Microarray is widely used to monitor gene expression changes in breast cancer. The transcriptomic changes in breast cancer is commonly occured during the transition of normal cells to cancerous cells. This is the first study on gene expression profiling of multi ethnic of Malaysian breast cancer patients (Malays, Chinese and Indian). We aim to identify differentially expressed genes between tumors and normal tissues. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001.
Gene expression patterns distinguish breast carcinomas from normal breast tissues: the Malaysian context.
Specimen part, Disease stage, Race
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part, Treatment
View SamplesThis study examined the effect of early pregnancy on the gene expression profiles of stromal and various epithelial mammary cell subpopulations in mice.
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part
View SamplesThis study examined the gene expression profile of mammary tumors derived from Lgr5- and K8-positive cell-of-origins
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part
View SamplesThis study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from Lgr5-creERT2/PIK3CA H1047R mice
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Specimen part, Treatment
View SamplesThis study examined the effect of mutant PIK3CAH1047R expression in mammary subsets of preneoplastic mammary glands from K8-creERT2/PIK3CA H1047R mice
PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours.
Treatment, Time
View SamplesVCaP cells expressing inducible shRNAs for either ERG or a non-targeting control were treated with Doxycycline for 1, 3, 7 and 10 days prior to collection
TMPRSS2:ERG blocks neuroendocrine and luminal cell differentiation to maintain prostate cancer proliferation.
No sample metadata fields
View SamplesA transgenic TMPRSS2:ERG mouse model was engineered in FVB background and compared to its wildtype counterpart in the absence of any treatment This experiment is designed to look at ERG-dependent changes in phenotype and gene expression Overall design: A loxP-GFP-loxP-hERG exon 4-11 cassette was inserted into a BAC clone containing the TMPRSS2 locus using a recombineering kit. This modified BAC was used for pronuclear injection and generation of germline-transmitting mice. One line expressing high GFP was used for pronuclear injection of Cre protein and one sub-line that transmitted the TMPRSS2:ERG transgene into the germline was subsequently bred to homozygosity.
TMPRSS2:ERG blocks neuroendocrine and luminal cell differentiation to maintain prostate cancer proliferation.
No sample metadata fields
View SamplesThe mechanisms involved in the maintenance of memory IgE responses are poorly understood, and the role played by germinal center (GC) IgE cells in these memory responses is particularly unclear. IgE B-cell differentiation is characterized by a transient GC phase, a bias towards the plasma cell (PC) fate, and dependence on sequential switching for the production of high-affinity IgE. We show here that IgE GC B cells are unfit to undergo the conventional GC differentiation program due to impaired B-cell receptor function and increased apoptosis. IgE GC cells fail to populate the GC light zone and are unable to contribute to the memory and long-lived PC compartments. Furthermore, we demonstrate that direct and sequential switching are linked to distinct B-cell differentiation fates: direct switching generates IgE GC cells, whereas sequential switching gives rise to IgE plasma cells. We propose a comprehensive model for the generation and memory of IgE responses.
The distinctive germinal center phase of IgE+ B lymphocytes limits their contribution to the classical memory response.
Specimen part, Treatment
View SamplesPEST-domain-enriched tyrosine phosphatase (PEP) is a cytoplasmic protein tyrosine phosphatase that regulates immune cell functions, including mast cell functions. Using bone marrow derived mast cells (BMMCs) from PEP+/+ and PEP-/- mice, RNA-seq data showed that dinitrophenol (DNP) - activated PEP-/- BMMCs have misregulated gene expression, with some cytokine/chemokine genes (eg.TNFa, IL13, CSF2) showing reduced gene expression in the dinitrophenol (DNP) - activated PEP-/- BMMCs compared to (DNP)-activated PEP+/+ BMMCs. Also, the ability of the glucocorticoid dexamethasone (Dex) to negatively regulate DNP - induced COX-2 gene expression in PEP-/- BMMCs was inhibited compared to the PEP+/+ BMMCs. Overall design: Biological replicates are sequenced and analyzed. The samples are either wild-type or mutant for PEP and cells were sensitized with Ig-E, activated with Dinitrophenol and glucocorticoid treatment done with Dexamethasone.
Transcriptomic data on the role of PEST-domain-enriched tyrosine phosphatase in the regulation of antigen-mediated activation and antiallergic action of glucocorticoids in mast cells.
Sex, Specimen part, Cell line, Treatment, Subject
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