title: Gene expression of SCP-1 cells after incubation with conditioned medium of the breast carcinoma cell line MCF-7.

status: Public on Aug 14 2013

city: Dresden

first: Manja

last: Wobus

address: Fetscherstr. 74

department: Hematology/Oncology

institute: University Hospital Dresden

summary: Disseminated tumor cells (DTCs) in the bone marrow can be detected in patients with solid tumors early on in disease progression. Via interaction with mesenchymal stromal cells (MSCs) these tumor cells may interfere with hematopoiesis. Using appropriate co-culture models, we investigated whether DTCs can change the bone marrow microenvironment by modulating MSC function with a special emphasis on their chemoattractive activity towards hematopoietic stem and progenitor cells (HSPCs). Human bone marrow derived MSCs as well as an immortalised MSC line (SCP-1) were co-cultured with MCF-7, MDA-MB231 breast carcinoma or MCF-10A non-malignant breast epithelial cells or their conditioned medium. Gene expression analysis of SCP-1 cells cultured with MCF-7 conditioned medium revealed SDF-1/CXCL12 as one of the significantly downregulated genes. Both tumor cell lines caused an inhibited SDF-1 promoter activity in SCP-1 cells, whereby MCF-7 medium decreased it to 77% and MDA-MB231 to 47%. Moreover, the SDF-1 mRNA and protein levels were significantly reduced. As a functional consequence of lower SDF-1 levels, we detected a decreased trans-well migration potential of CD34+ HSPC to MSC/tumor cell co-cultures or conditioned medium. The specificity of this chemokine mediated effect was confirmed by blocking studies with the CXCR4 antagonist AMD3100. Downregulation of SP1 transcription factor and increased miR23a levels in MSCs after contact with tumor cell medium as well as an enhanced TGFb1 expression were identified as potential molecular regulators of SDF-1 activity in MSCs. We propose an additional mechanism by which tumor cells affect the niche environment of HSPCs and therefore negatively impact hematopoiesis.

overall_design: Gene expression of human immortalized mesenchymal stromal cells (SCP-1) was investigated after incubation with conditioned medium of the breast carcinoma cell line MCF-7 for 24, 48, and 72 hours. Three independent experiments were performed at each time.

first: Martin

last: Bornhäuser


title: Genome-wide analysis of interleukin (IL) -6 and IL-11 responsive genes in murine gastric tumors

status: Public on Aug 10 2013

city: Heidelberg - Melbourne

first: Stefan

last: Thiem

state: Victoria

address: 145 Studley Road

department: Cancer Research

country: Australia

institute: Olivia Newton-John Cancer Research Institute

summary: We performed micrarrays to analyse gene expression in spontaneously arising gastric tumors from gp130Y757F/F mutant mice (Tebbutt et al., 2002) following administration of recombinant human IL-6 or IL-11. The present study was designed to assess differences in gene expression in response to IL-6 and IL-11, two cytokines which both activate the shared gp130 receptor and downstream Stat3 signalling pathway. Since gastric tumorigenesis in gp130Y757F/F mice is strictly dependent on IL-11, but not IL-6 signalling (Ernst et al., 2008) the study aimed to identify IL-6 and IL-11 specific target genes which may account for the IL-11 dependent tumor development.

overall_design: Total RNA was obtained from gastric tumor tissue of gp130Y575F/F mice collected 60 min after a single systemic (i.p.) administration of PBS (vehicle control), recombinant human IL6 or IL11 (5 ug). The gene expression profile of the IL-6 and IL-11 treated samples were separately compared to the PBS (vehicle) treated control samples, resulting in two lists of responsive genes (”IL-6 vs control” and “IL-11 vs control”).

first: Matthias

last: Ernst


title: Profile of H4K16 acetylation in undifferentiated ES cells [Illumina BeadArray data]

status: Public on Aug 23 2013

city: Edinburgh

first: Gillian

last: Taylor

address: MRC HGU Crewe Road South

country: United Kingdom

institute: IGMM

summary: Level of H4K16ac on highest and lowest expressed genes in undifferentiated ES cells

overall_design: 3 biological replicates in undifferentiated ES cells

first: Ragnhild

last: Eskeland

first: Madapura

middle: M

last: Pradeepa

first: Wendy

last: Bickmore


title: Gene expression analysis in mice with heart muscle-specific repression of CELF activity (MHC-CELFdelta)

status: Public on Aug 26 2013

city: Cleveland

first: Andrea

last: Ladd

state: OH

address: 9500 Euclid Avenue

department: Cell Biology

country: USA

institute: Cleveland Clinic Lerner Research Institute

summary: Members of the CUG-BP, Elav-like family (CELF) regulate alternative splicing in the heart.  In MHC-CELFdelta transgenic mice, CELF splicing activity is inhibited postnatally in heart muscle via expression of a nuclear dominant negative CELF protein under an a-myosin heavy chain promoter.  MHC-CELFdelta mice develop dilated cardiomyopathy characterized by alternative splicing defects, enlarged hearts, and severe contractile dysfunction.  In this study, gene expression profiles in the hearts of wild type, high- and low-expressing lines of MHC-CELFdelta mice were compared using microarrays.  Gene ontology and pathway analyses identified contraction and calcium signaling as the most affected processes.  Network analysis revealed that the serum response factor (SRF) network is highly affected.  Downstream targets of SRF were up-regulated in MHC-CELFdelta mice compared to the wild type, suggesting an increase in SRF activity.  Although SRF levels remained unchanged, known inhibitors of SRF activity were down-regulated.  These results suggest a role for CELF-mediated alternative splicing in the regulation of contractile gene expression, achieved in part through modulating the activity of SRF, a key cardiac transcription factor.

overall_design: Microarray analysis was performed on total RNA extracted from whole hearts of three MHC-CELFdelta-10 and three MHC-CELFdelta-574 females collected at weaning (three weeks old).  Three female wild type littermates from each line were used as controls (n = 6 wild type in total).

first: Twishasri

last: Dasgupta

first: Samantha

middle: J

last: Stillwagon

middle: N


title: Bone marrow-derived macrophages express distinct transcriptional programs when activated by LPS, IFN-gamma and PAO.

status: Public on Aug 08 2013

city: Houston

first: Chad

last: Creighton

state: TX

address: One Baylor Plaza, Mail Stop: BCM305

department: Biostatistics, Ducan Cancer Center

institute: Baylor College of Medicine

summary: mRNA microarray analysis of bone marrow derived macrophages treated under four conditions, including Naïve (N).  Bone marrow derived macrophages (BMDM) were derived from the bone marrow of mice and cultured in the presence of PAO, IFN-gamma, or lipopolysaccharide (LPS). Profiled groups include Naive, LPS, IFN, PAO.

overall_design: Compared each of the  groups (PAO, LPS, IFN) with Naïve group.

first: Valentine

last: Ongeri

first: Farrah

last: Kheradmand

first: David

last: Corry

first: Yiqun

last: Zhang


title: mRNA expression profiles of 71 esophageal squamous cell carcinoma cases

status: Public on Sep 01 2013

city: beppu

first: sawada

last: genta

address: tsurumihara

country: Japan

institute: kyushu university

summary: Analysis of primary esophageal squamous cell carcinoma (ESCC) from 71 patients in japan. Integrative analysis of gene expression profiles and genomic alterations obtained from array-CGH and NGS provided us new insight into the pathogenesis of ESCC

overall_design: Gene expression levels obtained from 71 microdissected ESCC tumors. We used the commercially available Human Whole Genome Oligo DNA Microarray Kit (Agilent Technologies). Labeled cRNAs were fragmented and hybridized to an oligonucleotide microarray (Whole Human Genome 4×44K Agilent G4112F). Fluorescence intensities were determined with an Agilent DNA Microarray Scanner. The gene expression profiles (GE) obtained from microarray data were quintile normalized. The batch effect in microarray experiments was also adjusted by an empirical Bayesian approach

first: Koshi

last: Mimori

first: Masaki

last: Mori


title: Expression analysis of Prdm4 mutant and overexpressing mouse embryonic stem cells

city: Coventry

first: Andrew

middle: Christopher

last: Nelson

address: Gibbet Hill Campus

department: School of Life Sciences

institute: University of Warwick

summary:
Expression profiling of wild-type, Prdm4 null and Prdm4-EGFP overexpressing mouse embryonic stem cells using Illumina whole genome V2 arrays.
The hypothesis tested was that Prdm4 regulates gene expression consistant with Prdm4 genomic binding identified by ChIP-seq

overall_design: Prdm4 null embryonic stem cells were generated by gene targeting.  Prdm4-EGFP overexpressing cells were generated through stable transfection.  Total RNA was obtained from six wild-type ES cell clones, four Prdm4 null mutant ES cell clones and six Prdm4-EGFP overexpressing ES cell clones and hybridized to Illumina WG6_V2 arrays

first: D

last: Bogani

first: M

last: Morgan

first: A

first: J

last: McGouran

first: B

last: Kessler

first: E

last: Bikoff

last: Robertson


title: The differentially expressed genes in SRSF3 siRNA-treated HCT116 cells

status: Public on Aug 04 2013

city: Tokushima

first: Ken

last: Kurokawa

address: 3-18-15 Kuramoto

department: Health Biosciences

institute: The University of Tokushima Graduate School

summary: Several members of SRSF family play wide-ranging roles in the regulation of transcription and post-splicing processes as well as splice sites selection. Although the expression of SRSF3 was reported to be overexpressed in several cancers, the roles of SRSF3 in the cancer cells are almost unknown. We analyzed differentially expressed genes in SRSF3 siRNA-treated HCT116 cells and identified the specific pathways regulated by SRSF3.

overall_design: After treatment of HCT116 cells with SRSF3 (sample 02) or control (sample 01) siRNA, total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA). The quality of the purified RNA and its applicability for microarray analysis were assessed by the Agilent 2100 Bioanalyzer using a RNA 6000 Nano Labchip kit (Agilent Technologies, Palo Alto, CA, USA). Total RNA (400 ng) was used for amplification, labeling and hybridization to a whole human genome oligoDNA microarray (4x44k; Agilent) according to the manufacture’s instructions.


title: HDAC inhibitor kinetic rate constants correlate with cellular histone acetylation but not transcription and cell viability

status: Public on Aug 01 2013

city: South San Francisco

first: Josh

last: Kaminker

state: CA

address: 1 DNA Way

department: Bioinformatics and Computational Biology

institute: Genentech

summary: Histone deacetylases (HDACs) are critical in the control of gene expression and dysregulation of their activity has been implicated in a broad range of diseases including cancer, cardiovascular and neurological diseases. HDAC inhibitors (HDACi) employing different zinc chelating functionalities such as hydroxamic acids and benzamides have shown promising results in cancer therapy. While it has also been suggested that HDACi with increased isozyme-selectivity and potency may broaden their clinical utility and minimize side effects, the translation of this idea to the clinic remains to be investigated. Moreover, a detailed understanding of how HDACi with different pharmacological properties affect biological functions in vitro and in vivo is still missing. Here we show that a panel of benzamide-containing HDACi are slow tight-binding inhibitors with long residence times unlike the hydroxamate-containing HDACi SAHA and TSA. Characterization of changes in H2BK5 and H4K14 acetylation following HDACi treatment in the neuroblastoma cell line SH-SY5Y revealed that the timing and magnitude of histoneacetylation mirrored both the association and dissociation kinetic rates of the inhibitors. In contrast, cell viability and microarray gene expression analysis indicated that cell death induction and changes in transcriptional regulation do not correlate with the dissociation kinetic rates of the HDACi. Therefore, our study suggests that the evaluation of different classes of HDACi compounds using recombinant HDACs or histone acetylation is insufficient to predict their functional impact on cell activity.

overall_design: Control, SAHA 6hr, SAHA 24hr, SAHA 24hr (pulsed), C1 6hr, C1, 24hr, C1 24hr (pulsed)

first: Joshua

middle: S

first: Pascal

last: Steiner

first: Christopher

middle: E

last: Heise

first: Benjamin

last: Lauffer

first: Zora

last: Modrusan

first: Grazyna

last: Fedorowicz


title: Expression changes in IC GABA receptors in the auditory midbrain of young adult and aging presbycusis mice.

status: Public on Aug 06 2013

city: Tampa

first: Robert

last: Frisina

state: FL

address: 4202. E. Fowler Avenue ENB 118

department: Department of Chemical & Biomedical Engineering

institute: university of south florida

summary:
We performed a microarray analysis of auditory midbrain (inferior colliculus, IC) mRNA from young adult CBA mice (controls) with good hearing, middle aged (MA) with good hearing, and old mild (MP) and severe (SP) presbycusic CBA mice. Fold Change data derived from RMA normalization revealed that the overall GABA receptor alpha 6 expression profiles for MA, MP and SP were down-regulated relative to young adult controls with good hearing. Relative real-time PCR for five GABA receptors confirmed this age-related down regulation quantitatively. Functional hearing data: Auditory Brainstem Responses (ABR) enriched the analysis to select the probe-sets that changed with age and hearing loss by the linear regression best-fit line model technique. GABA receptor genotype-phenotype correlations with auditory functional data indicated that GABA-receptor subtypes are under expressed in SP mice.  Hierarchical clustering (HC) analyses yielded statistical significance of normalized GeneChip data Real-time PCR showed that Gabra6, GABA B receptor 1 (Gabbr1), and Gaba transporter protein Slc32a1 may be involved in physiological changes that occur in age-related hearing loss.
Presbycusis – age-related hearing loss – is the number one communicative disorder of our aged population. In this study we analyzed gene expression for a set of GABA receptors in the inferior colliculus of aging CBA mice using the Affymetrix GeneChip MOE430A. Functional phenotypic hearing changes from RMA normalized microarray data (39 replicates) in four age-groups, Young Controls and Middle aged mice with good hearing, mild and sever e presbycusis from old mice. Fold change gene expression derived from RMA normalized data were first subjected to one-way ANOVA, and then linear regression was performed. The selected gene expression changes were confirmed by relative real-time relative to young adult controls with good hearing. Statistically significant and real time PCR confirmed GABA receptor genes; Gabra6, GABA B receptor 1 (Gabbr1), and Gaba transporter protein Slc32a1, may be involved in physiological changes that occur in age-related hearing loss.  Lastly, gene expression measures of each age group were correlated with pathway/network relationships relevant to the inferior colliculus  using Pathway Architect, to identify key pathways consistent with the gene expression changes observed

overall_design: In the study of Expression changes in IC GABA receptors in the Auditory Midbrain of young adult and aging presbycusis mice total of thirty nine chips were used. The normal aging mice were in Four groups Young adults Controls with good hearing (8 mice, 8 MOE430A GeneChips), Middle aged group  with good hearing  ( 17 mice, 17 MOE430A GeneChips), Mild Presbycusis with limited hearing loss (9 mice, 9 MOE430A GeneChips) and Severe Presbycusis (5 mice, 5 MOE430A GeneChips).

first: Mary

last: D'Souza

first: Xiaoxia

last: Zhu

first: Martha

middle: L

last: Zettel

middle: D


title: SHAE003: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.

status: Public on Jul 31 2013

city: Seattle

first: Michael

last: Katze

state: WA

address: Rosen Building 960 Republican St.

department: Microbiology

institute: University of Washington

summary: HAE cultures were infected with SARS-CoV, SARS-ddORF6 or SARS-BatSRBD and were directly compared to A/CA/04/2009 H1N1 influenza-infected cultures.  Cell samples were collected at various hours post-infection for analysis.

overall_design: Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV.  Time Points = 0, 24, 48, 60, 72, 84 and 96 hrs post-infection forSARS-ddORF6 and SARS-BatSRBD.  Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1.  Done in triplicate/quadruplicate for RNA  Triplicates/quadruplicates are defined as 3/4 different wells, plated at the same time and using the same cell stock for all replicates.  Time matched mocks done in triplicate from same cell stock as rest of samples.  Culture medium (the same as what the virus stock is in) will be used for the mock infections.  Infection was done at an MOI of 2.

first: Ralph

last: Baric

first: Amy

last: Sims

first: G

last: Law

first: Jean

last: Chang


title: SHAE002: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.

summary: HAE cultures were infected with SARS-CoV, SARS-dORF6 or SARS-BatSRBD and were directly compared to A/CA/04/2009 H1N1 influenza-infected cultures.  Cell samples were collected at various hours post-infection for analysis.

overall_design: Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV, SARS-dORF6 and SARS-BatSRBD.  Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1.  Done in triplicate or quadruplicate for RNA  Triplicates/quadruplicates are defined as 3/4 different wells, plated at the same time and using the same cell stock for all replicates.  Time matched mocks done in triplicate from same cell stock as rest of samples.  Culture medium (the same as what the virus stock is in) will be used for the mock infections.  Infection was done at an MOI of 2.


title: Asthmatics with exacerbation during acute respiratory illness exhibit unique transcriptional signatures.

status: Public on Aug 02 2013

city: Chicago

first: Peter

last: McErlean

state: Illinois

address: 240 E. Huron, McGaw M-530h

department: Allergy Immunology

institute: Northwestern University

summary: Acute respiratory illness (ARI) is the leading cause of asthma exacerbations yet the mechanisms underlying this association remain unclear. To address the deficiencies in our understanding of the molecular mechanisms driving ARI-induced asthma exacerbations, we undertook a transcriptional profiling study of the nasal mucosa over the course of ARI amongst individuals with a history of asthma, allergic rhinitis and no underlying respiratory disease. We found that ARI is characterized by dynamic, time-specific transcriptional profiles whose magnitudes of expression are influenced by underlying respiratory disease and the mucosal repair signature evoked during ARI. Most strikingly, we report that asthmatics that experience ARI-induced exacerbations are characterized by a reduced but prolonged inflammatory immune response, inadequate activation of mucosal repair and the expression of a newly described exacerbation-specific signature. Findings from our study represent a significant contribution towards clarifying the complex molecular interactions which typify ARI-induced asthma exacerbations.

overall_design: Upon the onset of ‘common cold’, volunteers were instructed to attend the first of three required visits to the study clinic. The first and second visits were designed to obtain samples and clinical data during the early and late stages of symptomatic illness respectively, whereas the third visit would occur when volunteers were asymptomatic and serve as a prospective baseline (BL) for the study.

first: Sergejs

last: Berdnikovs

first: Silvio

last: Favoreto Jr

first: Junqing

last: Shen

first: Assel

last: Biyasheva

first: Rebecca

last: Barbeau

first: Chris

last: Eisley

first: Andrea

last: Barczak

first: Theresa

last: Ward

middle: P

last: Schleimer

first: David

last: Erle

first: Homer

middle: A

last: Boushey

first: Pedro

middle: C

last: Avila


title: FGFR2 Signaling Underlies p63 Oncogenic Function in Squamous Cell Carcinoma

city: Boston

first: Matthew

last: Ramsey

state: MA

address: 77 Ave Louis Pasteur, HIM 668

department: Dermatology

institute: Brigham and Women's Hospital

summary: This study was designed to examine the requirement for the p63 transcription factor in Squamous Cell Carcinoma (SCC) tumor maintenance in an in vivo murine system.  A tamoxifen-inducible Keratin 14-driven Cre recombinase transgene was used to conditionally excise p63 in advanced murine SCC tumors.  These data show the context-dependent regulation of p63 target genes in cancer.

overall_design: Total RNA from murine Squamous Cell Carcinoma tumors was examined 1-3 days following genomic excision of TP63 in Keratin 14-expressing tumor cells.

middle: R

first: Leif

middle: W

last: Ellisen


title: SHAE004: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.

first: Michael

last: Katze

overall_design: Time Points = 0, 12, 24, 36, 48, 60, 72, 84 and 96 hrs post-infection for SARS-CoV, SARS-dORF6 and SARS-BatSRBD.  Time Points = 0, 6, 12, 18, 24, 36 and 48 hrs post-infection for H1N1.  Done in triplicate for RNA  Triplicates are defined as 3 different wells, plated at the same time and using the same cell stock for all replicates.  Time matched mocks done in triplicate from same cell stock as rest of samples.  Culture medium (the same as what the virus stock is in) will be used for the mock infections.  Infection was done at an MOI of 2 for SARS viruses and an MOI of 1 for H1N1.

first: Ralph

last: Baric

first: Amy

last: Sims

last: Law


title: Gene Expression Profiles of Lymphocytes Obtained from Mice treated with Glatimer Acetate and ither Glatiramatoids

city: Natanya

first: Tal

middle: Haim

last: Hasson

address: Hatrufa 12

department: Analytical R&D

country: Israel

institute: Teva Pharmaceuticals

summary: Glatiramer acetate (GA; Copaxone), is a complex mixture of synthetic polypeptides approved for treatment of multiple sclerosis (MS). GA is an altered peptide ligand (APL) of myelin basic protein (MBP), an encephalitic autoantigen implicated in MS. GA induces GA-reactive T cells, which upregulate expression of anti-inflammatory and neurotrophic substances in the CNS. The antigenic sequences in glatiramoids cannot be completely characterized; nevertheless, differences among them can cause toxicity. We conducted microarray analyses to determine whether gene expression by GA-reactive lymphocytes from mouse spleens could differentiate GA from other glatiramoids. Expression of 135 genes was unique to cells reactivated by GA vs by intentionally altered GA and other glatiramoids. Significantly (p<0.01) altered expression of 207 genes was observed by cells reactivated by GA vs purported generic GA. Some APLs of MBP have caused serious adverse effects in MS patients. The influence of altered gene expression on glatiramoid safety warrants further investigation.

overall_design:
Glatiramoid samples for SPL cell activation were grouped into four categories: 1) Verified GA, which included GA-RS (22 samples) and GA drug product (GA-DP, 34 samples from 30 batches) manufactured by Teva; 2) Deliberately Modified GA (DM-GA; 9 samples), which included glatiramoids made by Teva that were similar to GA but modified in a variety of ways: prepared with different ingredients (e.g., missing a constituent amino acid); prepared with the same amino acids in the same molar ratio as GA, but with defined amino acid sequences and different molecular weights (referred to as peptide markers TV-35 and TV-66); synthesized by a different process (e.g., changing acetolytic cleavage conditions, alternating polymerization initiator); exposed to destabilizing conditions (e.g., degradation by acid, base, and heat); 3) Unverified Glatiramoids, which included 4 samples, TV-5010 and 3 glatiramoids synthesized to be similar to GA but not manufactured using the Teva-patented manufacturing process; and 4) Unverified Generic GA, which included samples from 2 glatiramoids (“GA-N” 11 samples from 5 different batches, and 2 “GA-C” samples from a single batch) marketed as generic GA manufactured by companies other than Teva.

Please note that GSE61901 is another series on the same data as GSE40566.  GSE61901 includes the individual  technical replicates, and was utilized for the manuscript: Towfic F, Funt JM, Fowler KD, Bakshi S et al. Comparing the biological impact of glatiramer acetate with the biological impact of a generic. PLoS One 2014;9(1):e83757. PMID: 24421904.  GSE40566 was preprocessed to average the technical replicates, and was utilized for the manuscript: Bakshi S, Chalifa-Caspi V, Plaschkes I, Perevozkin I et al. Gene expression analysis reveals functional pathways of glatiramer acetate activation. Expert Opin Ther Targets 2013 Apr;17(4):351-62. PMID: 23469939.

first: Shlomo

last: Bakshi

first: Vered

last: Caspi

first: Inbar

last: Plaschkes

first: Igor

last: Perevozkin

first: Riki

last: Schwartz


status: Public on Jul 30 2013

city: Cambridge

first: Giuliano

middle: Giuseppe

last: Stirparo

state: Cambridgeshire

address: 418 Cambridge Science Park Milton Rd

institute: Cerevance ltd

summary: Genome-wide  gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile  that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage.

overall_design: To test the identity and the degree of differentiation of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice.  Global gene expression profiles by microarray was obtained in c-kitpos eCSCs, c-kitpos eCSC-derived YFPpos CMs and normal adult CMs. c-kitposCD45neg eCSCs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice and harvested at 4th passage (n=3). YFPpos cardiomyocytes were FACS sorted from left ventricle apex of Lentirius-c-kit/cre recombined B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice 28 days after ISO (N=3). Normal adult CMs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice (n=3).

first: Carla

last: Vicinanza

first: Iolanda

last: Aquila

middle: G

first: Daniele

last: Torella

first: Bernardo

last: Nadal-Ginard


title: TPL-2;ERK1/2 signaling promotes host resistance against intracellular bacterial infection by negative regulation of type I interferon production [Set 1]

status: Public on Sep 05 2013

city: London

first: Fin

last: McNab

address: The Ridgeway, Mill Hill

institute: MRC NIMR

summary:
Analysis of Mtb infected murine macrophages derived from C57Bl/6 WT, TPL2KO, IFNARKO & TPL2IFNAR DKO mice [Set 1]
Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a leading cause of mortality and morbidity worldwide, causing approximately 1.4 million deaths per year. Key immune components for host protection during tuberculosis include the cytokines IL‐12, IL‐1 and TNF‐α, as well as IFN‐γ and CD4+ Th1 cells. However, immune factors determining whether individuals control infection or progress to active tuberculosis are incompletely understood. Excess amounts of type I interferon have been linked to exacerbated disease during tuberculosis in mouse models and to active disease in patients, suggesting tight regulation of this family of cytokines is critical to host resistance. In addition, the immunosuppressive cytokine IL‐10 is known to inhibit the immune response to Mtb in murine models through the negative regulation of key pro-inflammatory cytokines and the subsequent Th1 response. We show here, using a combination of transcriptomic analysis, genetics and pharmacological inhibitors that the TPL-2-ERK1/2 signaling pathway is important in mediating host resistance to tuberculosis through negative regulation of type I interferon production. The TPL-2-ERK1/2 signalling pathway regulated production by macrophages of several cytokines important in the immune response to Mtb as well as regulating induction of a large number of additional genes, many in a type I IFN dependent manner. In the absence of TPL-2 in vivo, excess type I interferon promoted IL-10 production and exacerbated disease. These findings describe an important regulatory mechanism for controlling tuberculosis and reveal mechanisms by which type I interferon may promote susceptibility to this important disease.

overall_design: Macrophages were derived from C57Bl/6 bone marrow, plated and infected with Mtb H37Rv (or not) in duplicate wells. Samples were then harvested for RNA at time 0 (uninfected only), 15m, 30m, 1hr, 3hr, 6hr and 24hr.

first: Finlay

first: John

last: Ewbank

first: Ricardo

last: Rajsbaum

first: Evangelos

last: Stavropoulos

first: Anna

last: Martirosyan

first: Paul

last: Redford

first: Xuemei

last: Wu

first: Christine

last: Graham

first: Margarida

last: Saraiva

first: Philip

last: Tsichlis

first: Damien

last: Chaussabel

first: Steven

last: Ley

first: Anne

last: O’Garra


title: Human glioma cell line T98G: BAP-PCBP2 RIP vs. BAP-GFP RIP (Control)

status: Public on Jul 24 2013

city: Beijing

first: zhong

middle: xiao

last: peng

address: 5 Dong Dan San Tiao

country: China

institute: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences

summary: RIP-Chip analysis of PCBP2 and identification of preferentially associated mRNAs. T98G cells were transfected transiently with BAP-tagged constructs. BAP-tagged proteins were biotinylated in vivo by the co-transfected hBirA enzyme. RNPs were recovered via precipitation with Steptavidin-sepharose beads. Finally, RNAs were purified and analyzed on microarrays. BAP-GFP as control was used in three independent sets of experiments.

overall_design: Two-condition experiment, BAP-PCBP2 vs. BAP-GFP cells. Biological replicates: 3 BAP-PCBP2 replicates, 3 BAP-GFP (Control) replicates

first: Wei

last: Han


title: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.

first: Michael

last: Katze

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Distinct genetic alterations occur in ovarian tumor cells selected for combined resistance to carboplatin and docetaxel

status: Public on Jul 22 2013

city: Sudbury

first: Baoqing

last: Guo

state: ON

address: 41 Ramsey Lake Road

department: Tumor Biology

country: Canada

institute: Advanced Medical Research Institute of Canada

summary: Background: Current protocols for the treatment of ovarian cancer include combination chemotherapy with a platinating agent and a taxane. However, many patients experience relapse of their cancer and the development of drug resistance is not uncommon, making successful second line therapy difficult to achieve. The objective of this study was to develop a cell line resistant to both carboplatin and docetaxel (dual drug resistant ovarian cell line A2780CBNDXL), along with single agent resistant lines (docetaxel resistant A2780DXL and carboplatin resistant A2780CBN), to investigate the mechanisms which underlie the development of dual drug resistance.  Methods: The A2780 epithelial ovarian cancer cell line was used to select for isogenic carboplatin, docetaxel and dual drug resistant cell lines. A selection method of gradually increasing drug doses was implemented to avoid clonal selection. Resistance was confirmed using a clonogenic assay. Changes in gene expression associated with the development of drug resistance were determined by microarray analysis compared to parental co-culture control A2780CC. Changes in selected genes were validated by QPCR and immunoblotting. Results: Three isogenic cell lines were developed and resistance to each drug or the combination of drugs was confirmed. Development of resistance was accompanied by a reduced growth rate. The microarray and QPCR analyses showed that unique changes in gene expression occurred in the dual drug resistant cell line and that genes known to be involved in resistance could be identified in all cell lines. Conclusions: Novel changes in gene expression can occur in the development of dual drug resistance, indicating that dual drug resistance is not a simple combination of the changes occurring in single agent resistance

overall_design: Carboplatin, docetaxel (GSE26129) and carboplatin/docetaxel dual resistant cell lines of ovarian A2780 were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with two replicate of both forward and reverse labellings for each cell line. Four arrays were used for this experiments. And it was four replicate of both forward and reverse labellings for A2780 cells. Eight arrays were used for this experiments

first: Stephen

last: Armstrong

first: Rashmi

last: Narendrula

first: Amadeo

middle: M

last: Parissenti

first: Katherine

last: McCallum

first: Stephanie

last: Cull

first: Carita

last: Lanner


title: Expression analysis of LM8 osteosarcoma cells overexpressing human Prolyl Hydroxylase Domain Protein-4 (PHD4) and LM8 control cells

status: Public on Aug 09 2013

city: Dresden

first: Georg

last: Breier

department: Institut für Pathologie

country: Germany

institute: TU Dresden

summary:
PHD4 regulates the expression of Hypxia-inducible Factor 2 (HIF-2) alpha in LM8 osteosarcoma cells. PHD4 overexpression inhibits the growth of experimental tumor in syngenic mice but stimulates angiogenesis via Transforming Growth-Factor (TGF)-alpha.
We used microarrays to investigate the gene expression of stable LM8 cell line overexpressing human PHD4 in comparison to the LM8 control line, transfected with the empty vector.

overall_design: RNA was prepared from cultured cells and used for hybridization on Affymetrix microarrays.

first: Marianne

last: Grosser


title: Requirement for Lyl1 in a model of Lmo2-driven early T-cell precursor ALL

status: Public on Jul 25 2013

city: Clayton

last: Shi

address: Wellington Rd

institute: Monash University

summary: To determine the requirement for Lyl1 in Lmo2-driven T-ALL, microarray data was perepared from sorted CD4-CD8 double negative thymocytes of wild-type, Lmo2 transgenic and Lmo2-transgenic, Lyl1 knockout mice.

overall_design: Total RNA obtained from sorted CD4-CD8 double-negative thymocytes

first: Matthew

last: McCormack


title: ETV4 promotes metastasis in response to combined activation of PI3kinase and RAS signaling in a mouse model of advanced prostate cancer

status: Public on Jul 23 2013

city: Newark

first: Antonina

last: Mitrofanova

state: NJ

address: 65 Bergen Street, Rm 923B

institute: Rutgers University

summary:
Analysis of the transcriptome of mouse models of prostate cancer. NP (Nkx3.1CreERT2/+; Ptenfloxed/floxed) mice develop non-metastatic tumors while NPK (Nkx3.1CreERT2/+; Ptenfloxed/floxed; KrasG12D/+) mice develop metastatic tumors
The NPK mice are also analyzed at early and late stages of tumorigenesis (1 vs. 3 months after induction)

overall_design: Total RNA obtained from prostate tumors of different genotypes and at different stages of dissease as indicated

first: Alvaro

last: Aytes

first: Carolyn

last: Kinkade

first: Celine

last: Lefebvre

first: Ming

last: Lei

first: Vanessa

last: Phelan

first: H

last: Le

first: Jason

last: Koutcher

first: Robert

last: Cardiff

first: Andrea

last: Califano

last: Shen

first: Cory

last: Abate-Shen


title: Psychotropic drug-induced gene expression alterations in mouse striatum

status: Public on Jul 18 2013

city: Krakow

first: Marcin

last: Piechota

address: Smetna 12

department: Molecular Neuropharmacology

country: Poland

institute: Institute of Pharmacology PAS


title: Psychotropic drug-induced gene expression alterations in mouse striatum I

summary: To identify the molecular mechanisms that may initiate therapeutic effects, whole-genome expression profiling (Illumina Mouse WG-6 microarrays) of drug-induced alterations in the mouse brain was undertaken, with a focus on the time-course (1, 2, 4 and 8h) of gene expression changes produced by eighteen major psychotropic drugs: antidepressants, antipsychotics, anxiolytics, psychostimulants and opioids. The resulting database is freely accessible at www.genes2mind.org. Bioinformatics approaches led to the identification of three main drug-responsive genomic networks and indicated neurobiological pathways that mediate the alterations in transcription. Each tested psychotropic drug was characterized by a unique gene network expression profile related to its neuropharmacological properties. Functional links that connect expression of the networks to the development of neuronal adaptations (MAPK signaling pathway), control of brain metabolism (adipocytokine pathway), and organization of cell projections (mTOR pathway) were found. The additional data-sets are available at GEOX1 and GEOX2.

overall_design: The microarray experiment was performed to analyze time-course of drug-induced transcriptional response in C57BL/6J mouse striatum. Three antidepressants (imipramine 10 mg/kg, fluoxetine 20 mg/kg and tianeptine 20 mg/kg, i.p.) were selected for the comparison. Drug doses were previously reported as effective in mice and further tested in our laboratory. To analyze dynamics of early, intermediate and relatively late changes of mRNA abundance the experiment was performed in four time points (1, 2, 4 and 8h after drug administration). To exclude influence of drug injection and circadian rhythm on gene expression profile, control groups of saline treated and naïve animals were prepared for each time point. Design of the experiment assumed pooling of two animals per each array and using of three independent arrays per group. To provide appropriate balance in the whole dataset groups were equally divided between the array hybridization batches.

first: M

last: Korostynski


title: Psychotropic drug-induced gene expression alterations in mouse striatum II

overall_design: The microarray experiment was performed to analyze time-course of drug-induced transcriptional response in C57BL/6J mouse striatum. Three antidepressants (bupropion 20 mg/kg, tranylcypromine 20 mg/kg, mianserin 20 mg/kg, i.p.), three anxiolytics (diazepam 5 mg/kg, buspirone 10 mg/kg, hydroxyzine 10 mg/kg, i.p.), and three antipsychotics (clozapine 3 mg/kg, risperidone 0.5 mg/kg, haloperidol 1 mg/kg) were selected for the comparison. Drug doses were previously reported as effective in mice and further tested in our laboratory. To analyze dynamics of early, intermediate and relatively late changes of mRNA abundance the experiment was performed in four time points (1, 2, 4 and 8h after drug administration). To exclude influence of drug injection and circadian rhythm on gene expression profile, control groups of saline or tween (1% Tween 80) treated and naïve animals were prepared for each time point. Design of the experiment assumed pooling of two animals per each array and using of three independent arrays per group. To provide appropriate balance in the whole dataset groups were equally divided between the array hybridization batches.


title: Identification of GLI1 direct target genes in human pancreatic cancer cell line Panc-1

city: Aichi

first: Shingo

last: Inaguma

address: Nagakute

department: Department of Pathology and Promoting Center for Clinical Research

institute: Aichi Medical University School of Medicine

summary:
Panc-1GLI1ER and Panc-1ER were established from human pancreatic cancer cell line Panc-1. Panc-1GLI1ER cells express a chimeric transgene composed of an enhanced green fluorescent protein (EGFP)-tagged version of the amino-terminal half of GLI1, fused to the AF2 domain of the mouse estrogen receptor 1(Esr1) cDNA. On the other hand, Panc-1ER harbor only EGFP-tagged AF2 domain.
To identify GLI1 direct target genes, total RNAs were purified from the cells before and 3 hours after the beta-estradiol (E2) treatment.
Gene expression profiles were analyzed by AGILENT human 4x44 cDNA microarray.

Keywords: Expression profiling by genome tiling array

overall_design: GLI1 direct target genes were identified in Panc-1 cells. Gene expression profiles of Panc-1GLI1ER and Panc-1ER cells were analyzed by AGILENT human 4x44 cDNA microarray before and 3 hours after treatment of beta-estradiol (E2) at doses of 10nM.

first: Kenji

last: Kasai

first: Hiroshi

last: Ikeda


title: Gene expression profile of breast cancer cells.

status: Public on Jul 12 2013

city: Baltimore

first: Francescopaolo

last: Di Cello

state: MD

address: 1650 Orleans Street

institute: The Johns Hopkin University School of Medicine

summary: We compared the gene expression profile of 26 breast cancer cell lines to identify variations associated with different phenotypes and molecular subtype. The panel includes 13 estrogen receptor negative (ER-) and 13 ER+ cell lines. Four of the ER- cell lines and 5 of the ER+ cell lines are HER2 positive.

overall_design: We have used 2-color gene expression arrays for two separate studies. The one described here compares the intensities of one color channel across 26 cell lines, as normalized signal intensities. The second color channel is not analyzed here and will be used in a separate study.

first: Cynthia

last: Zahnow

first: Huili

last: Li


title: Genome-wide mRNA expression analysis of primary cultured mouse brain microvascular endothelial cells after inhibition of PKC-beta

status: Public on Jul 08 2013

city: Heidelberg

first: Tobias

middle: Volker

last: Lanz

address: Im Neuenheimer Feld 280

department: Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology

institute: German Cancer Research Center (DKFZ)

summary: Pharmacological inhibition of protein kinase C beta (PKC-beta) # by the compound LY317615 has been tested on primary cultured mouse brain microvascular endothelial cells, stimulated in-vitro for 8h at a concentration of 5 µM. The aim of the study was the question if inhibition of PKC-beta leads to inhibition of genes responsible for T-cell migration in order to investigate LY-317615 as a possible experimental therapy for multiple sclerosis.

overall_design: primary cultured mouse brain microvascular endothelial cells (MBMEC) have been prepared from new-born mice and cultured for one week. Then stimulated for 8h with 5 µM LY317615. Two samples had been treated for the last 24h with 500 µM TNF-alpha and 500 µM IFN-gamma (inflamed) whereas two samples had been left untreated (naive). RNA was prepared using TRIZOL according to standard protocols.

middle: V

first: Michael

last: Platten


title: Conditional knockout of p300 and Cbp in mouse rod photoreceptors

status: Public on Jul 29 2013

city: St. Louis

first: Jinsheng

last: Yu

state: MO

address: 660 S. Euclid Ave.

department: Genetics

institute: Washington University School of Medicine

summary: Ep300 and/or CrebBP were conditionally knocked out in differentiating mouse rod photoreceptors using opsin-driven Cre recombinase to elucidate the role of these transcription coactivators in photoreceptor gene expression regulation.

overall_design: Total RNA was isolated from retinas of 3 male and 3 female P14 mice of each genotype.  Each microarray sample contained pooled RNA from a male and female littermate of the same genotype, to control for any sex-related differences; three samples of each genotype were tested.  There were three control (C57Bl/6, RCre+, and cre neg dbl Fl/Fl) and 5 test genotypes (p300KO, CbpKO, p300 CH, Cbp CH, R-DCKO).

first: Anne

middle: K

last: Hennig

first: Shiming

last: Chen


title: Transcriptome signature of mouse embryonic stem cell-derived microglia is closely related to primary cultured microglia

status: Public on Jul 11 2013

city: Bonn

first: Joachim

last: Schultze

state: NRW

address: Carl-Troll-Strasse 31

department: Genomics and Immunoregulation

institute: LIMES (Life and Medical Sciences Center Genomics and Immunoregulation)

summary:
Preparation of primary microglial cultures from postnatal mice is tedious with a low yield, high variability and risk of astrocytic contamination. Microglia derived from embryonic stem cells (ESdM) have been suggested as alternative source, but it is unclear how closely ESdM resemble the molecular phenotype of primary microglia.
Here, we performed a whole transcriptome analysis of ESdM in comparison to primary cultured and flow cytometry-sorted microglia and compared the microglial transcriptome to other cell types. Cultured microglia and ESdM were related to sorted microglia, but clearly distinct from other myeloid cell types, T cells, astrocytes and neurons. ESdM and primary cultured microglia showed strong overlap in their transcriptome. Only 144 gene transcripts were differentially expressed between both cell types, mainly derived from immune-related genes with a higher activation status of pro-inflammatory and immune defense genes in primary microglia compared to ESdM. Flow cytometry analysis of cell surface markers CD54, CD74 and CD274 selected from the microarray confirmed the close phenotypic relation between ESdM and primary cultured microglia. Thus, assessment of genome-wide transcriptional regulation demonstrates that microglia are distinct from other macrophage cell types and that mouse pluripotent stem cell-derived microglia are closely related to cultured postnatal microglia.

overall_design: Comparison of different primary neuronal cells with ES-cell derived microglial cells

first: Marc

last: Beyer


title: Gender bias in autoimmunity is influenced by microbiota

first: Aly

middle: Azeem

last: Khan

state: IL

address: 6045 S. Kenwood Ave.

institute: University of Chicago

summary: Gender bias and the role of sex hormones in autoimmune diseases are well established. In specific-pathogen free (SPF) non-obese diabetic (NOD) mice females have 1.3-4.4 times higher incidence of Type 1 diabetes (T1D). Germ-free (GF) mice lose the gender bias (female/male ratio 1.1-1.2). Gut microbiota differed in males and females, a trend reversed by male castration, confirming that androgens influence gut microbiota. Colonization of GF NOD mice with defined microbiota revealed that some but not all lineages overrepresented in male mice supported a gender bias in T1D, and protection did not correlate with androgen levels. However, hormone-supported selective microbial lineage variation may work as a positive feedback mechanism contributing to the sexual dimorphism of autoimmune diseases. Gene expression analysis suggested pathways involved in protection of males from T1D by microbiota.

overall_design: We compared gene expression patterns in the pancreatic lymph nodes (PLNs) between four groups of mice (two genders in SPF and GF conditions, respectively). PLNs were isolated from 9-10 week old GF and SPF male and female NOD mice with 3 mice in each group, for a total of 12 samples.

first: Leonid

last: Yurkovetskiy

last: Burrows

first: Alexander

last: Chervonsky


title: CD146 expression in mesenchymal stem cells is associated with vascular smooth muscle commitment

status: Public on Jul 04 2013

city: Toulouse

first: Nicolas

last: Espagnolle

address: Bâtiment INCERE 4 bis, avenue Hubert Curien

country: France

institute: STROMALab, Université de Toulouse, CNRS  ERL5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, France

summary: Bone-marrow mesenchymal stem cells (MSCs) are plastic adherent cells that can differentiate into various tissue lineages, including osteoblasts, adipocytes and chondrocytes. However, this progenitor property is not shared by all cells within the MSC population. In addition, MSCs vary in their proliferation capacities and expression of markers. Because of heterogeneity of CD146 expression in the MSC population, we compared CD146-/Low and CD146High cells under clonal and non-clonal (sorted MSCs) conditions to determine whether this expression is associated with specific functions. CD146-/Low and CD146High MSCs did not differ in colony-forming unit-fibroblast number, osteogenic and adipogenic differentiation or in vitro hematopoietic supportive activity. However, CD146-/Low clones proliferated slightly but significantly faster than did CD146High clones. In addition, a strong expression of CD146 molecule was associated with a commitment towards a vascular smooth muscle cell lineage with upregulation of calponin-1 expression. Thus, within a bone-marrow MSC population, certain subpopulations characterized by high expression of CD146, are committed toward a vascular smooth muscle cell lineage.

overall_design: Clonal MSC were selected on the basis of CD146 level at their surface (CD146Low and CD146 High) and non-clonal MSC were compared from 4 different donors.

first: Fabien

last: Guilloton


title: Myeloid-derived suppressor cell development is regulated by a STAT/IRF-8 axis

status: Public on Jul 05 2013

city: Buffalo

first: Qiang

last: Hu

state: NY

address: Elm & Carlton Streets

institute: Roswell Park Cancer Institute

summary:
Interferon Regulatory Factor-8, an Integral Determinant of Myeloid-Derived Suppressor Cell Subset Development.

Myeloid-derived suppressor cells (MDSC) are a major barrier to anticancer responses. Although much is known about how MDSC promote tumor progression, little is known about how they develop. We hypothesized that MDSC develop as a consequence of tumor-induced downregulation of interferon regulatory factor-8 (IRF-8), a key myeloid developmental transcription factor. We showed that: 1) IRF8-deficiency in mice generated myeloid populations highly homologous to tumor-induced MDSC; 2) IRF-8 overexpression in mice reduced MDSC accumulation and retarded tumor growth; 3) MDSC-inducing factors, G-CSF or GM-CSF, facilitated IRF-8 downregulation via STAT3- or STAT5-dependent pathways, respectively; and 4) IRF-8 levels in MDSC-like subsets of breast cancer patients were depressed compared to healthy donors. Altogether, our data implicate IRF-8 as a novel MDSC-dependent transcription factor.

overall_design: Splenic CD11b+Gr-1high cell populations from tumor-bearing mice, IRF8 knockout mice or non-tumor-bearing control mice  were purified in two independent experiments by flow cytometry (> 97% purity) and subjected to whole genome expression profiling using Illumina microarrays.

first: Jeremy

last: Waight

first: Mary

last: Hensen

first: Austin

last: Miller

first: Song

last: Liu

first: Paul

last: Bogner

first: Kebin

first: Scott

middle: I

last: Abrams


title: Gene expression profile in the diaphragm following contractile inactivity during thoracic surgery

status: Public on Jul 03 2013

city: Amsterdam

first: Daoud

last: Sie

address: De Boelelaan 1117

department: Pathology

country: Netherlands

institute: Vrije Universiteit Medical Center

summary: Recent work revealed the development of marked diaphragm muscle fiber weakness during two hours of thoracic surgery. This loss of muscle fiber function was not part of a generalized muscle weakness as function of the non-respiratory latissimus dorsi muscle was preserved. To disentangle the molecular processes that might underlie the development of diaphragm muscle fiber weakness during thoracic surgery we studied changes in the gene expression profile.

overall_design: Analyzed were diaphragm samples at t0 vs t2 and latissimus dorsi at t0 vs t2.  In total 8 Diaphragm samples and 6 latissimus dorsi samples were analyzed.

first: Coen

last: Ottenheijm


title: Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: PLZF_HEK]

city: Berlin

first: Daniela

last: Zaade

address: Hessische Straße 3-4

department: Center for Cardiovascular Research

institute: Charité

summary: Within the overall project, we performed a set of microarray and chromatin-immunoprecipitation (ChIP)-chip experiments using siRNA against the (pro)renin receptor ((P)RR), stable overexpression of PLZF, the PLZF translocation inhibitor genistein and the specific V-ATPase inhibitor bafilomycin to dissect transcriptional pathways downstream of the (P)RR.

overall_design:
In this dataset, we include the expression data obtained from stable PLZF overexpression in HEK293T cells. Three intervention samples and three control samples were analyzed. We generated the following pairwise comparisons using Chipinspector (Genomatix Software GmbH) and a FDR of 1%.
ChipInspector carries out significance analysis on the single probe level. Normalized probe set level data not provided for individual Sample records. Processed data is available on Series record.

first: Heiko

last: Funke-Kaiser


title: Genome-wide analysis of gene expression in response to bortezomib treatment [mouse cell lines I]

status: Public on Jul 02 2013

city: Minneapolis

first: Aaron

last: Sarver

state: MN

address: 425 East River Road

department: Masonic Cancer Center

institute: University of Minnesota

summary:
Genome-wide analysis of gene expression in response to bortezomib treatment (33 nM) in cell lines before and after selection for resistance.
Multiple myeloma (MM) is a hematologic malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow. While the first-to-market proteasome inhibitor bortezomib/VELCADE has been successfully used to treat myeloma patients, drug resistance remains an emerging problem. In this study, we identify signatures of bortezomib sensitivity and resistance by gene expression profiling (GEP) using pairs of bortezomib-sensitive and -resistant cell lines created from the Bcl-XL/Myc double transgenic mouse model of MM. Finally, these data reveal complex heterogeneity within MM and suggest resistance to one drug class reprograms resistant clones to make them more sensitive to a distinct class of drugs. This study represents an important next step in translating pharmacogenomic profiling and may be useful for understanding personalized pharmacotherapy of MM patients.

overall_design: Transcript profiling timecourses after treatment with Bortezomib treatment (33nm) in Multiple Myeloma derived cell lines.


title: Genome-wide analysis of gene expression in response to bortezomib treatment [mouse cell lines II]

summary:
Genome-wide analysis of gene expression in response to bortezomib treatment(33 nM) in cell lines before and after selection for resistance.
Multiple myeloma (MM) is a hematologic malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow. While the first-to-market proteasome inhibitor bortezomib/VELCADE has been successfully used to treat myeloma patients, drug resistance remains an emerging problem. In this study, we identify signatures of bortezomib sensitivity and resistance by gene expression profiling (GEP) using pairs of bortezomib-sensitive and -resistant cell lines created from the Bcl-XL/Myc double transgenic mouse model of MM. Finally, these data reveal complex heterogeneity within MM and suggest resistance to one drug class reprograms resistant clones to make them more sensitive to a distinct class of drugs. This study represents an important next step in translating pharmacogenomic profiling and may be useful for understanding personalized pharmacotherapy of MM patients.


title: Pilot study to identify technical variation in microarray data of mouse lungs in the context of inter-animal variation

city: Bethesda

first: Marlene

last: Brandes

address: 9000 Rockville Pike

department: Laboratory of Systems Biology

institute: NIH, NIAID

summary: Prior to generation of microarray data for a Top-down Systems analysis of influenza A infection, we evaluated the degree and origin of technical variation in gene expression microarray data from mouse lungs and compared this to inter-animal variation. Technical variation in these microarray data in the context of inter-animal variation supported a choice of biological rather than technical replicates.

overall_design:
A) One mouse (260) was infected with 0.6LD50 of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at 72h post infection and processed to yield whole lung RNA that was used for microarray analysis.
The RNA was extracted in 3 individual batches (I, II, III), each batch of RNA was amplified in 2 separate batches (1,2), and the individual batches of amplified product were again hybridized in 2 batches. This dataset contains 18 microarrays covering 1 experimental condition with 1 biological replicate and a matrix of technical replicates.

B) 3 mice (245, 246, 247) were infected with 0.6LD50 of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at 72h post infection and processed to yield whole lung RNA that was used for microarray analysis.
From each animal, RNA was extracted, the RNA was amplified in three separate batches (A, B, C), and the individual batches of amplified product were again hybridized in 2 batches. This dataset contains 24 microarrays covering 1 experimental condition with 3 biological replicates and a matrix of technical replicates.

Datasets A) and B) are linked to two biological datasets - one comparing the transcriptomes of 5 different cell types isolated from individual lungs of influenza A-infected or control animals (contains 75 microarrays covering 25 experimental conditions) and one comprising whole lung microarrays from sham-infected or influenza H1N1-infected animals (contains 138 microarrays, 19 experimental conditions, 7 biological replicates).

first: Marlène

first: Ronald

middle: N

last: Germain


summary:
Identification of biological processes that distinguish lethal from non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity to during lethal influenza infection.

For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology.

overall_design:
Multiple mice were either sham infected, infected with the seasonal H1N1 influenza A virus TX91 (10^6PFU), or infected with various sublethal or lethal doses of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at various time points (24h, 48h, 72h and 240h post infection) and processed to yield whole lung RNA that was used for microarray analysis. The dataset contains 138 microarrays covering 20 experimental conditions with 7 biological replicates each. As an exception, the alternative non-infectious control condition (Alum treatment) contains 5 biological replicates.

This dataset is linked to a dataset comparing the transcriptomes of 5 different cell types isolated from individual lungs of influenza A-infected or control animals (contains 75 microarrays covering 25 experimental conditions).


title: Microarray gene expression analysis of mouse fetal liver erythroblasts after plek2 knockdown

status: Public on Jun 28 2013

city: Chicago

first: Peng

last: Ji

address: 303 E Chicago Ave

institute: Northwestern University

summary: The goal of this experiment is to determine the expression levels of the genes that are influenced by the downregulation of plek2.

overall_design: TER119 negative mouse fetal liver erythroblasts were purified and infected with control and plek2 shRNA retroviruses and cultured in Epo free medium for 24 hours followed by Epo medium for 24 hours. Microarray gene expression profile analysis was performed using an Illumina platform with a biological triplicate of the same experiment.

first: Ji

last: Peng

first: Ganesan

last: Keerthivasan


title: A Top-down Systems Analysis Identifies an Innate Feed-forward Inflammatory Circuit Leading to Lethal Influenza Infection

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Med1 overexpression induces cell proliferation

first: Navin

last: Viswakarma

summary: Med1 overexpression leads to induction of a wide spectrum of genes. Adenovirally-driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control and liver specific genes as observed at day 3 and day 5 post injection. Med1 gene is amplified in a number of cancers so in this study we tested the hypothesis that Med1 by itself has the capacity to induce cell proliferation. Analysis of the Med1- induced gene expression showed a robust induction of a wide spectrum of genes involved in hepatocellular proliferation.

overall_design: Med1 floxed mice (Med1fl/fl) were injected with Ad-His-Med1 (adenovirus expressing Med1 gene) via tail vein and killed 3 or 5 days after injection. Ad-LacZ (adenovirus expression beta-galactosidase gene) injected mouse liver served as control. Total RNA were isolated from the liver and subjected to the microarray.

first: N

first: Y

last: Jia

first: L

last: Bai

first: Janardan

last: Reddy


title: Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: Geni_Bafi]

overall_design:
In this dataset, we include the expression data obtained from KELLY cells incubated with genistein or bafilomycin A1. Five intervention samples and three control samples were analyzed. We generated the following pairwise comparisons using Chipinspector (Genomatix Software GmbH) and a FDR of 0.5% (bafilomycin), 5% (genistein): genistein- versus DMSO- and bafilomycin- versus DMSO-treated cells.
ChipInspector carries out significance analysis on the single probe level. Normalized probe set level data not provided for individual Sample records. Processed data is available on Series record.


title: Genome-wide analysis of mRNA expression differences from various stem cell enriched sub-populations of mouse mammary epithelial cells

status: Public on Jun 27 2013

city: Toronto

first: carl

last: virtanen

state: Ontario

address: 101 College St

department: Princess Margaret Genomics Centre

institute: University Health Network

summary: Microarrays were used to examine gene expression differences in four different sub-populations of mammary epithelial cells obtained through flow cytometry of stem cell markers for H2BGFP, CD24, and CD29. The present study aims to find the specific differences between these populations that influence their ability to repopulate mammary structures in vivo during transplantation assays. H2GFP+/CD24+/CD29lo cells were found to be multipotent and able to give rise to mammary structures capable of lactation, and this ability increased dramatically if the recipient mice were pregnant.

overall_design: Total RNA obtained from sorted sub-populations of mammary epithelial cells.

first: Alice

middle: S

last: Kaanta

first: Benjamin

last: Neel

first: Joan

last: Brugge

first: Laura

last: Selfors

first: Carl

last: Virtanen


title: Human prostate carcinoma cell line 22Rv1 overexpressing ESE1

status: Public on Jun 20 2013

city: Biella

first: giovanna

last: chiorino

address: via malta 3

department: Cancer Genomics

country: Italy

institute: Fondo Edo Tempia

summary: Activation of the inflammatory circuits occurs frequently in cancer cells. However the molecular details linking inflammation to transformation and progression are still unknown. In this study we report for the first time, that activation of the ETS factor ESE1 is a key event connecting inflammatory signaling with prostate cancer progression. We report that ESE1 is induced upon IL-1 beta stimulation by NFKB and mediates key transcriptional changes involving cell adhesion, migration and invasion. ESE1 activation in turn induces NFKB transcriptional activation and intranuclear translocation and mediates the transforming phenotypes linked to the activation of IL-1B. Transcriptional signatures and immunohistochemistry revealed that this ESE1-NFKB regulatory circuit also operates in prostate tumors, particularly in those with significant elevation of ESE1. Thus, ESE1 promotes an inflammatory feed forward loop positively leading to prostate cancer progression.  Pharmacological NFKB inhibition reverted the transformed status of ESE1 cell lines providing a rationale for context-dependent therapeutic strategies in ESE1 activated tumors. These studies find a previously unrecognized link between ETS and activation of the NFKB pathway and open new avenues for prostate cancer treatment.

overall_design: Gene expression analysis of a control cell line (22Rv1-pcDNA3.1) and a testing cell lines (22Rv1-ESE1), with two replicates, with dye swap, performed for each sample.

first: Nicole

last: Longoni

first: Manuela

last: Sarti

first: Anastasia

last: Malek

first: Erika

last: Ortelli

first: Sandra

last: Pinton

first: Maurizia

last: Mello-Grand

first: Paola

last: Ostano

first: Domenico

last: Albino

first: Gioacchino

last: D’Ambrosio

first: Fausto

last: Sessa

first: George

last: Thalmann

first: Giovanna

last: Chiorino

first: Carlo

last: Catapano

first: Gioseppina

last: Carbone


first: Marlene

last: Brandes

summary:
Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity during lethal influenza infection.

For acutely lethal influenza infections, the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity remain unresolved. Here, we take a top-down systems approach to this question. Multigene transcriptional signatures from infected lungs suggested that elevated activation of inflammatory signaling networks distinguished lethal from sublethal infections. Flow cytometry and gene expression analysis involving isolated cell subpopulations from infected lungs showed that neutrophil influx largely accounted for the predictive transcriptional signature. Automated imaging analysis together with these gene expression and flow data identified a chemokine-driven feed-forward circuit involving pro-inflammatory neutrophils potently driven by poorly contained lethal viruses. Consistent with these data, attenuation but not ablation of the neutrophil-driven response increased survival without changing viral spread. These findings establish the primacy of damaging innate inflammation in at least some forms of influenza-induced lethality and provide a roadmap for the systematic dissection of infection-associated pathology.

overall_design:
Multiple mice were either sham infected, infected with the seasonal H1N1 influenza A virus TX91 (10^6PFU), or infected with various sublethal or lethal doses of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at 48h or 72h post infection. 5 different cell types were purified by flow sorting from lungs of individual animals and then processed to yield total RNA that was used for microarray analysis. The dataset contains 75 microarrays covering 25 experimental conditions with 3 biological replicates.

This dataset is linked to a dataset containing 138 microarrays of whole lungs covering 20 experimental conditions.

first: Marlène

first: Ronald

last: Germain


title: The global gene expression profile of superficial zone articular cartilage in P1 wildtype and Prg4 transgenic mice

status: Public on Jun 24 2013

city: Houston

first: Merry

last: Ruan

address: One Baylor Plaza

institute: Baylor College of Medicine

summary: To examine the unbiased global gene expression of over-expression of Prg4 in superficial zone articular chondrocytes in mice.  This approach allows us to define novel signaling changes caused by the over-expression of Prg4 in superficial zone articular chondrocytes

overall_design: Total RNA was isolated from superficial zone chondrocytes in P1 articular cartilage in hind limbs (n=3) by laser capture microdissection. Same tissue from wild type mice served as control

first: Brian

last: Dawson


title: Differential expression in adipose derived stem cells

status: Public on Jun 25 2013

city: Shanghai

first: Min

last: Li

address: 50 Chifeng Rd., Yangpu District

department: Life Sciences and Technology

institute: Tongji University

type:
Expression profiling by array
Non-coding RNA profiling by array

platform_organism:
Homo sapiens
Mus musculus
Rattus norvegicus
Human alphaherpesvirus 1
Human alphaherpesvirus 2
Human betaherpesvirus 5
Murid betaherpesvirus 1
human gammaherpesvirus 4
JC polyomavirus
Human immunodeficiency virus 1
synthetic construct
Murid gammaherpesvirus 4
Human gammaherpesvirus 8
Merkel cell polyomavirus
Betapolyomavirus hominis
Betapolyomavirus macacae


title: Crosstalk between the effects of extracellular vesicles (Evs) and TNF on U937 human monocyte cell line

status: Public on Jun 19 2013

city: Budapest

first: Katalin

last: Szabo-Taylor

address: Nagyvárad tér 4.

department: Department of Genetics, Cell- and Immunobiology

country: Hungary

institute: Semmelweis University

summary: Under physiological conditions, extracellular vesicles (EVs) are present simultaneously in the extracellular compartment together with cytokines. Thus, we hypothesized that EVs in combination with cytokines induce different responses of monocyte cells compared to EVs or cytokines alone. Human monocyte U937 cells were incubated with EV-containing or EV-free CCRF human T-cell supernatant, with or without the addition of TNF.

overall_design: U937 cells cultured in EV-free supernatant, supernatant containing CCRF t-cell derived Evs, TNF or both. Each treatment option was measured in 3 replicates.

first: Tamas

last: Szabo

first: Bettina

last: Tarr

first: Krisztna

last: Paloczi

last: Eder

first: Agnes

last: Kittel

first: Sara

last: Toth

first: Bence

last: Gyorgy

first: Maria

last: Pasztoi

first: Andrea

last: Nemeth

first: Xabier

last: Osteikoetxea

first: Eva

last: Pallinger

first: Edit

last: Buzas


title: Screening Hub Genes Related to the Recovery Phase of Irradiation Injury by Microarray Analysis Combined with Integrated Gene Network

status: Public on Jun 17 2013

first: Ming

last: Yin

address: No.800 RD Dongchuan

department: School of Pharmacy

institute: Shanghai Jiao Tong University

summary: Microarray analysis was used to identify the differentially expressed genes. Bioinformatics analyses integrated with databases and text-mined gene network were conducted to understand irradiation-related hub genes, pathways and biological processes. Our hypothesis in these paper are: 1) the expression profiles of irradiation damaged bone marrow tissue are not identical in injury phase and recovery phase; and 2) some hub genes potentially vital to BM recovery can be screened out by means of microarray analysis and bioinformatics analysis. The results provide basic information to explain the radiation-related biological processes and hub genes.

overall_design: The five mRNA samples in total bone marrow cells were profiled by using gene chip at 3, 7, 11 and 21 days after irradiation and 0 day (sham-irradiation) as control. Each time point contains one sample.

first: Jing

last: Zhang

first: Yue

last: Yang

first: Yin

last: Wang

first: Jinyuan

first: Zejian

first: Xudong

last: Shen


title: Gene Expression in Perivenous Hepatocytes: A Laser Capture Microdissection and Transcriptomic Analysis.

status: Public on Jun 26 2013

city: St. John's

first: John

middle: Thomas

last: Brosnan

state: NL

address: 232 Elizabeth Avenue

department: Biochemistry

institute: Memorial University of Newfoundland

summary: Differential expression of genes and proteins, as well as physiological processes, along the hepatic acinus, known collectively as hepatic zonation, is a fundamental feature of hepatic physiology. However, the precise cellular location of only a relatively small proportion of the ~14,000 genes expressed in the liver is known. This is critical information for understanding hepatic physiology as well as for the accurate targeting of gene transfer vectors for gene therapy.  We have employed laser capture microdissection (LCM) and unbiased transcriptomic analysis of the normal adult mouse liver to define gene expression in a very distinct population of cells in the acinus, the glutamine-synthetase sub-compartment of perivenous hepatocytes, encompassing a one- to two-layer of cells surrounding the centrilobular vein. We confirmed the location of a number of genes whose expression is known to be restricted to these cells by virtue of immunohistochemistry or in situ hybridization (Slc1a2, Glul, Rhbg). We also identified genes whose expression had not previously been reported to be enriched in these cells (e.g. Sp5, Vldlr, Lpl, Gabrb3, Rcan2). Transcription factor analysis of the differentially expressed genes suggested important roles, in these cells, for members of the polycomb group, Wt1 and Tbx3. Collectively, our findings highlight the utility of combined LCM and transcriptome analysis for the identification of novel functions of distinct subclasses of hepatocytes. We plan to extend this approach to the mapping of physiological function across hepatic acini of the human liver.

overall_design:
Comparison of mRNA expression by two hepatic cell populations: the glutamine synthetase-subcompartment of the perivenous compartment and zones 1+2 of the hepatic acinus
Cells were isolated by laser capture microdissection and mRNA extracted by standard protocol.

first: Margaret

middle: E

middle: T

first: Molly

last: Bray

first: Martin

last: Young

first: Lourdes

last: Pena-Castillo

first: Robert

last: Cabrera

first: Angela

last: Major

first: Milton

middle: J

last: Finegold


title: Differential expression of genes in adipose derived stem cells

first: Min

last: Li

summary: Human adipose derived stem cells (hADSCs) are an attractive multipotent stem cell source with therapeutic applicability in diverse fields for the repair and regeneration of acute and chronically damaged tissues. In the last few years there has been increased interest in hADSCs for tissue engineering applications; however, the molecular mechanisms underlying the regulation of hADSCs proliferation and differentiation are not fully understood. In an effort to reveal the functions essential for this process, we performed microarray (Agilent 4x44K Whole Human Genome Microarray Kit) to profile the global gene expression in the hADSCs by including human endothelial and fibroblast cells as controls.

overall_design: To identify the genes significantly expressed in human adipose derived stem cells, eight samples were analyzed using Agilent whole human genome microarray including six hADSCs samples and human endothelial and fibroblast cells as controls.

first: Xiaoqing

last: Liu

first: Cizhong

last: Jiang

first: Guangfeng

last: Chen

first: Xiujuan

last: Shi

first: Qing

last: Zhou


title: Genome-wide analysis of gene expression in response to bortezomib treatment

first: Aaron

last: Sarver

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Gene expression signatures in gastric gastrointestinal stromal tumors (GISTs)

status: Public on Jun 14 2013

city: Seoul

first: Kyoung-Mee

last: Kim

address: #50 Irwon-dong

country: South Korea

institute: Samsung Medical Center

summary: To explore mechanisms underlying wild-type GISTs, gene expression analysis was performed on 15 gastric GISTs.

overall_design: 11 KIT-mutant, 1 PDGFRA-mutant and 3 wild-type GISTs

first: Eui-Jin

last: Lee

first: Guhyun

last: Kang

first: Shin-Woo

first: Kee-Taek

last: Jang

first: Jeeyun

first: Joon-Oh

last: Park

first: Cheol-Keun

first: Tae-Sung

last: Sohn

first: Sung


title: Age and Space Irradiation Modulate Tumor Progression: Implications for Carcinogenesis Risk

status: Public on Jun 13 2013

city: Boston

first: christine

middle: elaine

last: briggs

address: 736 Cambridge Street

department: Center for Cancer Systems Biology

institute: christine briggs

summary: Age plays a major role in tumor incidence and is an important consideration when modeling the carcinogenesis process or estimating cancer risks. Epidemiological data show that from adolescence through middle age, cancer incidence increases with age. This effect is commonly attributed to a lifetime accumulation of cellular, particularly DNA, damage. However, during middle-age, the incidence begins to decelerate and, for many tumor sites, it actually decreases at sufficiently advanced ages. We investigated if the observed deceleration and potential decrease in incidence could be attributed to a decreased capacity of older hosts to support tumor progression, and whether HZE (high atomic number (Z), high energy (E)) radiation differentially modulates tumor progression in young versus middle-age hosts, issues relevant to estimating carcinogenesis risk for astronauts. Lewis lung carcinoma (LLC) cells were injected into syngeneic mice (143 and 551 days old), which were then subject to whole-body 56Fe irradiation (1GeV/amu). Three findings emerged: 1) among unirradiated animals, substantial inhibition of tumor progression and significantly decreased tumor growth rates were seen for middle-aged mice compared to young mice; 2) whole-body 56Fe irradiation (1GeV/amu) inhibited tumor progression in both young and in middle-aged mice (with greater suppression seen in case of young animals), with little effect on tumor growth rates; and 3) 56Fe irradiation (1GeV/amu) suppressed tumor progression in young mice, to a degree not significantly different than transiting from young to middle-aged. Thus, 56Fe irradiation (1GeV/amu) acted similar to aging with respect to tumor progression. We further investigated the molecular underpinnings driving the radiation modulation of tumor dynamics in young and middle-aged mice. Through global gene expression analysis, the key players, FASN, AKT1, and the CXCL12/CXCR4 complex, were determined to be contributory. In sum, these findings demonstrate a reduced capacity of middle-aged hosts to support the progression phase of carcinogenesis and identify molecular factors contributory to HZE radiation modulation of tumor progression as a function of age.

overall_design: For genome-wide expression profiling of tumor tissue, Mouse WG-6 BeadArray chips (Illumina, San Diego, CA) were used. Total RNA was amplified with the Ambion Illumina TotalPrep Amplification Kit (Ambion, Austin, TX) and labeled from all replicate biological samples for each condition. The number of tumor sample replicates used from each condition is as follows: 10 samples from young unirradiated mice, 8 samples from young irradiated mice, 7 samples from middle-aged unirradiated mice, 5 samples from middle-aged irradiated mice. Total RNA was isolated and purified using Trizol (Invitrogen) or RNeasy (Qiagen), quantified and qualified using Agilent Bioanalyzer (Agilent) and samples were deemed suitable for amplification and hybridization if they had O.D. 260/280 = 1.7 - 2.1, 28s/18s = 2:1, RIN (RNA integrity number) >7. Total RNA of 500ng per sample was amplified using Ambion TotalPrep (Ambion), and 1.5µg of the product was loaded onto the chips. Following hybridization at 55C, the chips were washed and then scanned using the Illumina iScan (Illumina), and the data were analyzed using GenomeStudio (Illumina). Data were first analyzed for gene expression and then culled for present genes (genes that meet the criteria of detection p-value < 0.05). Expression above background was included in an expressed genes working data set for further analyses. Rank variant normalization was applied to the data before extensive analysis. Differential gene expression analysis was used to compare to the reference group, young unirradiated mice, and genes were then evaluated and validated.

first: Afshin

last: Beheshti

first: Rainer

last: Sachs

first: Michael

last: Peluso

first: Edward

last: Rietman

first: Philip

last: Hahnfeldt

first: Lynn

last: Hlatky


title: Genome wide analysis of Adrenal Gland tissue from Gata6 conditional knockout versus Control Adrenal tissue

status: Public on Jun 06 2013

city: Ann Arbor

middle: Dale

last: Brooks

state: Michigan

address: 2800 Plymouth Rd Building 26 Rm 329S

department: Internal Medicine

institute: University of Michigan

summary: Transcription factor GATA6 is expressed in the fetal and adult adrenal cortex and has been implicated in steroidogenesis. To characterize the role of GATA6 in adrenocortical development and function, we generated mice in which Gata6 was conditionally deleted using Cre-LoxP recombination with Sf1-cre. The adrenal glands of adult Gata6 conditional knockout (cKO) mice were small and had a thin cortex with thickened capsule. Cytomegalic changes were evident in the adrenal glands of fetal and adult cKO mice, and chromaffin cells were ectopically located at the periphery of the glands. The secretion of corticosterone in response to exogenous ACTH was blunted in cKO mice. Cells expressing gonadal-like markers, including Gata4, Amhr2, and Tcf21, accumulated in the adrenal capsule and subcapsule of cKO mice, suggesting aberrant adrenocortical progenitor/stem cell differentiation. Gonadectomy triggered the overexpression of sex steroidogenic differentiation markers, such as Lhcgr and Cyp17, in the adrenal glands of male and female cKO mice. Nulliparous female and orchiectomized male cKO mice lacked an adrenal X-zone. Microarray hybridization identified Pik3c2g as a novel X-zone marker that is downregulated in the adrenal glands of nulliparous female Gata6 cKO mice. Our findings offer genetic proof of the longstanding hypothesis that GATA6 regulates the differentiation of steroidogenic progenitors into corticoid-producing cells.

overall_design: 3 replicates from both conditional knockout of Gata6 in the adrenal gland and control adrenal glands from non-knockout mice were compared

first: Marjut

last: Pihlajoki

first: Elisabeth

last: Gretzinger

first: Rebecca

last: Cochran

first: Antti

last: Kyrönlahti

first: Laura

last: Sullivan

last: Shoykhet

first: Erica

middle: L

last: Schoeller

middle: D

first: Markku

last: Heikinheimo

first: David

middle: B

last: Wilson


title: The ERRalpha metabolic nuclear receptor controls growth of colon cancer cells

city: Sherbrooke

first: Julie

last: Carrier

state: Québec

address: 3001, 12ième avenue nord

department: Médecine(Gastroentérologie)

institute: Université de Sherbrooke

summary:
Estrogen-Related Receptor alpha (ERRα) is a nuclear receptor that acts principally as a regulator of metabolism processes particularly in tissues subjected to high-energy demand. Besides its implication in energy metabolism and mitochondrial biogenesis, ERRα was recently associated with tumorigenesis. Notably, increased expression of ERRα was noted in different cancerous tissues as breast, ovary and colon.  However, supplemental studies are required to better understand the role of ERRα in colon carcinoma.
We used microarrays to detail  gene expression during ERRalpha knockdown in HCT116 cells and identified distinct classes of up and down-regulated genes.

overall_design: Triplicate of HCT116 cell line was infected witn shscrambled(shCTL) and shERRalpha lentivirus and used  for RNA extraction and hybridization on Affymetrix microarrays.

first: Gérald

last: Bernatchez

first: Véronique

last: Giroux

first: Thomas

last: Lassalle

first: André

last: Carpentier

first: Nathalie

last: Rivard

middle: C


title: Gene expression data in over expressed Human Fetal Lung Fibroblasts with IPF downregulated miRNAs

city: Pittsburgh

first: Luai

last: Huleihel

state: PA

address: 450 technology drive

department: Regenerative medicine

institute: University of Pittsburgh

summary: Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition.miRNA let-7d and mir30b were found to be signifcantly down regulated in IPF. Compared to control we over expressed these miRNAs in Human Fetal Lung Fibroblast cell line

overall_design: Fetal lung tissues were collected through the University of Pittsburgh Tissue Bank through approved IRB protocol 0506140.  The samples were de-identified using an honest broker system and immediately transferred to the IRB exempt protocol PRO09040459 (PI: D. Carlisle).  Total RNA was labeled with Cy3 and hybridized on Agilent 8X44K gene expression array (Agilent Technologies, Santa Clara, CA). After 17 hours hybridization, arrays were washed and scanned according to the manufacturer’s protocol.

first: Naftali

last: Kaminski


title: Constitutively Active Foxo3 in Oocytes Preserves Ovarian Reserve in Mice

status: Public on Jun 08 2013

city: Paris

first: Chris

last: Ottolenghi

address: rue des Saint-Peres

institute: Inserm/Univ.Paris Descartes

summary: During female reproductive life, the reserve of ovarian follicles is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. We asked if overexpression of a constitutively active FOXO3 protein can increase long-lasting ovarian reproductive capacity in mice.

overall_design: Trangenic vs non-transgenic mice onto Foxo3+/- vs Foxo3-/- genotype

first: Emanuele

last: Pelosi


title: miR-29 affect on DC gene expression

status: Public on Jun 01 2013

city: Oxford

first: Oliver

last: Brain

state: Oxfordshire

address: Headley Way

department: TGU

institute: Nuffield Dept of Medicine

summary: Transcriptional profiling of human monocyte-derived dendritic cells (MDDCs), comparing cells transfected with miR-29a mimic, or miR-29b mimic, or negative control.

overall_design: 3 condition experiment, control versus miR-29a, and control versus miR-29b. 3 biological replicates for each condition and control.

first: Alison

last: Simmons


title: The differentially expressed genes identified in oncospheres derived from CRC cells and its metastatic variants

status: Public on May 30 2013

first: Li

last: Qingquan

address: No.138，Yixueyuan Rd.

institute: fudan university

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Tissue selective effects of topoisomerase II inhibitors in vivo

status: Public on Jun 04 2013

city: Palo Alto

first: Baoxu

last: Pang

state: CALIFORNIA

address: 3165 Porter Drive

department: Genetics

institute: Stanford University

summary: One major class of anti-cancer drugs targets topoisomerase II to induce DNA double-strand breaks and cell death of fast growing cells. In vitro experiments showed that doxorubicin can induce histone eviction as well as DNA damage, while etoposide can only induce DNA damage. Here, we compare the transcription responses of different tissues to doxorubicin or etoposide treatment in vivo.

overall_design: Total RNA from respective tissues in FVB mice 1 day or 6 days post indicated drug treatment were extracted and compared to un-treated mice. Two mice were used for each treatment.

first: Arno

last: Velds

first: Ron

last: Kerkhoven

first: Xiaohang

last: Qiao

first: Olaf

last: van Tellingen

first: Sven

last: Rottenberg

first: Jacques

last: Neefjes


title: The differentially expressed genes identified in oncospheres derived from CRC108 and its metastatic variants.

summary: Migrating cancer stem cells (MCSCs) are believed to be tumorigenic initiators of metastasis. However, the relevance of MCSCs for organ-specific metastasis in colorectal cancer remains unclear. Using in vivo selection, transcriptomic analysis and functional verification, we cultured colorectal cancer stem cells and discovered specific cell surface markers of MCSCs exhibiting distinct abilities to metastasize to the liver and lung. These results have important clinical implications as selection criterion for post-operative adjuvant therapy.

overall_design: The human primary colorectal cancer cells from  colorectal cancer patient (CRC108) were orthotopically injected into NOG mice. The cancer cells in the liver or lung metastases were orthotopically injected into a new set of mice. After six selection cycles, we obtained cancer cells that produce spontaneous liver (CRC108LM) or lung metastases (CRC108PM). Under serum-free conditions, all individual cells produced nonadherent, multicellular oncospheres. Total RNA extracted from oncospheres of organ-specific metastasizing variants and their parental cells was used to generate biotinylated complementary RNA (cRNA) by following the standard Agilent GeneChip protocol.

first: Qing-Quan

last: Li


title: The differentially expressed genes identified in oncospheres derived from CRC102 and its metastatic variants.

overall_design: The human primary colorectal cancer cells from  colorectal cancer patient (CRC102) were orthotopically injected into NOG mice. The cancer cells in the liver or lung metastases were orthotopically injected into a new set of mice. After six selection cycles, we obtained cancer cells that produce spontaneous liver (CRC102LM) or lung metastases (CRC102PM). Under serum-free conditions, all individual cells produced nonadherent, multicellular oncospheres. Total RNA extracted from oncospheres of organ-specific metastasizing variants and their parental cells was used to generate biotinylated complementary RNA (cRNA) by following the standard Agilent GeneChip protocol.


title: Gene expression microarray during Human NK cell development; 1-, 7- and 14-day cultured cells after differentiation induction

status: Public on May 31 2013

city: Cheongwon-gun

first: Su Ui

last: Lee

address: Ochang-eup

institute: Korea Research institute of Bioscience & Biotechnology

summary: To identify differentially expressed genes during human NK cell development, we performed mRNA arrays analysis by using total RNA isolated from 1-, 7- or 14-day cultured cells after the addition of medium supplemented with IL-15 in HSCs isolated from human umbilical cord blood (UCB).

overall_design: Two-condition experiment, 1-day(control) vs. 7-day  and 1-day(control) vs 14-day cultured cells .

first: Tae-Don

last: Kim

first: Inpyo

last: Choi

first: Su

middle: U

first: Sohyun

last: Yun

first: Jung

middle: M


title: Cluster analysis reveals differential transcript profiles associated with resistance training-induced human skeletal muscle hypertrophy

status: Public on May 24 2013

city: Ithaca

first: Anna

last: Thalacker-Mercer

address: 109 Savage Hall

institute: Cornell University

summary: Overall, the widely disparate transcriptomes identified prior to RT among the three clusters support the notion that at least some of the inter-individual heterogeneity in propensity for RT-induced myofiber hypertrophy is likely pre-determined.

overall_design: Baseline comparisons of skeletal muscle transcript profiles from 44 subjects previously clustered (K-means cluster analysis) as non-, modest-, and extreme-responders (Non, n=15; Mod, n=14; Xtr, n=15) based on the magnitudes of change in vastus lateralis myofiber cross-sectional area (CSA) following 16-wk, 3-d/wk, high-intensity RT.

first: Marcas

last: Bamman

first: Xiangqin

last: Cui

first: Michael

last: Stec

first: James

last: Cross

first: Samuel

last: Windham


title: Cell host-response to infection with novel human coronavirus EMC predict potential antivirals and important differences with SARS-coronavirus.

status: Public on May 03 2013

city: Seattle

last: Katze

state: WA

address: Rosen Building 960 Republican St.

department: Microbiology

institute: University of Washington

summary: Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection.

overall_design:
Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or mock infected.  Samples were collected 0, 3, 7, 12, 18 and 24 hpi.
There are 3 mock and 3 infected replicates for each time point, except for 12 hpi for which there are only 2 infected replicates (one replicate did not pass RNA quality check).  There were no mock sampes at 18 hpi, and therefore infected samples at 18 hpi were compared with mocks at 24 hpi.
For direct comparison with SARS-CoV infected cells, raw data from HCoV-EMC experiments were quantile normalized together with the SARS-CoV dataset (GEO Series accession number GSE33267).

first: Laurence

last: Josset

first: Vineet

last: Menachery

first: Lisa

last: Gralinski

first: Sudhakar

last: Agnihothram

first: Pavel

last: Sova

first: Victoria

last: Carter

first: Boyd

last: Yount

first: Rachel

last: Graham

first: Ralph

last: Baric

middle: G


title: Integrated array CGH and expression profiling revealed candidate biomarkers in gastrointestinal stromal turmor

first: Kyoung-Mee

last: Kim

type: Genome variation profiling by genome tiling array


title: Expression profile of Pten loss and ERG overexpression in mouse prostate

status: Public on May 10 2013

city: New York

first: Yu

last: Chen

address: 1275 York Ave, Box 20

department: Human Oncology and Pathogenesis Program

institute: Memorial Sloan Kettering Cancer Center

summary:
We performed expression mouse profiling of prostates of 3 month WT, ERG, PTEN f/f and Pten f/f;ERG mice.
For WT and ERG prostates, entire prostates were dissected and total RNA immediated harvested. For Pten f/f and Pten f/f;ERG prostates, the Ventral Lobe was dissected.

overall_design: Mice are in the C57B6 background. The prostate were harvested and RNA isolated by standard protocols and analyzed by expression profiling.

first: Charles

last: Sawyers


title: Autoantigen promotes progression to aggressive TCL1 leukemia

status: Public on May 01 2013

city: Manhasset

first: ShihShih

address: 350 community dr

institute: Feinstein Institute

summary: Activated BCR signaling in Murine CLL leukemia cells responsive to autoantigen phosphatidylcholine

overall_design: Murine CLL cells obtained from spleen and peritoneum were compared for the genetic signatures associated with autoantigen responsiveness

first: Nicholas

last: Chiorazzi

first: Shih-Shih


title: Global gene expression analysis of PB-Oct4.2A.cherry iPS-/-, PB-Oct4.2A.cherry (low) iPS-/- and ES cells

status: Public on Apr 30 2013

city: Cambridge

first: Jose

last: Silva

state: Cambridgeshire

address: Tennis Court Road

institute: Wellcome Trust Centre for Stem Cell Research

summary: We have generated iPS cell lines with constitutive Oct4 expression at ES-cell level or 3 times lower. The aim of the experiment was to compare the global gene expression profile between these two cell lines and also between each of them and wild type ES cells.

overall_design: We have analysed two biological replicates of each cell line

first: Aliaksandra

last: Radzisheuskaya


title: Whole genome mRNA analysis of wild-type and Id2-deficient virus-specific CD8+ T cells after influenza infection

city: Parkville

first: Moshe

last: Olshansky

state: Victoria

address: 1G Royal Pde

department: Bioinformatics

institute: Walter & Eliza Hall Institute of Medical Research

summary: The transcription factor Inhibitor of DNA binding 2 (Id2) modulates T cell fate decisions but the molecular mechanism underpinning this regulation is unclear. Here, using whole genome mRNA analysis we show that loss of Id2 programs CD8+ T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. Our findings reveal that the Id2-E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation.

overall_design: Wild-type and Id2fl/flLckCre+ DbNP366-specific CD8+ T cells were isolated from the spleen of  PR8-primed/HKx31-infected Ly5.2+Id2fl/flLckCre+:Ly5.1+ mixed bone marrow chimeric mice ten days after intranasal influenza infection and analysed by whole genome mRNA analysis. Three biological replicates of each genotype were subjected to microarray analysis.

first: Frederick

last: Masson

first: Gabrielle

last: Belz