Filters
Technology
Platform
GSE31552
Homo sapiens
131 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Lung cancers are a heterogeneous group of diseases with respect to biology and clinical behavior. Currently, diagnosis and classification are based on histological morphology and immunohistological methods for discrimination between two main histologic groups: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) which account for 20% and 80% of lung carcinomas, respectively. NSCLCs, which are divided into the three major subtypes adenocarcinoma, squamous cell carcinoma and dedifferentiated large cell carcinoma, show different characteristics such as the expression of certain keratins or production of mucin and lack of neuroedocrine differentiation. The molecular pathogenesis of lung cancer involves the accumulation of genetic und epigenetic alterations including the activation of proto-oncogenes and inactivation of tumor suppressor genes which are different for lung cancer subgroups. The development of microarray technologies opened up the possibility to quantify the expression of a large number of genes simultaneously in a given sample. There are several recent reports on expression profiling on lung cancers but the analysis interpretation of the results might be difficult because of the heterogeneity of cellular components. The methods used for sample selection and processing can have a strong influence on the expression values obtained through microarray profiling. Laser capture microdissection (LCM) provides higher specificity in the selection of target cells compared to traditional bulk tissue selection methods, but at an increased processing cost.
Publication Title
Lung cancer transcriptomes refined with laser capture microdissection.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Rattus norvegicus
- 15 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Neuronal differentiation of PC12 cells in response to NGF is a prototypical model in which signal duration determines a biological response. Sustained ERK activity induced by NGF, as compared to transient activity induced by EGF, is critical to the differentiation of these cells. To characterize the transcriptional program activated preferentially by NGF, we compared global gene expression profiles between cells treated with NGF and EGF for 2-4 hrs, when sustained ERK signaling in response to NGF is most distinct from the transient signal elicited by EGF. This analysis identified 69 genes that were preferentially upregulated in response to NGF.
Publication Title
Global expression analysis identified a preferentially nerve growth factor-induced transcriptional program regulated by sustained mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) and AP-1 protein activation during PC12 cell differentiation.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We propose the hypothesis that loss of estrogen receptor function which leads to endocrine resistance in breast cancer, also results in de-differentiation from an epithelial to a mesenchymal phenotype that is responsible for increased aggressiveness and metastatic propensity. siRNA mediated silencing of the estrogen receptor in MCF7 breast cancer cells resulted in estrogen/tamoxifen resistant cells (pII) with altered morphology, increased motility with rearrangement and switch from an actin to a vimentin based cytoskeleton, and ability to invade simulated components of the extracellular matrix. Phenotypic profiling using an Affymetrix Human Genome U133 plus 2.0 GeneChip indicated fold changes 3 in approximately 2500 identifiable unique sequences, with about 1270 of these being up-regulated in pII cells. Changes were associated with genes whose products are involved in cell motility, loss of cellular adhesion and interaction with the extracellular matrix. Selective analysis of the data also showed a shift from luminal to basal cell markers and increased expression of a wide spectrum of genes normally associated with mesenchymal characteristics, with consequent loss of epithelial specific markers. Over-expression of several peptide growth factors and their receptors are indicative of an increased contribution to the higher proliferative rates of pII cells as well as aiding their potential for metastatic activity. Signalling molecules that have been identified as key transcriptional drivers of epithelial to mesenchymal transition were also found to be elevated in pII cells. We suggest that these data support our hypothesis that induced loss of estrogen receptor in previously antiestrogen sensitive cells is a trigger for the concomitant loss of endocrine dependence and onset of a series of possibly parallel events that changes the cell from an epithelial to a mesenchymal type. Inhibition of this transition through targeting of specific mediators may be a useful supplementary strategy to circumvent the effects of loss of endocrine sensitivity.
Publication Title
Estrogen receptor silencing induces epithelial to mesenchymal transition in human breast cancer cells.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Objective: To quantify changes in adipogenic gene expression in the presence of ritonavir (RTV) or tenofovir (TDF), and determine whether conjugated linoleic acid (CLA) isomers (cis9,trans11 or trans10,cis12) can mitigate detrimental effects of antiretoviral drugs.
Publication Title
Microarray Analysis Reveals Altered Lipid and Glucose Metabolism Genes in Differentiated, Ritonavir-Treated 3T3-L1 Adipocytes.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 52 Downloadable Samples
Illumina HiSeq 1000
Description
We report differences in mRNA gene expression in rectal biopsies from MSM compared to controls and for MSM timed with episodes of CRAI. Overall design: Rectal biopsies were obtained from MSM at two study timepoints: 1. after who abstaining from CRAI for >72 hours and 2.after engaing in CRAI within the last 24 hours. Rectal biopsies were also obtained from men who never engaged in AI.
Publication Title
Short Communication: Anatomic Site of Sampling and the Rectal Mucosal Microbiota in HIV Negative Men Who Have Sex with Men Engaging in Condomless Receptive Anal Intercourse.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 55 Downloadable Samples
- Illumina HiSeq 2000
Description
The goal of this study was to identify potential AMH-induced genes and regulatory networks controlling regression by RNA-Seq transcriptome analysis of differences in Müllerian Duct mesenchyme between males (AMH signaling on) and females (AMH signaling off) in purified fetal Müllerian Duct mesenchymal cells. This analysis found 82 genes up-regulated in males during MD regression and identified Osterix (Osx)/Sp7, a key transcriptional regulator of osteoblast differentiation and bone formation, as a novel downstream effector of AMH signaling during MD regression. Overall design: Müllerian Duct mesenchymal cells mRNA profiles from 2-7 embryonic day 14.5 embryos were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000.
Publication Title
<i>Osterix</i> functions downstream of anti-Müllerian hormone signaling to regulate Müllerian duct regression.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This study compared gene expression in murine bcr-abl positive acute lymphoblastic leukemia cells in vivo in allogeneic BMT recipients compared to syngneneic BMT recipients.
Publication Title
Differential gene expression in acute lymphoblastic leukemia cells surviving allogeneic transplant.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The effect of CLA on gene expression in Caco-2 cells
Publication Title
Conjugated linoleic acid alters global gene expression in human intestinal-like Caco-2 cells in an isomer-specific manner.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Analysis of adult retinas from tripartite motif-containing domain 9 knockouts and wild type littermates. Trim9 belongs to the TRIM family of E3 ubiquitin ligases. Results provide insight into possible roles for Trim9 in the retina.
Publication Title
The Trim family of genes and the retina: Expression and functional characterization.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed.
Publication Title
Wild-type tumor repressor protein 53 (Trp53) promotes ovarian cancer cell survival.
Sample Metadata Fields
Age, Specimen part
View Samples