JMJD2B is expressed in a high proportion of human breast tumors, and the expression levels significantly correlate with estrogen receptor (ER) positivity. To assess the effect of JMJD2B depletion on the ER signaling pathway, we performed genome-wide gene expression analysis using the Affymetrix Human Gene 1.0 ST array.
Histone demethylase JMJD2B functions as a co-factor of estrogen receptor in breast cancer proliferation and mammary gland development.
Sex, Specimen part, Cell line, Treatment
View SamplesThe goal was to capture the transcriptional activity due to over-expression of AKT, BAD, ERBB2, IGF1R, RAF1 and KRAS(G12V) genes .Overexpressions were validated using Western Blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in TPM . Overall design: Profiles of gene expression, downstream of AKT, BAD, ERBB2, IGF1R, RAF1 and KRAS(G12V) over-expression, were generated in cells derived from breast and used to generate a gene-expression signatures.
Activity of distinct growth factor receptor network components in breast tumors uncovers two biologically relevant subtypes.
Specimen part, Subject
View SamplesComparison of global transcription profiles in mouse E12.5 embryonic lung from Shh-Cre;Sin3a flox/+ control with Shh-Cre;Sin3a flox/flox revealed a large change genes due to loss of Sin3a in early lung development. Overall design: Examination of 2 different transcriptomes in 2 genotypes with three replicates.
Sin3a regulates epithelial progenitor cell fate during lung development.
Specimen part, Subject
View SamplesExpression profiles of acute myeloid leukemia patient samples.
Identification of genes with abnormal expression changes in acute myeloid leukemia.
No sample metadata fields
View SamplesAcute myeloid leukemia (AML) is one of the most common and deadly forms of hematopoietic malignancies. We hypothesized that microarray studies could identify previously unrecognized expression changes that only occur only in AML blasts. We were particularly interested in those genes with increased expression in AML, believing that these genes may be potential therapeutic targets.
Identification of genes with abnormal expression changes in acute myeloid leukemia.
Sex, Disease
View SamplesThe goal was to capture the transcriptional activity due to over-expression of AKT, BAD, ERBB2, IGF1R, RAF1 and ERK1 genes.Over-expressions were validated using Western Blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in TPM . Overall design: Profiles of gene expression, downstream of AKT, BAD, ERBB2, IGF1R, RAF1 and ERK over-expression, were generated in cells derived from breast and used to generate a gene-expression signatures.
Combating subclonal evolution of resistant cancer phenotypes.
No sample metadata fields
View Samples