional profiling between laboratory mice and rats suggests that similar molecular processes are unfolding in response to prion infection. At the level of individual transcripts, however, variability exists between mice and rats and many genes deregulated in mouse scrapie are not affected in rats. Notwithstanding these differences, many transcriptome responses are conserved between mice and rats infected with scrapie. Our findings highlight the usefulness of comparative approaches to understanding neurodegeneration and prion diseases in particular.
Transcriptomic responses to prion disease in rats.
Specimen part, Disease
View SamplesA total number of 1,511 probe sets in the bone marrow showed at least two-fold changes with FDR < 0.05, of which 256 probe sets had over four-fold changes. A group of 63 genes in the bone marrow of NDLD mice had more than a 4-fold change with FDR < 0.0001. From 503 genes encoding proteins with ITIM motif that binds to Ptpn6, 109 were up-regulated and 83 were down-regulated.
A differential gene expression study: Ptpn6 (SHP-1)-insufficiency leads to neutrophilic dermatosis-like disease (NDLD) in mice.
Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptome instability in colorectal cancer identified by exon microarray analyses: Associations with splicing factor expression levels and patient survival.
Specimen part
View SamplesColorectal cancer is a heterogeneous disease molecularly characterized by inherent genomic instabilities, chromosome instability and microsatellite instability. In the present study we propose transcriptome instability as an analogue to genomic instability on the transcriptome level. Exon microarray data from two independent series of altoghether 160 colorectal cancer tissue samples was used for global alternative splicing detection using the FIRMA algorithm (aroma.affymetrix). The sample-wise amounts of these alternative splicing scores exceeding a defined threshold (deviating exon usage amounts) were summarized to provide the basis for description of transcriptome instability. This characteristic was shown to be associated with splicing factor expression levels and patient survival in both independent sample series.
Transcriptome instability in colorectal cancer identified by exon microarray analyses: Associations with splicing factor expression levels and patient survival.
Specimen part
View SamplesColorectal cancer is a heterogeneous disease molecularly characterized by inherent genomic instabilities, chromosome instability and microsatellite instability. In the present study we propose transcriptome instability as an analogue to genomic instability on the transcriptome level. Exon microarray data from two independent series of altoghether 160 colorectal cancer tissue samples was used for global alternative splicing detection using the FIRMA algorithm (aroma.affymetrix). The sample-wise amounts of these alternative splicing scores exceeding a defined threshold (deviating exon usage amounts) were summarized to provide the basis for description of transcriptome instability. This characteristic was shown to be associated with splicing factor expression levels and patient survival in both independent sample series.
Transcriptome instability in colorectal cancer identified by exon microarray analyses: Associations with splicing factor expression levels and patient survival.
Specimen part
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