Background: MYC is a transcription factor encoded by the c-MYC gene (thereafter termed MYC). MYC is key transcription factor involved in many central cellular processes including ribosomal biogenesis. MYC is overexpressed in the majority of human tumours including aggressive B-cell lymphoma especially Burkitt's lymphoma. Although Burkitt's lymphoma is a highlight example for MYC overexpression due to a chromosomal translocation, no global analysis of MYC binding sites by chromatin immunoprecipitation (ChIP) followed by global next generation sequencing (ChIP-Seq) has been conducted so far in Burkitt's lymphoma.
Deep sequencing of MYC DNA-binding sites in Burkitt lymphoma.
Specimen part, Cell line
View SamplesTranscriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by mono- and complex co-culture with oral commensal S. gordonii and pathogenic P. gingivalis.
The degree of microbiome complexity influences the epithelial response to infection.
No sample metadata fields
View SamplesThe canonical role of eEF1A is to deliver the aminoacyl tRNA to the ribosome, we have used the yeast model system to investigate further roles for this protein.
Inappropriate expression of the translation elongation factor 1A disrupts genome stability and metabolism.
No sample metadata fields
View SamplesThe intention was to detect genes that are determining trastuzumab efficiency in HER2-positive breast cancer cell lines with different resistance phenotypes. While BT474 should be sensitive to the drug treatment, HCC1954 is expected to be resistant due to a PI3K mutation. The cell line BTR50 has been derived from BT474 and was cultured to be resistant as well. Based on RNA-Seq data, we performed differential expression analyses on these breast cancer cell lines with and without trastuzumab treatment. In detail, five separate tests were performed, namely resistant cells vs. wild type, i.e. HCC1954 and BTR50 vs. BT474, respectively, and untreated vs. drug treated cells. The significant genes of the first two tests should contribute to resistance. The significant genes of the test BT474 vs. its drug treated version should contribute to the trastuzumab effect. To exclude false positives from the combined gene set (#64), we removed ten genes that were also significant in the test BTR50 vs. its drug treated version. This way we ended up with 54 genes that are very likely to determine trastuzumab efficiency in HER2-positive breast cancer cell lines. Overall design: mRNA profiles of human breast cancer cell lines were generated by deep sequencing using Illumina HiSeq 2000. The cell lines BT474 and HCC1954 were analyzed with and without trastuzumab treatment. HCC1954 is known to be trastuzumab resistant. Additionally, the cell line BTR50 was generated as resistant version of BT474, and was analyzed with and without trastuzumab as well.
mRNA profiling reveals determinants of trastuzumab efficiency in HER2-positive breast cancer.
No sample metadata fields
View SamplesImmune interferon beta and gamma are essential for mammalian host defence against intracellular pathogens.
GBPs Inhibit Motility of Shigella flexneri but Are Targeted for Degradation by the Bacterial Ubiquitin Ligase IpaH9.8.
Cell line
View SamplesERG overexpression was conducted in stably transfected K562 cell line with a tet-on inducible plasmid habouring ERG3. Prolonged induction of ERG (8 days) produced spindle cell shape changes whereas non-induced cells retained the round morphology. In oder to determine the genes responsible for inducing cell shape changes, a genome wide transcriptional screen was conducted.
ERG induces a mesenchymal-like state associated with chemoresistance in leukemia cells.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Candidate DNA methylation drivers of acquired cisplatin resistance in ovarian cancer identified by methylome and expression profiling.
Disease, Cell line
View SamplesMultiple DNA methylation changes have been associated with the acquisition of drug resistance; however it remains uncertain how many of these changes may represent critical DNA methylation drivers of chemoresistance. Using gene expression profiling method on HGU133plus2 array, we identified a total of 1370 genes showing significant gene expression changes with 687 genes going up and 683 genes going down in the resistant (cp70) versus sensitive cell lines (A2780) by Rank Product (FDR<5%). Combining expression profiling with methylation profiling data we found out of 245 hypermethylated and down-regulated genes in the resistant cell line, 41 genes were up-regulated following Decitabine treatment alone, 45 genes up-regulated following combined treatment of Decitabine and PXD101, and only 10 genes up-regulated following PXD101 treatment alone. Altogether we found a small set of genes as being potential key drivers of chemoresistance and should be further evaluated as predictive biomarkers, both to existing chemotherapies, but also to epigenetic therapies used to modulate drug resistance.
Candidate DNA methylation drivers of acquired cisplatin resistance in ovarian cancer identified by methylome and expression profiling.
Cell line
View SamplesBACKGROUND
Emmprin and survivin predict response and survival following cisplatin-containing chemotherapy in patients with advanced bladder cancer.
No sample metadata fields
View SamplesING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is required to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the impact of ING1-GADD45a on gene expression, we compared the expression profile of wildtype mouse embryonic fibroblasts (MEFs) with Ing1- and Gadd45a- single- or double-knockout (DKO) MEFs. Overall design: Gene expression profiling in all 4 genotypes of undifferentiated MEFs in triplicates.
Impaired DNA demethylation of C/EBP sites causes premature aging.
Sex, Specimen part, Cell line, Subject
View Samples