title: Runx3 function in IL-2-activated splenic CD8+ T cells.

city: Rehovot

first: Joseph

last: Lotem

department: Molecular genetics

country: Israel

institute: Weizmann institute of science

summary: CD8+T cells are immune cells that recognize foreign antigens on infected and tumor cells, leading to cytokine-dependent expansion and activation of cytotoxicity towards the targets.

overall_design: To identify Runx3 regulated genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-)  of CD8+ T cells were separately obtained from individual mice, TCR activated and cultured for 4 days with IL-2.

first: Dena

last: Leshkowitz

first: Yoram

last: Groner


title: Gene signatures of normal hTERT immortalized ovarian epithelium and fallopian tube epithelium (paired cultures from 2 donor patients)

status: Public on Nov 25 2013

city: Boston

first: Melissa

middle: Amy

last: Merritt

state: MA

address: 450 Brookline Ave

department: Biostatistics and Computational Biology

country: USA

institute: Dana-Farber Cancer Institute

summary: Most epithelial ovarian cancers are thought to arise from different cells in the ovarian or fallopian tube epithelium. We hypothesized that these distinct cells-of-origin may play a role in determining ovarian tumor phenotype and also could inform the molecular classification of ovarian cancer. To test this hypothesis, we developed new methods to isolate and culture paired normal human ovarian (OV) and fallopian tube (FT) epithelial cells from multiple donors without cancer and identified a cell-of-origin gene expression signature that distinguished these cell types within the same patient. Application of the OV versus FT cell-of-origin gene signature to gene expression profiles of primary ovarian cancers permitted identification of distinct OV and FT-like subgroups among these cancers. Importantly, the normal FT-like tumor classification correlated with a significantly worse disease-free survival. This work describes a new experimental method for culture of normal human OV and FT epithelial cells from the same patient. These findings provide new evidence that cell-of-origin is an important source of ovarian tumor heterogeneity and the associated differences in tumor phenotype.

overall_design: We analyzed 12 samples from two donor patients and established cultures of both ovarian epithelium and fallopian tube epithelium (hTERT immortalized), each with 3 replicates (different culture passages).

middle: A

first: Tan

last: Ince


title: Expression data from WEEV infected BE(2)-C/m cells

status: Public on Nov 23 2013

city: Ann Arbor

first: David

last: Miller

state: MI

address: 3560B MSRB II, 1150 W. Medical Center Dr.

department: Internal Medicine

institute: University of Michigan

summary: Analysis of transcription response of differentiated human BE(2)-C/m neuronal cells to infection with WEEV at 12 h and 24 h after infection.

overall_design: Two independent sets of BE(2)-C/m cells uninfected or infected with WEEV at an MOI=10 and harvested at 12 h or 24 h after infection.  Total RNA was harvested analyzed with Affymetrix U133 Plus 2.0 chips.

middle: J


title: Role of miR-146a in colon cancer cells

status: Public on Nov 20 2013

city: Taipei

first: Wei-Lun

last: Hwang

address: No.155, Sec.2, Linong Street

department: Department of Biotechnology and Laboratory Science in Medicine

country: Taiwan

institute: National Yang Ming Chiao Tung University

summary: miRNAs exert various biological functions by targeting different cellular targets. Studying miR-146a functions in colon cancer cells helps to understand colorectal cancer (CRC) malignancy and progression.

overall_design: HT29 miR-146a-expressing cells and empty control cells were established for mining the gene expression profiles upon miR-146a expression.

first: W

middle: L

first: H

middle: W

last: Wang


title: Pdx1 maintains β-cell identity and function by repressing an α-cell program

status: Public on Nov 19 2013

city: Philadelphia

first: Tao

last: Gao

state: PA

address: 421 Curie Blvd, BRB II/III, Room 527

institute: University of Pennsylvania

summary:
To get a more complete picture of the transcriptional changes associated with Pdx1 loss in β-cells, we conducted an mRNA microarray comparing normal islet β-cells and a-cells to the reprogrammed cells from PKO mice.
Islet beta cells are from mice which has a single copy of Pdx1 flox (Pdx1L/+) allele, but is considered normal based on normal islet morphology, gene profiling, and euglycemic status. We chose to use heterozygous mice as control to avoid the litter effect. Islet alpha cells  are from normal mice.

overall_design: To enrich for genes directly affected by Pdx1 loss, we chose the early time-point for analysis of PKO mice (5d after TAM administration). Control mRNA profiling was performed on FACS sorted islet YFP+ β-cells and a-cells obtained from 2 month-old glucagon-Cre; RosaYFP and RIP-CreER; Pdx1fl/+, RosaYFP mice, respectively.

first: Brian

last: Mckenna

first: Changhong

last: Li

first: Maximilian

last: Reichert

first: James

last: Nguyen

first: Tarjinder

last: Singh

first: Chenghua

last: Yang

first: Archana

last: Pannikar

first: Nicolai

last: Doliba

first: Tingting

last: Zhang

first: Doris

last: Stoffers

first: Helena

last: Edlund

first: Franz

last: Matchinsky

first: Roland

last: Stein

first: Ben

middle: Z

last: Stanger


title: Runx3 function in CD8+ splenic T cells

status: Public on Nov 18 2013

first: Joseph

last: Lotem

overall_design: To identify Runx3 responsive genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-)  of freshly isolated CD8+ T cells (resting) were separately obtained from individual mice.

first: Dena

last: Leshkowitz

first: Yoram

last: Groner


title: Expression data of ALDH+ breast cancer cells

status: Public on Nov 14 2013

city: Houston

first: yang

last: CONG

state: TX

address: 6565 Fannin St.,

department: Department of Systems Medicine and Bioengineering

institute: Houston Methodist Research Institution

summary:
It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse.  Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations.
Based on established breast cancer cell lines, as well as primary tumor samples and xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites.

overall_design: Breast cancer cells from patient were sorted using flow cytometry to select for cells that were ALDH+.  Gene expression profiles of these cells were compared with profiles of ALDH- cells.

first: Daniel

last: Birnbaum

first: Christophe

last: Ginestier

first: Emmanuelle

last: Charafe-Jauffret


title: Transcriptional events in human skeletal muscle at the outset of concentric resistance exercise training

status: Public on Nov 15 2013

city: Loughborough

first: Andrew

last: Murton

state: Leicestershire

address: Sutton Bonington Campus

department: Division of Nutritional Sciences

country: United Kingdom

institute: The University of Nottingham

summary: We sought to ascertain the time-course of transcriptional events that occur in human skeletal muscle at the outset of resistance exercise (RE) training in RE naïve individuals, and determine if the magnitude of any response was associated with exercise induced muscle damage. Sixteen RE naïve males were recruited, 8 underwent 2 sessions of 5x30 maximum, isokinetic knee extensions (180°.s-1) separated by 48 hrs. Muscle biopsies of the vastus lateralis were taken at baseline and 24 hrs after each exercise bout.  Eight individuals acted as non-exercise controls with biopsies obtained at the same time intervals. Transcriptional changes were assessed by microarray, and binding of HSP27 and αB-crystallin to insoluble proteins by immunohistochemistry as a measure of muscle damage. In control subjects, no probesets were significantly altered (FDR<0.05) and HSP27 and αB-crystallin binding remained unchanged throughout the study. In exercised subjects, significant inter-subject variability following the initial bout of RE was observed in the muscle transcriptome, with greatest changes occurring when HSP27 and αB-crystallin binding was elevated. Following the second bout of RE, the transcriptome response was more consistent among subjects revealing a cohort of probesets associated with immune activation, the suppression of oxidative metabolism and protein ubiquitination as differentially regulated. The results reveal that the initial transcriptional response to RE is highly variable in RE naïve volunteers, is associated with muscle damage, and unlikely to reflect longer-term adaptations to RE training. These results highlight the importance of considering multiple time-points when determining the transcriptional response to RE and associated physiological adaptation.

overall_design: 16 healthy male subjects were recruited and attended the laboratory fasted on 4 consecutive days. Biopsies from the vastus lateralis muscle were obtained on Days 0, 1 and 3, with total RNA extracted for gene expression analysis by microarray. During this period, 8 subjects performed isokinetic leg extension exercise using an isokinetic dynamometer (180 degrees per second; maximum intensity) on two occassions (days 0 and 2). Data for 7 exercise subjects presented in this study.  8 further subjects acted as non-exercised controls and did not participate in any exercise during the study period.  A number of technical replicates were included and are identified in the sample list. Insufficient muscle biopsy sample or inadequate RNA quality accounted for 8 missing data points (TechRep1 N=40 as opposed to 48).

first: Rudolf

last: Billeter

first: Francis

middle: B

last: Stephens

first: Shelley

middle: G

last: Des Etages

first: Franziska

last: Graber

first: Roger

last: Hill

first: Kanagara

last: Marimuthu

first: Paul

last: Greenhaff


title: Hypothalamic gene expression of appetite regulators in a cancer-cachectic mouse model [Dataset 1]

city: Wageningen

first: Guido

last: Hooiveld

address: HELIX, Stippeneng 4

department: Div. Human Nutrition & Health

country: Netherlands

institute: Wageningen University

summary: Appetite is frequently affected in cancer patients, leading to anorexia and consequently insufficient food intake. In this study, we report on hypothalamic gene expression profile of a cancer cachectic mouse model with increased food intake. In this model, mice bearing C26 colon adenocarcinoma have an increased food intake subsequently to the loss of body weight. We hypothesize that in this model, appetite regulating systems in the hypothalamus, which apparently fail in anorexia, are still able to adapt adequately to changes in energy balance. Therefore studying the changes that occur on appetite regulators in the hypothalamus might reveal targets for treatment of cancer-induced eating disorders. By applying transcriptomics, many appetite regulating systems in the hypothalamus could be taken into account, providing an overview of changes that occur in the hypothalamus during tumour growth. We show that hypothalamic expression of orexigenic neuropeptides NPY and AgRP was higher, whereas expression of anorexigenic genes CCK and POMC were lower in TB compared to controls. In addition, serotonin and dopamine signalling pathways were found to be significantly altered in TB mice. Serotonin levels in brain showed to be lower in TB mice compared to control mice, while dopamine levels did not change. Moreover, serotonin levels inversely correlated with food intake. Transcriptomic analysis of the hypothalamus of cachectic TB mice with an increased food intake showed changes in NPY, AgRP and serotonin signalling. Serotonin levels in the brain showed to correlate with changes in food intake. Targeting these systems seems a promising strategy to avoid the development of cancer-induced eating disorders.

overall_design: C26-colon adenocarcinoma cells were subcutaneously inoculated in CDF1 mice. After 20 days, hypothalami were dissected and subjected to gene expression profiling. The total dataset consists of 2 parts; dataset 1, a pilot stuy in which mice were injected with increasing number of tumour cells and pooled samples were arrayed; and dataset 2, the main study in which mice were injected with 1 million tumour cells and samples were individually arrayed.

first: Jvalini

middle: T

last: Dwarkasing

first: Francina

last: Dijk

first: Mark

middle: V

last: Boekschoten

first: Joyce

last: Faber

first: Josep

middle: M

last: Argilès

first: Alessandro

last: Lavianio

first: Michael

last: Müller

first: Renger

middle: F

last: Witkamp

first: Klaske

last: van Norren


title: Brown Adipogenic Reprogramming Induced by a Small Molecule

city: San Francisco

first: Baoming

last: Nie

state: CA

address: 1650 Owens St.

department: GICD

institute: Gladstone Institutes

summary:
Transcriptome analysis of early adipogenesis induced by  basal adipogenesis medium(AM) and AM+Bex for 2 days in C2C12 cells
Global gene expression profiling has shown Bex induced adipogenic genes expression change

overall_design: We analyzed 4 samples from basal adipogenesis medium(AM) and AM+Bex(10uM) treated C2C12 cells using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed by Affymetrix Expression Console and Transcriptome Analysis Console (TAC) software.

first: Jiazhun

last: Zheng


title: Affymetrix gene chip analysis for the whole mouse genome transcripts of epithelial and stromal cells from mouse uterine primary co-culture treated with either vehicle or E2

city: Cincinnati

first: Daesuk

last: Chung

state: OH

address: 3333 Burnet Ave.

institute: Cincinnati Childrens Hospital Medical Center

summary: In the present study, to identify potential paracrine factor for the stromal regulation of E2-induced epithelial cell proliferation, we treated epithelial and stromal cell populations of mouse uterine primary co-culture with either oil or E2. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 119 genes and down-regulation of 28 genes in epithelial cell populations and up-regulation of 144 genes and down-regulation of 192 genes in stromal cell population.

overall_design: We analyzed whole gnenome transcription from epithelial and stromal cell populations of mouse uterine primary co-culture using the Affymetrix GeneChip® Mouse Gene 1.0 ST Array (vehicle vs. E2). 3 replicates were performed.

first: Fei

last: Gao

first: Sanjoy

middle: K

last: Das


title: The long non-coding RNA Paupar regulates the expression of both local and distal genes [Paupar KD]

status: Public on Nov 21 2013

city: Oxford

first: Stephen

last: Sansom

state: Oxfordshire

address: Roosevelt Drive

department: NDORMS

institute: Kennedy Institute of Rheumatology

summary: Although some long noncoding RNAs (lncRNAs) have been shown to regulate gene expression in cis, it remains unclear whether lncRNAs can directly regulate transcription in trans by interacting with chromatin genome-wide independently of their sites of synthesis. Here, we describe the genomically local and more distal functions of Paupar, a vertebrate-conserved and central nervous system-expressed lncRNA transcribed from a locus upstream of the gene encoding the Pax6 transcription factor. Knockdown of Paupar disrupts the normal cell cycle profile of neuroblastoma cells and induces neuronal differentiation. Paupar acts in a transcript-dependent manner both locally, to regulate Pax6, as well as distally by binding and regulating genes on multiple chromosomes, in part through physical association with Pax6 protein. Paupar binding sites are enriched near promoters and can function as transcriptional regulatory elements whose activity is modulated by Paupar transcript levels. Our findings demonstrate that a lncRNA can function in trans at transcriptional regulatory elements distinct from its site of synthesis to control large-scale transcriptional programmes.

overall_design: N2A cells transfected with a non-targeting control vector were compared to N2A cells transfected with a Paupar knockdown construct. Three biological replicates of each condition were analysed on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

first: Keith

last: Vance

middle: N

first: Sheena

last: Lee

first: Vladislava

last: Chalei

first: Lesheng

last: Kong

first: Sarah

middle: E

last: Cooper

first: Peter

last: Oliver

first: Chris

middle: P

last: Ponting


title: Gene expression comparison of E14.5 Foxd1 null and wild type kidneys

city: Scarborough

first: Jennifer

last: Fetting

state: ME

address: 81 Research Dr.

institute: Maine Medical Center Research Institute

summary:
Forkhead transcription factors are essential for diverse processes in early embryonic development and organogenesis. Foxd1 is required during kidney development and its inactivation results in failure of nephron progenitor cell differentiation. Foxd1 is expressed in interstitial cells adjacent to nephron progenitor cells, suggesting an essential role for the progenitor cell niche in nephrogenesis. To better understand how cortical interstitial cells in general, and FOXD1 in particular, influence the progenitor cell niche, we examined the differentiation states of two progenitor cell subtypes in Foxd1-/- tissue. We found that while nephron progenitor cells are retained in a primitive CITED1-expressing compartment, cortical interstitial cells prematurely differentiate. To identify pathways regulated by FOXD1, we used microarray analysis and screened for target genes by comparison of Foxd1 null and wild type tissues.
We chose the E14.5 timepoint because at this stage nephron differentiation is present in wild type kidneys but absent from Foxd1 null kidneys. We examined genes that were upregulated or downregulated in the Foxd1 null compared to wild type.

overall_design: Embryonic kidneys were harvested from Foxd1-/- and wild type littermates from three E14.5 litters. Three biological replicates were generated per genotype, each containing two non-littermate kidney pairs. Sex of embryos was not determined.

first: Justin

last: Guay

first: Leif

last: Oxburgh


title: Vastus lateralis biopsies from healthy and COPD patients before and after 8 weeks of exercise training

status: Public on Nov 16 2013

city: Birmingham

last: Turan

address: University of Birmingham, Edgbaston

institute: University of Birmingham

summary: Study the training exercise effects in chronic obstructive pulmonary disease (COPD) patients and aged-matched healthy individuals. Skeletal muscle biopsies from 9 stable COPD patients with normal fat free mass index (FFMI, 21Kg/m2) (COPDN), 6 COPD patients with low FFMI  (16Kg/m2) (COPL), and 12 healthy sedentary subjects (FFMI 21Kg/m2) before and after 8 weeks of a supervised endurance exercise program were analyzed.

overall_design: Samples were collected from open biopsies from the musculus vastus lateralis of COPD patients and healthy individuals before and after 8 weeks of exercise training. Constant-work rate exercise at 70% of pre-training Watts peak (Wpeak) (CardiO2 cycle Medical Graphics Corporation, USA) was carried out before and after 8 weeks of supervised interval training with a cycloergometer until pre-training endurance time exhaustion. Measurements before and after training were obtained at isowork-rate and iso-time.

first: Susana

last: Kalko

first: Francesco

last: Falciani

first: Josep

last: Roca


title: DNA methylation analysis of subcutaneous adipose tissue abdominal versus subcutenaous adipose tissue gluteal

city: Hamburg

first: Sandra

last: Gehrke

address: Unnastraße 48

department: Applied Skin Biology

country: Germany

institute: Beiersdorf AG

type: Methylation profiling by genome tiling array

summary: In humans, adipose tissue is distributed in subcutaneous abdominal and subcutaneous gluteal depots that comprise a variety of functional differences. Whereas energy storage in gluteal adipose tissue has been shown to mediate a protective effect, an increase of abdominal adipose tissue is associated with metabolic disorders. However, the molecular basis of depot-specific characteristics is not completely understood yet. Using array-based analyses of transcription profiles, we identified a specific set of genes that was differentially expressed between subcutaneous abdominal and gluteal adipose tissue. To investigate the role of epigenetic regulation in depot-specific gene expression, we additionally analyzed genome-wide DNA methylation patterns in abdominal and gluteal depots. By combining both data sets, we identified a highly significant set of depot-specifically expressed genes that appear to be epigenetically regulated. Interestingly, the majority of these genes form part of the homeobox gene family. Moreover, genes involved in fatty acid metabolism were also differentially expressed. Therefore we suppose that changes in gene expression profiles might account for depot-specific differences in lipid composition. Indeed, triglycerides and fatty acids of abdominal adipose tissue were more saturated compared to triglycerides and fatty acids in gluteal adipose tissue. Taken together, our results uncover clear differences between abdominal and gluteal adipose tissue on the gene expression and DNA methylation level as well as in fatty acid composition. Therefore, a detailed molecular characterization of adipose tissue depots will be essential to develop new treatment strategies for metabolic syndrome associated complications.

overall_design: DNA methylation profiles of abdominal adipose tissue (6 samples) and gluteal adipose tissue (6 samples) were generated using Infinium methylation 450K BeadChips from Illumina (Illumina, San Diego, USA).

first: Marc

last: Winnefeld

first: Sabine

last: Hagemann


title: Expression data of CD24-CD44+ and ALDH+ cells

status: Public on Nov 13 2013

first: yang

last: CONG

summary:
It has been suggested that breast cancers are driven and maintained by a cellular subpopulation with stem cell properties. These breast cancer stem cells (BCSCs) mediate metastasis and by virtue of their resistance to radiation and chemotherapy, contribute to relapse.  Although several BCSC markers have been described, it is unclear whether these markers identify the same or independent BCSC populations.
Based on established breast cancer cell lines, as well as primary tumor xenografts, we show that BCSCs exist in distinct mesenchymal-like (epithelial-mesenchymal transition, EMT) and epithelial-like (mesenchymal-epithelial transition, MET) states characterized by expression of distinct markers, proliferative capacity and invasive characteristics. The gene expression profiles of mesenchymal-like and epithelial-like BCSCs are remarkably similar across the different molecular subtypes of breast cancer and resemble those of distinct basal and luminal stem cells found in the normal breast. We propose that the plasticity of BCSCs allowing them to transition between EMT- and MET-like states endows these cells with the capacity for tissue invasion, dissemination and growth at metastatic sites.

overall_design: Breast cancer cell lines, primary xenografts and normal breast cells from patient were sorted using flow cytometry to select for cells that were CD24-,CD44+ and ALDH+. Gene expression profiles of CD24-CD44+ cells were compared with non-CD24-CD44+ cells. Gene expression profiles of ALDH+ cells were compared with ALDH- cells.

first: Suling

last: Liu

first: Joe

last: Washburn

first: Craig

last: Johnson


title: Hypothalamic gene expression of appetite regulators in a cancer-cachectic mouse model

first: Guido

last: Hooiveld

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

overall_design: Refer to individual Series


title: Expression data for minimally invasive glioblastoma stem-like cell (GSC) plasma membrane markers

city: Madison

first: Michael

last: Zorniak

state: WI

address: 600 Highland Ave

department: Neurological Surgery

institute: University of Wisconsin-Madison

type:
Expression profiling by array
Third-party reanalysis

summary: We compared whole genome expression profiles of GSCs with normal human cortex, human neural stem cells (hNSC) from fetal cortex, glioblastoma (GBM) primary, and recurrent tumors to find GSC-specific plasma membrane transcripts.

overall_design: All of the expression profiles were batch normalized by a robust multichip average (RMA) algorithm using Geospiza GeneSifter (PerkinElmer) online microarray database and analysis software. The data was then exported into Microsoft Office Excel 2010 and organized for GSC transcripts with raw intensity values 10 fold or higher over normal brain, hNSCs, GBM primary and recurrent tumor samples. The reverse sorting algorithm was done to obtain downregulated GSC trascripts.

first: Paul

last: Clark

first: John

middle: S

last: Kuo


title: Gene expression and DNA methylation analysis of subcutaneous abdominal and gluteal adipose tissue


title: Mepenzolate bromide displays beneficial effects in a mouse model of chronic obstructive pulmonary disease

city: Bunkyo-ku

first: Kaoru

last: Mogushi

state: Tokyo

address: 2-1-1 Hongo

department: Intractable Disease Research Center

country: Japan

institute: Juntendo University

summary: For the clinical treatment of chronic obstructive pulmonary disease (COPD), it is important not only to improve the airflow limitation by bronchodilation but also to suppress emphysema by controlling inflammation.  In this study, we have screened for compounds that prevent elastase-induced airspace enlargement in mice from medicines already used clinically.  Mepenzolate bromide, a muscarinic antagonist used to treat gastrointestinal disorders was selected.  Intratracheal administration or inhalation of mepenzolate bromide decreased the severity of elastase-induced airspace enlargement, alteration of lung mechanics and respiratory dysfunction. While mepenzolate bromide showed bronchodilatory activity, most of other muscarinic antagonists tested did not improve the elastase-induced pulmonary disorders.  Mepenzolate bromide suppressed elastase-induced pulmonary inflammatory responses and production of superoxide anions, and reduced the level of cigarette smoke-induced airspace enlargement and alteration of lung mechanics.  Based on these results, we propose that this drug is therapeutically effective for COPD as a consequence of both its anti-inflammatory and bronchodilatory activities.

overall_design: In order to understand the mechanism governing mepenzolate-dependent decrease in inflammatory responses and oxidative stress, we performed DNA microarray analysis at the lung of mepenzolate-administered (or control) mice. We then analyzed gene sets that were differently expressed at 25 hours after administration of mepenzolate using Gene Set Enrichment Analysis (GSEA).

first: Ken-ichiro

last: Tanaka

first: Tomoaki

last: Ishihara

first: Toshifumi

last: Sugizaki

first: Daisuke

last: Kobayashi

first: Yasunobu

last: Yamashita

first: Kayoko

last: Tahara

first: Naoki

last: Yamakawa

first: Kumiko

last: Iijima

first: Hiroshi

first: Keizo

last: Sato

first: Hidekazu

last: Suzuki

first: Tohru

last: Mizushima


title: Expression data of growth plate chondrocytes isolated from control or conditional Lkb1 mutant mice at postnatal day 30

city: Los Angeles

first: Lick Pui

last: Lai

address: 1425 San Pablo St, 3rd fl

institute: University of Southern California

summary: We have shown that removal of Lkb1 in chondorcytes results in enchondroma-like structure in postnatal mouse long bones. To furhter understand the role of Lkb1 in this process, we performed microarrrays to compare the transcriptional profile between control and conditional Lkb1 mutant (Col2a1-Cre; Lkb1c/c) chondrocytes.

overall_design: Postnatal day 30 mouse growth plate chondorcytes from control and mutant mouse femurs and tibiae were isolated for RNA extraction and hybridization on Affymetrix microarrays.

first: Lick

first: Andrew

last: McMahon


title: HDAC3deltaIEC

status: Public on Nov 12 2013

first: Theresa

last: Alenghat

address: 240 Albert Sabin Way, S5.409

department: Division of Immunobiology


title: Regulation of gene expression in IECs by HDAC3 under germ-free conditions

summary: The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria.  However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3ΔIEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation.  Critically, conventionally-housed HDAC3ΔIEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria.  In addition, HDAC3ΔIEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis.  Strikingly, rederivation of HDAC3ΔIEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria.  Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.

overall_design: In this study, we performed gene expression profiling to examine how the transcriptional profiles in primary live, EpCAM+ IECs from the large intestine differed between germ-free control HDAC3FF mice (3 biological replicates) and germ-free IEC-intrinsic knockout HDAC3ΔIEC mice  (3 biological replicates).

first: David

last: Artis


title: Regulation of gene expression in IECs by HDAC3

overall_design: In this study, we performed gene expression profiling to examine how the transcriptional profiles in primary live, EpCAM+ IECs from the large intestine differed between control HDAC3FF mice (3 biological replicates) and IEC-intrinsic knockout HDAC3ΔIEC mice  (3 biological replicates).


title: Variability in functional p53 reactivation by Prima-1Met/APR-246 in Ewing sarcoma

city: Vienna

first: Maximilian

last: Kauer

address: Zimmermannplatz 10

department: Molecular Biology

country: Austria

institute: CCRI, St.Anna Children Cancer Research Institute

summary:
Though p53 mutations are rare in Ewing sarcoma, there is a strong indication that p53-mutant tumors form a particularly bad prognosis group. As such, novel treatment strategies are warranted that would specifically target and eradicate tumor cells containing mutant-p53 in this subset of ES patients.
PRIMA-1Met/APR-246 is a small organic molecule which has been shown to restore tumor suppressor function primarily to mutant p53 and to also induce cell death in various cancer cell types.

overall_design: We analyzed the apoptosis inducibility on Ewing sarcoma cells harbouring different p53 mutations upon exposure to APR-246. Gene expression profiles of three STA-ET-7 cell lines established from the same patient at different stages of the disease was assessed by microarray analysis as these cell lines responded variably to APR-246.

first: Dave

last: Aryee

first: Stefan

last: Niedan

first: Jozef

last: Ban

first: Raphaela

last: Schwentner

first: Karin

last: Muehlbacher

first: Max

first: Reinhard

last: Kofler

first: Heinrich

last: Kovar


title: Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

city: Nashville

first: Claudia

middle: D

last: Andl

state: TN

address: 1161 21St Ave S

department: Surgery

institute: Vanderbilt University

summary:
Esophageal cancer is one of the deadliest cancers as patients present at late stages of disease. Frequent gene alterations include the loss of E-cadherin and TGFb receptor type II. The goal of this study was to establish a model of esophageal cancer by introducing dominant-negative mutants of E-cadherin and TGFb receptor II.
To analyze the functional consequences and gene expression chages induced by E-cadherin and TGFb receptor type II loss in esophageal cancer.

overall_design: Human esophageal keratinocytes were retrovirally transfected with wild-type full length E-cadherin, dominant-negative E-cadherin and dominant-negative TGFb receptor type II. Grown in organotypic cultures on a collagen/matrigel matrix with embedded fibroblast, the generated cell lines were analyzed for their potential to invade into the underlying matrix. Each cell lines was grown in duplicate in organotypic culture and therefore 2 replicates analyzed. Gene expression changes in invasive versus non-invasive areas were analyzed after RNA isolation using laser-capture microdissection resulting in 2 samples representing a normal esophageal epithelium (Ecad), 2 each of dominant-negative Ecad (Ecyto) non-invasive and invasive. To model the genetic alterations in esophageal cancer dominant-negative E-cadherin and dominant-negative TGFb receptor type II (Ecyto-dnTGFR) were expressed and 2 samples each, non-invasive and invasive, analyzed.

first: Anil

last: Rustgi

first: Hung-Chung

last: Huang

first: Zhongming

last: Zhao


title: Brain tumor initiating cell response to microglia

status: Public on Nov 06 2013

city: Calgary

first: Voon

middle: Wee

last: Yong

state: Alberta

address: 3330 Hospital drive NW

department: Clinical Neurosciences

country: Canada

institute: University of Calgary

summary:
Determination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis.
We subjected brain tumor initiating cells to microarray to determine the genes involved in BTICs growth and differentiation when exposed to microglia conditioned medium (MCM) for 6h.

overall_design: BTICs were grown in MCM or control medium for 6h, and media was removed and then the cells were subjected for RNA extraction and hybridization on Affymatrix microarrays. Three (3) control and four (4) MCM samples were generated. The overall objective was to collect the RNA from the MCM exposed differentiated BTICs.

first: V

first: Susobhan

last: Sarkar


title: Gene expression data from 131 human subjects in Detroit, Michigan

city: Chapel Hill

first: Rebecca

middle: Catherine

last: Fry

address: 1213 MHRC

department: Environmental Sciences and Engineering

institute: UNC-Chapel Hill

summary:
Background
Complex diseases are often difficult to diagnose, treat and study due to the multi-factorial nature of the underlying etiology. Large data sets are now widely available that can be used to define novel, mechanistically distinct disease subtypes (endotypes) in a completely data-driven manner. However, significant challenges exist with regard to how to segregate individuals into suitable subtypes of the disease and understand the distinct biological mechanisms of each when the goal is to maximize the discovery potential of these data sets.

Results
A multi-step decision tree-based method is described for defining endotypes based on gene expression, clinical covariates, and disease indicators using childhood asthma as a case study. We attempted to use alternative approaches such as the Student’s t-test, single data domain clustering and the Modk-prototypes algorithm, which incorporates multiple data domains into a single analysis and none performed as well as the novel multi-step decision tree method. This new method gave the best segregation of asthmatics and non-asthmatics, and it provides easy access to all genes and clinical covariates that distinguish the groups.

Conclusions
The multi-step decision tree method described here will lead to better understanding of complex disease in general by allowing purely data-driven disease endotypes to facilitate the discovery of new mechanisms underlying these diseases. This application should be considered a complement to ongoing efforts to better define and diagnose known endotypes. When coupled with existing methods developed to determine the genetics of gene expression, these methods provide a mechanism for linking genetics and exposomics data and thereby accounting for both major determinants of disease.

overall_design: We collected peripheral blood samples from 131 children for RNA extraction and hybridization of target cDNA onto Affymetrix Human U133 Plus 2.0 whole genome array.

first: ClarLynda

middle: R

last: Williams-DeVane

first: David

last: Reif

first: Elaine

middle: C

last: Hubal

first: Pierre

last: Bushe

first: Edward

last: Hudgens

first: Jane

last: Gallagher

first: Stephen

last: Edwards


title: Alleviation of telomere dysfunction and mitochondria defects of telomerase deficient somatic cells by reprogramming

status: Public on Nov 11 2013

city: Beijing

first: le

middle: rong

last: rong

state: Beijing

department: Gaoshaorong lab

country: China

institute: NIBS

summary: Somatic cell nuclear transfer (SCNT) and induced pluripotent stem cells (iPSCs) represent two major approaches for somatic cell reprogramming. However, little attention has been paid to the ability of these two strategies in rejuvenating cells from donors with aging associated syndrome. Here, we utilized telomerase deficient (Terc-/-) mice to probe this question. SCNT-derived embryonic stem cells (ntESCs) and iPSCs were successfully derived from second generation (G2) and third generation (G3) of Terc-/- mice, and ntESCs showed better differentiation potential and self-renewal ability. Telomeres lengthened extensively in cloned embryos while remained or slightly increased in the process of iPSCs induction. Furthermore, G3 ntESCs exhibited improvement of telomere capping function as evidenced by decreased signal free ends and chromosome end-to-end fusion events. In contrast, there was a further decline of telomere capping function in G3 iPSCs. In addition to telomere dysfunction, mitochondria function was severely impaired in G3 iPSCs as evidenced by oxygen consumption rate (OCR) decline, reactive oxygen species (ROS) accumulation and dramatically increased mitochondria genome mutations while these deficiencies were greatly mitigated in G3 ntESCs. Our data proved the principle that SCNT-mediated reprogramming appears more superior than transcription factors induced reprogramming in terms of the resetting of telomere quality and mitochondria function, and thus, providing valuable information for further improvement of transcription factors mediated reprogramming.

overall_design: We compared the gene expression profile of G3 Terc-/- ntES and G3 Terc-/- iPS. Three biological repeats were included for each cell line.

first: R

last: Le

first: S

last: Gao

first: Z

last: Ju


title: Expression profiling of the uteri of progesterone induced uterine gland knockout mice

status: Public on Nov 05 2013

city: Columbia

first: Thomas

last: Spencer

state: MO

address: 920 East Campus Drive

department: Animal Sciences

institute: University of Missouri

summary: To identify genes differentially expressed in the glandless uterus, whole uteri were collected from control (uterine glands present) and PUGKO (no uterine glands) mice at day of pseudopregnancy (DOPP) 3.5 (day DOPP 0.5= vaginal plug). Microarray analysis identified differentially expressed genes in the glandless uteri of PUGKO mice as compared to control mice.

overall_design: Whole uteri (control wild type  n=4;  PUGKO  n=4) were analyzed for differences in their transcriptome using a mouse microarray.

first: Justyna

last: Filant


title: Expression profiling of luminal and glandular epithelia in the neonatal and adult mouse uterus

summary: Laser capture microdissection coupled with microarray genes expression analysis were utilized in order to elucidate the regulatory networks active in epithelial cells of the neonatal and adult mouse uterus.

overall_design: Genes predominantly expressed in the glandular epithelium (GE) in the neonatal or adult uterus were determined by comparing transcripts in the isolated samples of luminal epithelium (LE) and GE from postnatal day (PD) 10, day of psudopregnancy (DOPP) 2.5 or DOPP 3.5 uteri (n=2/cell type/day).


title: Genome-wide expression study of the CD11b+  subsets of dermal myeloid cells and their migratory counterparts in the draining lymph node

status: Public on Nov 04 2013

city: Marseille

first: Marc

last: DALOD

address: Parc scientifique de Luminy, Case 906

department: Dendritic cells and antiviral defense

country: France

institute: Center of Immunology of Marseille Luminy (CIML)

summary: Numerous CD11b+ myeloid cells are present within the dermis. They are very heterogeneous and can be divided in dermal DCs, tissue monocytes and tissue macrophages. At steady state, only CD11b+ DC migrate from the dermis to the skin draining lymph nodes whereas upon DNFB-induced inflammation, CD11b+ DC as well as dermal monocytes migrated to the lymph nodes. The objective of this study was to use gene expression profiling to rigorously identify the different subsets of dermal CD11b+ myeloid cells at steady state and upon inflammation and to characterize their functional potential.

overall_design: This study includes data from DC, monocytes and macrophages purified by flow cytometry sorting from the blood (monocytes only), dermis and the cutaneous lymph nodes (migDC and mig mono) of WT C57BL6 mice, under steady-state or upon DNFB-mediated inflammation. Three independent replicates were made for each cell type, from three independent pools of mice,  and were hybridized on 3 separate batches of gene chips Affimetrix 1.0ST.

last: Tamoutounour

last: Henri

first: B

last: Malissen

first: M

last: Dalod

first: F

last: Montanana Sanchis

first: E

last: Ppollet

first: H

last: Liu


title: Transcriptional override: a regulatory network model of indirect responses to modulations in microRNA expression (mRNA)

city: Atlanta

first: Christopher

last: Hill

state: GA

address: 315 Ferst Dr

department: Biology

institute: Georgia Institute of Technology

summary: MicroRNAs are small non-coding molecules that have been shown to repress the translation of thousands of genes. Changes in microRNA expression in a variety of diseases, including cancer, are leading to the development of microRNAs as early indicators of disease, and to their potential use as therapeutic agents. A significant hurdle to the use of microRNAs as therapeutics is our inability to predict the molecular and cellular consequences of perturbations in the levels of specific microRNAs on targeted cells. While the direct gene (mRNA) targets of individual microRNAs can be computationally predicted and are often experimentally validated, assessing the indirect effects of microRNA variation remains a major challenge in molecular systems biology. We present experimental evidence for a computational model that quantifies the extent to which down-regulated transcriptional repressors contribute to the unanticipated upregulation of putative microRNA targets. An appreciation of the effects of these repressors may provide a more complete understanding of the indirect effects of microRNA dysregulation in diseases such as cancer, and to their successful clinical application.

overall_design: mRNA were collected from the surface epithelial cells of 10 normal ovaries and from laser capture microdisection of 10 ovarian tumors. mRNA expression was captured on Affymetrix U133 Plus 2 chips. Present/absent calls were generated using MAS5, while signals were calculated using GCRMA. All signals were then log2 normalized. Expression was compared between miRanda-mirSVR predicted target genes of upregulated microRNAs, non-predicted target genes, and genes putatively targeted by down-regulated transcriptional repressors.

first: C

first: L

last: Matyunina

last: Walker

first: J

last: McDonald


title: Transcriptome Analysis of Human Peripheral Blood Mononuclear Cells Exposed to Lassa Virus and to the Reassortant ML29, a Vaccine Candidate

city: Baltimore

first: Maria

last: Salvato

state: MD

address: 725 W Lombard Street

department: Institute of Human Virology

institute: University of Maryland School of Medicine

summary: The virulent Lassa fever virus (LASV) and the non-pathogenic Mopeia virus (MOPV) infect rodents and incidentally people in West Africa. The mechanism of LASV damage in human beings is unclear. A live-attenuated reassortant of MOPV and LASV protects rodents and primates from Lassa fever disease. Peripheral blood mononuclear cells from healthy human subjects were expose to either LASV or ML29 in order to identify early cellular responses that could be attributed to the difference in virulence between both viruses. Differential expression of interferon-related genes as well as coagulation-related genes could lead to an explanation for Lassa fever pathogenesis and lead to protective treatments for Lassa fever disease.

overall_design: 27 RNA sampes from Human PBMC exposed to Lassa and Mop/Las (see below):  1 uninf. PBMC  4hr, 8 hr, 24 hr   2 LASV PBMC  4hr, 8 hr, 24 hr   X 3  3 ML29 PBMC 4hr, 8 hr, 24 hr     There are 3 biological replicates of this experiment in that the PBMC of 3 different individuals have been used.

first: Juan

last: Zapata

first: Ricard

last: Carrion Jr.

first: Jean

middle: L

last: Patterson

first: Oswald

last: Crasta

first: Yan

last: Zhang

first: Sachin

last: Mani

first: Bhawna

last: Poonia

first: Mahmoud

last: Djavani

first: David

last: White

first: Igor

last: Lukashevich


title: Linking genomic lesions with minimal residual disease improves prognostic stratification in children with T-cell acute lymphoblastic leukaemia

city: Padova

first: Andrea

last: Zangrando

address: Via Giustiniani, 3

department: Woman and Child's Health

country: Italy

institute: University of Padova

summary: GEP class prediction in association with CI-FISH (42 candidate genes) and patient MRD stratification

overall_design:
Combined Interphase FISH (CI-FISH) for 42 candidate genes and Single Nucleotide Polymorphism (SNP) arrays were applied in a series of 51 T-ALL patients enrolled in Italy into the AIEOP-BFM ALL2000 protocol and stratified by Minimal Residual Disease (MRD). In 40 cases gene expression profiles (GEP) (Affymetrix HU-133 Plus 2.0 arrays) were available.

This submission represents the gene expression component of the study

first: Marco

last: Giordan


title: Gene expression profiling in neuroblastoma cells upon CHAF1A silencing

status: Public on Nov 01 2013

city: Houston

first: Eveline

last: Barbieri

state: Texas

address: 1102 Bates Street

department: Department of Pediatrics

institute: Baylor College of Medicine

summary:
We used an inducible ShRNA system and microarrays to detail the global programme of gene expression underlying neuroblastoma differentiation upon CHAF1A silencing .
CHAF1A is a subunit of the Chromatin Assembly Factor-1 (CAF1) and regulates H3K9-trimethylation. High expression of CHAF1A strongly correlates with neuroblastoma poor prognosis and  loss-of-function drives neuronal differentiation in vitro and in vivo.

overall_design: Total RNA was isolated using RNAeasy kit from IMR32 cells transduced with inducible CHAF1A ShRNA. Gene expression profiling was performed in neuroblastoma cells upon CHAF1A silencing over time course (0, 5, and 10 days) in triplicate.

first: Katleen

last: De Preter

first: Mario

last: Capasso

first: Zaowen

last: Chen

first: Danielle

last: Hsu

first: Gian

last: Tonini

first: Steve

last: Lefever

first: John

last: Hicks

first: Rogier

last: Versteeg

last: Pession

first: Frank

last: Speleman

first: Eugene

last: Kim

first: Jason

last: Shohet


title: NLRP7 promotes trophoblast lineage differentiation, YY1 binding and alters CpG methylation

first: Sangeetha

middle: Kaveri

last: Mahadevan

address: 1250 Moursund St, Room 1025

department: Obsterics and Gynecology

summary: Genome wide DNA methylation profiling of hESC in the untransduced, scrambled control and with knockdown of NLRP7 in undifferentiated and BMP4 differentiated states using the Illumina HumanMethylation 450 BeadChip. Several genomic sites exhibit altered methylation upon knocking down NLRP7.

overall_design: Bisulphite converted DNA from 3 replicates of untransduced, scrambled control and NLRP7 knockdown in the undifferentiated and BMP differentiated groups were hybridised to the Illumina Human Methylation 450 Beadchip.

first: Shu

last: Wen

first: Ying-Wooi

last: Wan

first: Hsiu-Huei

last: Peng

first: Subhendu

last: Otta

first: Zhandong

last: Liu

first: Michelina

last: Iacovino

first: Elisabeth

last: Mahen

first: Michael

last: Kyba

first: Bekim

last: Sadikovic

first: Ignatia

middle: B

last: Van den Veyver


title: Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

status: Public on Nov 03 2013

city: La Jolla

first: George

last: Sen

address: 9500 GIlman Drive

department: Dermatology/CMM

institute: UCSD

summary:
To determine if fibroblasts could be reprogrammed to a keratinocyte phenotype p63+KLF4 or LacZ expressing retroviruses were transduced into primary human neonatal fibroblasts.
Global gene expression profiling using U133 plus 2.0 arrays were used to deteremine the extent of reprogramming to a keratinocyte phenoypte upon transduction with p63+KLF4. Fibroblasts transduced with p63+KLF4 were also treated +/- high calcium to determine if treatment with calcium could induce differentiation of these cells. Microarray analysis was also performed on cells treated +/- calcium.

overall_design: For gene expression profiling, cultured human fibroblasts were infected with LacZ or p63+KLF4 expressing retroviruses. p63+KLF4 cells were also treated +/- calcium.  Microarray analysis using Affymetrix HG-U133 2.0 plus arrays was performed on duplicate samples.

first: Y

last: Chen

first: D

last: Mistry

first: G


title: Global reprogramming of the cellular translational landscape facilitates cytomegalovirus replication

city: LYON

first: Jiri

last: ZAVADIL

state: Other

address: 150 COURS ALBERT THOMAS

institute: IARC WHO

summary:
Genome-wide profiling establishes that human cytomegalovirus (HCMV) exerts an extensive, unforeseen level of specific control over which cellular mRNAs are recruited to or excluded from polyribosomes.
The landscape of translationally-regulated host mRNAs regulates HCMV replication. The HCMV imposed translational signature shares similarities with cancer cells

overall_design:
Two biological replicate experiments were performed profiling total and polysomal mRNAs from i) HCMV-infected vs mock-infected cells and ii) uninfected cells transduced with a lentivirus expressing doxycyclin (dox)-inducible HCMV UL38 +/- dox.
Analysis of translationally-controlled host genes in HCMV-infected cell and cells expressing the HCMV UL38 gene product

first: Caleb

last: McKinney

last: Zavadil

first: Christopher

last: Bianco

first: Lora

last: Shiflett

first: Stuart

last: Brown

first: Ian

last: Mohr


title: Dynamic changes of DNA methylome and hydroxymethylome during neural differentiation of hES cell (hMeDIP-Seq and MBD-Seq)

city: Daejeon

first: Mirang

last: Kim

address: 125 Gwahak-ro, Yuseong-gu

department: Personalized Genomic Medicine Research Center

country: South Korea

institute: KRIBB(Korea Research Institute of Bioscience and Biotechnology

type: Methylation profiling by high throughput sequencing

summary: DNA methylation and hydroxymethylation have been implicated in normal development and differentiation, but our knowledge about the genome-wide distribution of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) during cellular differentiation remains limited. Using in vitro model system of gradual differentiation of human embryonic stem (hES) cells into ventral midbrain-type neural precursor (NP) cells and terminally into dopamine (DA) neurons, we explored changes in 5mC or 5hmC patterns during lineage commitment. We used three techniques, 450K DNA methylation array, MBD-seq, and hMeDIP-seq, and found combination of these methods can provide comprehensive information on the genome-wide 5mC or 5hmC patterns. We observed dramatic changes of 5mC patterns during differentiation of hES cells into NP cells. Although genome-wide 5hmC distribution was more stable than 5mC, coding exons, CpG islands and shores showed dynamic 5hmC patterns during differentiation. In addition to the role of DNA methylation as a mechanism to initiating gene silencing, we also found DNA methylation as a locking system to maintain gene silencing. More than 1,000 genes including mesoderm development related genes acquired promoter methylation during neuronal differentiation even though they were already silenced in hES cells. Finally, we found that activated genes lost 5mC in transcription start site (TSS) but acquired 5hmC around TSS and gene body during differentiation. Our findings may provide clues for elucidating the molecular mechanisms underlying lineage specific differentiation of pluripotent stem cells during human embryonic development.

overall_design: Examination of hMeDIP-Seq and MBD-Seq in 3 cell types (human embryonic stem, neural precursor, and dopamine neuron cells)

first: Young-Kyu

last: Park

first: Tae-Wook

last: Kang

first: Sang-Hun

last: Lee

first: Yong-Hee

last: Rhee

first: Jong-Lyul

first: Hee

middle: J

first: Seon-Young

first: Daeyoup

first: Doheon

first: Yong


title: Gene expression data from PC3 prostate cells overexpressing control miR or miR-95

city: Toronto

first: Stanley

last: Liu

state: Ontario

address: 2075 Bayview Avenue

institute: Sunnybrook Research Institute

summary: We used microarrays to detail the global changes in gene expression resulting from miR-95 overexpression

overall_design: PC3 prostate cells stably overexpressing control miR or miR-95 were processed for Affymetrix gene array


title: An attenuated Lassa vaccine in SIV-infected rhesus macaques does not persist or cause renavirus disease but does elicit protective immunity

first: Maria

last: Salvato

summary: Lassa fever (LF) is a rodent-borne viral disease that can be fatal for human beings.  In this study, an attenuated Lassa vaccine candidate, ML29, was tested in SIV-infected rhesus macaques for its ability to elicit immune responses without instigating signs of virulent disease. ML29 is a reassortant between Lassa and Mopeia viruses that causes a transient infection in non-human primates and confers sterilizing protection from lethal Lassa viral challenge. However, since the LF endemic area of West Africa also has high HIV seroprevalence, it is important to determine whether vaccination could be safe in the context of AIDS.    SIV-infected and uninfected rhesus macaques were vaccinated with the ML29 virus and monitored for classical and non-classical signs of arenavirus disease.  Classical disease signs included viremia, rash, weight loss, high liver enzyme levels, and virus invasion of the central nervous system.  Non-classical signs derived from profiling the blood transcriptome of virulent and non-virulent arenavirus infections included increased expression of interferon response genes and decreased expression of COX2, IL-1?, coagulation intermediates and nuclear receptors needed for stress signaling.  Here it is demonstrated that SIV-infected and uninfected rhesus macaques responded similarly to ML29 vaccination, and that none developed signs of arenavirus disease or persistence. Furthermore, 5 of 5 animals given a heterologous challenge with a lethal dose of LCMV-WE survived without developing disease signs.

overall_design: 30 RNA samples from Monkey PBMC: 4 uninf. Monkey PBMC, 8 SIV-infected Monkey PBMC(From 8 Monkeys), 5 SIV+ML29-sc infected week1(Monkey PBMC), 5 SIV+ML29-sc infected week2(Monkey PBMC), 1 SIV+ML29-ig infected week1(Monkey PBMC),  1 SIV+ML29-ig infected week2(Monkey PBMC), 2 SIV+Arm-sc infected week1(Monkey PBMC), 2 SIV+Arm-sc infected week2(Monkey PBMC), 1 only ML29-iv infected week1(Monkey PBMC), 1 only ML29-iv infected week2(Monkey PBMC)

first: Juan

last: Zapata

first: Bhawna

last: Poonia

first: Joseph

last: Bryant

first: Harry

last: Davis

first: Eugene

last: Ateh

first: Lanea

last: George

first: Oswald

last: Crasta

first: Yan

last: Zhang

first: Tom

last: Slezak

first: Crystal

last: Jaing

first: C

first: Igor

last: Lukashevich


title: Re-specification of myeloid precursors from human pluripotent cells into engraftable multi-lineage progenitors

city: Seattle

first: Sergei

last: Doulatov

state: WA

address: 1795 NE Pacific Street

institute: University of Washington

summary:
Human pluripotent stem cells were differentiated into hematopoietic progenitors, which were then re-specified using defined transcription factors to resemble hematopoietic stem cells (HSC)
We used microarrays to establish the similarity between converted cells and purified human HSCs.

overall_design: The samples analyzed were: starting embryoid body progenitors, transcription factor-converted cells, and primary HSCs and progenitors from fetal liver and cord blood. All samples were flow sorted for CD34+ and CD38- to compare across a similar population of primitive cells.

first: Linda

middle: T

last: Vo

first: Stephanie

last: Chou

first: Andrea

last: Ditadi

first: Peter

middle: G

last: Kim

first: Natasha

last: Arora

first: Hu

last: Li

first: Brandon

last: Hadland

first: Irwin

last: Bernstein

first: James

last: Collins

first: Gordon

last: Keller

first: Leonard

middle: I

last: Zon

first: George

middle: Q

last: Daley


title: Towards understanding breast cancer mechanisms to metastasize

city: Rotterdam

first: Marcel

last: Smid

address: Dr. Molewaterplein 50

department: Medical Oncology

institute: Erasmus MC

summary: How organ-specific metastatic traits accumulate in primary tumors remains unknown. We identified a role of the primary tumor stroma in selecting breast cancer cells that are primed for metastasis in the bone. A fibroblast-rich stroma in breast tumors creates a microenvironment that is similar to that of bone metastases in its abundance of the cytokines CXCL12 and IGF1. Heterogeneous breast cancer cell populations growing in such mesenchymal environment evolve towards a preponderance of clones that thrive on CXCL12 and IGF1. Fibroblast-driven selection of bone metastatic clones in mammary tumors is suppressed by CXCL12 and IGF1 receptor inhibition. Thus, a fibroblast-rich stroma in breast tumors can pre-select bone metastatic seeds, promoting the evolution of metastatic traits and the interplay between a primary tumor and its distant metastases.

overall_design: Affymetrix U133 Plus2 arrays were hybridized according to the manufacturer's procedure using RNA extracted from 47 primary breast tumors. Specific gene sets were evaluated in this cohort.

first: Xiang

middle: H

last: Zhang

first: John

last: Foekens

first: Joan

last: Massagué


title: 14-3-3ζ overexpression-induced gene signature in MCF-10A cells

first: Jia

last: Xu

state: TX

address: 1515 Holcombe Blvd.

department: Molecular & Cellular Oncology

institute: UT-M.D. Anderson Cancer Center

summary:
To study the function of 14-3-3ζ, we established MCF-10A human mammary epithelial cells transduced with 14-3-3ζ (10A.ζ) and vector (10A.Vec)
We performed gene expression profiling on 10A.ζ cells and 10A.Vec cells, and normalized to profiling of MCF-10A parental cells

overall_design: Total mRNA were extracted from 10A.Parental cells, 10A.Vec cells, 10A.ζ cells which were cultured in 3D culture model for 16 days, and subjected to Affymetrix microarray analysis

first: Dihua

last: Yu


title: Expression data from 205432- or 206381-treated BE(2)-C cells

status: Public on Oct 31 2013

city: Ann Arbor

first: David

last: Miller

state: MI

address: 3560B MSRB II, 1150 W. Medical Center Dr.

department: Internal Medicine

institute: University of Michigan

summary: Analysis of transcription response of undifferentiated human BE(2)-C neuronal cells to stimulation with novel indole-2-carboxamide antivirals 205432 or 206381.

overall_design: Independent sets of BE(2)-C cells were treated with 25 uM of either 205432 or 206381, or DMSO as control.  Total RNA was harvested at 24 h after stimulation and analyzed with Affymetrix U133 Plus 2.0 chips.


title: Tmod3-/- mouse fetal liver compared with wild type

city: La jolla

first: Velia

last: Fowler

state: CA

address: 10550 North Torrey Pines Road

department: Department of Cell and Molecular Biology

institute: The Scripps Research Institute

summary: Tropomodulins (Tmods) cap the pointed ends of actin filaments in erythroid and nonerythoid cell types. Targeted deletion of mouse Tmod3 leads to embryonic lethality at E14.5-E18.5, with anemia due to defects in definitive erythropoiesis in the fetal liver. BFU-E and CFU-E colony numbers are greatly reduced, indicating defects in progenitor populations. Flow-cytometry of fetal liver erythroblasts shows late stage populations are also decreased, including reduced percentages of enucleated cells. AnnexinV staining indicates increased apoptosis of Tmod3-/- erythroblasts, and cell cycle analysis reveals that there are more Ter119hi cells in S-phase in Tmod3-/- embryos. Notably, enucleating Tmod3-/- erythroblasts are still in the process of proliferation, suggesting impaired cell cycle exit during terminal differentiation. Tmod3-/- late erythroblasts often exhibit multi-lobular nuclear morphologies and aberrant F-actin assembly during enucleation.  Furthermore, native erythroblastic island formation was impaired in Tmod3-/- fetal livers, with Tmod3 required in both erythroblasts and macrophages. In conclusion, disruption of Tmod3 leads to impaired definitive erythropoiesis, due to reduced progenitors, impaired erythroblastic island formation, and defective erythroblast cell cycle progression and enucleation. Tmod3-mediated actin remodeling may be required for erythroblast-macrophage adhesion, coordination of cell cycle with differentiation, and F-actin assembly and remodeling during erythroblast enucleation.

overall_design: Total RNAs from Tmod3+/+ and Tmod3-/- fetal livers at E14.5 were extracted and prepared for  micro-array analysis using the MoGene-1_0-st-v1 Affymetrix chip in the Scripps Research  Microarray Core Facility. Each experiment was repeated with three independent embryos.

first: Zhenhua

last: Sui

first: Andrea

last: Bacconi

middle: M


title: Gene expression in Bach2-deficient and wildtype CD4 single-positive thymocytes from mixed chimeric animals

city: Doha

first: Francesco

middle: Maria

last: Marincola

address: Al Nasr Tower, AL Corniche Street, PO Box 26999

country: Qatar

institute: Sidra Medical and Research Center

summary: The role of FoxP3+ regulatory T (Treg) cells in the maintenance of immunological tolerance is well established. Recently, genome-wide association studies (GWAS) in humans have associated polymorphisms within the BACH2 locus encoding the transcription factor BTB and CNC homology 1, basic leucine zipper transcription factor 2 (Bach2) with diverse allergic and autoimmune diseases including asthma, multiple sclerosis, Crohn's disease, celiac disease, generalized vitiligo and type 1 diabetes. Common to these diseases is a failure to adequately maintain immunological tolerance. However, a role for Bach2 in this process has not been established. Here, by assessing the phenotype of mice in which the Bach2 gene is disrupted, we demonstrate a non-redundant role for Bach2 in the prevention of a spontaneous lethal inflammatory disorder predominantly affecting the lung and gut with excessive T helper 2 (Th2) responses and formation of circulating autoantibodies. Bach2 was necessary for efficient induction of FoxP3 expression both during thymopoesis and upon stimulation of naïve peripheral CD4+ T cells under Treg polarizing conditions in vitro. Consequently, in bone marrow reconstitution experiments, Bach2 expression within the haematopoetic system was necessary for suppression of lethal autoimmunity in a manner that was FoxP3 dependent. These findings demonstrate a requirement for Bach2 in early lineage commitment of both thymic and induced Treg cells and point to shared mechanisms that underlie diverse allergic and autoimmune disorders that may serve as targets in the development of novel therapeutic strategies.

overall_design: Six samples were collected from separate mice: three Ly5.1+ wildtype thymocyte samples (biological replicates) and three Ly5.1- Bach2 knockout thymocyte samples (biological replicates).


title: Expression of SUDHL-1 cell line treated by ALK inhibitors

city: Philadelphia

first: Wasik

middle: A

last: Mariusz

state: Pennsylvania

address: 422 Curie Blvd

institute: University of Pennsylvania

summary: In this study we compared the effects of ALK inhibitor on the gene expression, activation of cell signaling pathways, and functional properties of cells derived from a patient with Anaplastic Large Cell Lymphoma. we used microarrays to map the genome-wide gene expression patterns in ALK+TCL cells in response to ALK inhibition.

overall_design: The ALK+TCL Sudhl-1 cell line was treated in triplicates with the ALK inhibitor, CEP-14083, or the compound's solvent for 6 h. The isolated RNA was reverse-transcribed, biotin-labeled, and hybridized to the U133 Plus 2.0 array chips (Affymetrix). Microarray data were normalized using the MAS5 algorithm and analyzed using Partek GS (Partek).

first: Michal

last: Marzec

first: Krzysztof

last: Halasa

first: Xiaobin

last: Liu

first: Hong

middle: Y

last: Wang

first: Mangeng

last: Cheng

first: Donald

last: Baldwin

middle: W

last: Tobia

first: Stephen

last: Schuster

first: Anders

last: Woetmann

first: Qian

first: Suzanne

middle: D

last: Turner

first: Niels

last: Odum

first: Mariusz

last: Wasik


title: RORγt+ Innate lymphoid cells transcriptomes after aNKp44 and cytokine stimulation

status: Public on Oct 30 2013

city: Berlin

first: Johannes

last: Meisig

address: Chariteplatz 1

department: Institut für Pathologie

institute: Charite Universitätsmedizin

summary: RORγt+ innate lymphoid cells (ILC) are crucial players of innate immune responses and represent a major source of IL-22, which has an important role in mucosal homeostasis. The signals required by RORγt+ ILC to express IL-22 and other cytokines, including TNF, have only partially been elucidated. Here we show that RORγt+ ILC can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt+ ILC selectively activates a coordinated pro-inflammatory program, including TNF, while cytokine stimulation induces preferentially IL-22 expression. However, combined engagement of NKp44 and cytokine receptors results in a strong synergistic effect. These data support the concept that NKp44+ RORγt+ ILC can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus.

overall_design: Transcriptome analysis of CD56+CD127hi tonsil ILC, Ex vivo and after stimulation with aNKp44, IL-1/IL-7/IL-23 or aNKp44/IL-1/IL-7/IL-23 for 3.5h. RNA was extracted and pooled from 2 donors each, Amplified and labeled according to manufacturer´s instructions (GeneChipU133plus2® , Affymetrix). The analysis was performed in triplicates.

first: Timor

last: Glatzer

first: Monica

last: Killig

first: Chiara

last: Romagnani


title: Expression data from glioblastoma stem cell clones (GSC)

city: Los Angeles

first: Cho-Lea

last: Tso

address: 10833 Le Conte Avenue

department: Surgery

institute: University of California, Los Angeles

summary: Comparison of treatment sensitive GSC clones (TSGC) with treatment resistant GSC clones (TRGC). We used microarrays to identify molecular signatures of TRGC (upregulated genes).

overall_design: We used radiation treatment (RT) or RT plus TMZ to select treatment resistant GSC clones (TRGC)


title: Dynamic developmental signaling logic underlying lineage bifurcations during human endoderm induction and patterning from pluripotent stem cells [Expression data set]

status: Public on Nov 07 2013

city: Stanford

first: Kyle

middle: M.

last: Loh

address: 265 Campus Drive

department: Department of Developmental Biology

institute: Stanford University School of Medicine

summary:
The definitive endoderm germ layer is the provenance of multiple internal organs, including the lungs, liver, pancreas and intestines. Molecular events driving initial endoderm germ layer specification and subsequent anterior-posterior patterning of endoderm into distinct organ primordia remain largely cryptic.
Through microarray analyses, we captured genome-wide transcriptional dynamics driving successive stages of endoderm development with the intent of identifying novel regulatory genes or diagnostic markers that respectively drive or mark endoderm committment.

overall_design: HES3 human embryonic stem cells (hESCs) were differentiated into highly homogeneous endodermal progenitor populations, and microarray analyses were conducted of six different populations at different tiers of the endodermal lineage hierarchy: undifferentiated hESCs, anterior primitive streak (day 1 of in vitro differentiation), definitive endoderm (day 3) and anterior foregut, posterior foregut or midgut/hindgut patterned endoderm populations (day 7). Additionally, we compared hESCs differentiated using two alternative endoderm induction protocols, serum-based or AFBLy-based differentiation (both day 3 of differentiation).

first: Lay

last: Ang

first: Jingyao

last: Zhang

first: Vibhor

last: Kumar

first: Shyam

last: Prabhakar

first: Irving

last: Weissman

first: Bing

last: Lim


title: Expression data from IgE+ and IgG1+ B lymphocytes in mice infected with Nippostrongylus brasiliensis

city: Singapore

first: Michael

last: Poidinger

address: #04-06, 8A Biomedical Grove

department: Bioinformatics

country: Singapore

institute: Singapore Immunology Network

summary: The mechanisms involved in the maintenance of memory IgE responses are poorly understood, and the role played by germinal center (GC) IgE cells in these memory responses is particularly unclear. IgE B-cell differentiation is characterized by a transient GC phase, a bias towards the plasma cell (PC) fate, and dependence on sequential switching for the production of high-affinity IgE. We show here that IgE GC B cells are unfit to undergo the conventional GC differentiation program due to impaired B-cell receptor function and increased apoptosis. IgE GC cells fail to populate the GC light zone and are unable to contribute to the memory and long-lived PC compartments. Furthermore, we demonstrate that direct and sequential switching are linked to distinct B-cell differentiation fates: direct switching generates IgE GC cells, whereas sequential switching gives rise to IgE plasma cells. We propose a comprehensive model for the generation and memory of IgE responses.

overall_design: The purpose of this analysis was to: 1) identify expression differences between IgE and IgG1 B lymphocytes, 2) identify GC Dark Zone (DZ) and Light Zone (LZ) signatures of IgG1 GC cells. For that purpose, we compared in one experiment the gene expression patterns of IgE germinal center (GC) cells, IgG1 GC cells, IgE plasma cells (PC), IgG1 PC and naïve cells. In a second experiment, we compared the expression of IgG1 DZ GC cells with that of IgG1 LZ GC cells. Triplicates obtained from independent sorting experiments were used for all samples except two (IgG1 PC=2 samples; IgE PC=4 samples). Each sample was obtained from a pool of three individual mice. The mice used in the experiment were CeGFP BALB/c mice infected with the parasite N. brasiliensis. CeGFP mice carry an IRES-GFP KI cassette in the 3'UTR of membrane IgE. In these mice, GFP expression marks IgE cells, and a population of IgG1 cells with a rearrangement to Cepsilon in the non-productive (VDJ negative) IgH chromosome.

first: Maria

last: Curotto de Lafaille

first: Jin

middle: S

last: He

first: Geraldine

last: Koh

first: Francesca

last: Zolezzi


title: Tumor grafts derived from patients with head and neck squamous carcinoma.

status: Public on Oct 28 2013

first: Chad

last: Creighton

address: One Baylor Plaza, Mail Stop: BCM305

department: Biostatistics, Ducan Cancer Center

summary: Head and neck squamous cell carcinoma (HNSCC) is a deadly and disfiguring disease for which better systemic therapy is desperately needed.  The development of new therapies for HNSCC and the understanding of its biology both depend upon clinically relevant animal models.  An increasingly promising xenograft model, the patient derived xenograft (PDX), is developed by surgically implanting tumor tissue directly from a patient into an immunocompromised mouse. We transplanted 30 HNSCC primary tumors directly into mice.  The histology and stromal components were analyzed using immunohistochemistry. Gene expression analysis with Affymetrix U133A-microarrays was conducted on patient tumors, including third generation and one tenth generation PDX; one PDX-derived cell line; and 2 established HNSCC cell lines. Five of 30 (17%) transplanted tumors could be serially passaged and used for therapeutic and mechanistic studies.  One cell line has been established from a tongue primary.  The tumors maintained the histologic appearance of the parent tumor although human stromal components were lost upon engraftment.  One PDX model was derived from an HPV-positive tumor.  From the >54,000 probes tested, there were widespread differences in gene expression between the tumors growing in mice vs. the corresponding human tumors from which they were derived.  For genes differing between parent tumors and human cell lines in culture, the PDXs’ expression pattern was very similar to that of the parent tumors.  There were also widespread expression differences between the human tumors that subsequently grew in mice vs. those that did not - suggesting that this model enriches for cancers with distinct biological features. Our results demonstrate the feasibility of a PDX model of HNSCC.  Gene expression patterns suggest that the PDX more closely recapitulated the parental tumor than do cells in culture.  The histology of the tumors in mice is similar to that of the same tumor in humans.  Additionally, gene expression patterns and histology are stable over multiple generations.

overall_design: We transplanted HNSCC primary tumors directly into mice.  Gene expression analysis with Affymetrix U133A-microarrays was conducted on patient tumors, including third generation and one tenth generation PDX; one PDX-derived cell line; and 2 established HNSCC cell lines.

first: Faye

last: Johnson

first: Shaohua

last: Peng

first: Yiqun


title: Genome-wide profiling of DNA methylation and expression identifies CIMP in myelodysplastic syndrome [Illumina]

status: Public on Oct 29 2013

city: Shanghai

first: xiaoqin

last: wang

address: 12 wulumuqi road central

institute: Huashan  hospital

summary: To identify genes hypermethylated and transcriptionally downregulated, we have employed the Illumina Infinium HumanMethylation450 BeadChip and Agilent SurePrint G3 Human Gene Expression 8x60K. And we validated selected genes in cases and controls. eventually we estalished CIMP of MDS.

overall_design: Bisulphite converted DNA from the 4 patients and 4 controls were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

first: Xiaoqin

last: Wang

first: Xiaodong

last: Jia

first: Xiaoli

last: Zhao

first: Feng

last: Yang

first: Shuang

last: Li

first: Meixia

last: Liu

first: Shaoxu

last: Ying

first: Rong

last: Fan


title: Anticancer properties of distinct antimalaria drug classes

status: Public on Oct 26 2013

city: Freiburg

first: Jaga

last: Virayah

address: Am Flughafen 12-14

institute: Oncotest GmbH

summary:
Background: Antimalarials have anticancer potential.  Results: We have systematically tested five distinct antimalaria drugs in a panel of cancer cell lines.  Conclusion: Three antimalarial classes display potent antiproliferative activity, and their potency is correlated with cancer cell gene expression patterns.  Significance: We confirm and extend anticancer potential of these antimalarials and we discuss their therapeutic potential based on clinical data.
Key words: Malaria, Anticancer drug, Drug Discovery, Genomics, Gene Expression, Bioinformatics, Cancer

overall_design: Affymetrix® HG-U133 Plus 2.0 mRNA expression arrays were used to determine the expression. CEL result files were pre-processed using the RMA  (Irizarry et al, 2003) algorithm. This microarray analysis was performed for 91 cell lines.

first: Rob

last: Hooft van Huijsduijnen

first: Kip

last: Guy

first: Kelly

last: Chibale

first: Richard

last: Haynes

first: Ingmar

last: Peitz

first: Gerhard

last: Kelter

first: Margaret

last: Phillips

first: Jonathan

last: Vennerstrom

first: Yongyuth

last: Yuthavong

first: Timothy

middle: N

last: Wells


title: Gene expression profile of E. coli MG1655 cells grown at different growth rates in mixed substrates culture

status: Public on Oct 24 2013

city: Pittsburgh

first: Zoltan

last: Oltvai

state: PA

address: Rm. S701 Scaife Hall, 3550 Terrace St.

department: Department of Pathology

institute: University of Pittsburgh

summary:
E. coli MG155 cells were grown at different grwoth rates in mixed substrate culture. To facilitate different metaoblic status, cells adjust substrate consumption behavior which must be reflected in the gene expression profiles of metablism network. The metabolism network including the substrate transporter systems is our study focus.
We use microarrays to capture the adjustments and switches in substrate transporter and central metabolism network along growth rate changes.

overall_design: E. coli MG155 cells were cultured in a continuous-feed chemostat culture with growth rate control through dilution. Cells were confirmed with a stable growth rate then collected and analyzed 24 hrs after each dilution change.

first: Yi

last: Zhou

first: Alexei

last: Vazquez

first: Aaron

last: Wise

first: Tomoko

last: Warita

first: Katsuhiko

first: Ziv

last: Bar-Joseph


title: EGFR expression status associated with lymph node ratio

city: Sagamihara

first: Akira

last: Ema

state: Kanagawa

address: Kitasato 1-15-1, Minami-ku

department: Department of Surgery

institute: Kitasato University School of Medicine

summary:
We have tried to identify molecules associated with lymph node ratio expression by microarray.  Expression microarray data prioritized gene candidates according to average expression ratio and its frequency.
Among these genes, we examined particular EGFR expression by immunohistochemistry (IHC) in 167 advanced gastric cancer.

overall_design: We compared tumor specimens with high LNR (n=4) with those with low one (n=4) at mRNA level by Affymetrix microarray (harboring 54,675 genes) in stage III gastric cancer.  We then prioritized the expression data, and enriched genes correlated with LNR, and finally validated EGFR as such candidates in primary advanced gastric cancer who underwent standard treatment (n=167).

first: Mina

last: Waraya

first: Keishi

last: Yamashita

first: Kenichi

last: Kokubo

first: Hirosuke

last: Kobayashi

first: Keika

last: Hoshi

first: Yoshiko

last: Shinkai


title: Effects of Intestine-specifc SREBP2 overactivation on gene expression in mouse jejnum

city: Chicago

first: Waddah

last: Alrefai

state: IL

address: 820 S Damen Ave

department: Medicine

institute: University of Illinois at Chicago/Jesse Brown VA Medical Center

summary:
The active form of the SREBP2 transcription factor was specifically overexpressed in the intesitne. This was achieved by generating transgenic mouse model (designated as ISR2) in which the transgene represents the N-terminal active SREBP2 transcription factor driven by the villin promoter.
In this project, we investigated the effects of overactivation of SREBP2 on gene expression in mouse jejunum

overall_design: Gene expression profile in the jejunum of ISR2 was compared to gene expression profile in the jejunum of their wild type littermates.

first: Ke

last: Ma


title: Genome-wide profiling of DNA methylation and expression identifies CIMP in myelodysplastic syndrome

first: xiaoqin

last: wang

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

overall_design: Refer to individual Series


title: Remission in Juvenile Idiopathic Arthritis Achieved on Different Drug Regimens

city: Oklahoma City

first: Bart

last: Frank

state: OK

institute: OMRF

summary: Remission has become both the gold standard for clinical care and the end point for clinical trials for children with juvenile idiopathic arthritis (JIA). Using gene expression microarrays, we found that when remission induced by methotrexate (MTX) or MTX plus a TNF inhibitor (etanercept, Et) (MTX+Et) was compared with healthy controls, there were notable differences in gene expression patterns, demonstrating that remission is not a restoration of immunologic normalcy. Differences were detected in PBMC as well as in granulocytes.

overall_design: Total RNA was extracted from isolated PBMC and granulocytes from patients with polyarticular JIA and from healthy controls. Patients had achieved remission (clinical remission on medicine as defined by Wallace et al, Arthritis Rheum. 2005;52(11):3354-3562) using either MTX or MTX+Et.


title: Expression data from footpad of AIRmax and AIRmin mice submitted to pristane arthritis induction

status: Public on Oct 23 2013

city: Sao Paulo

first: Marcelo

last: De Franco

state: Sao Paulo

address: Avenida Vital Brasil 1500

department: Imunogenetica

country: Brazil

institute: Instituto Butantan

summary:
Mice selected for high and low acute inflammation were tested for pristane induced arthritis, showing to be susceptible and resistant, respectively.
We used microarrays to detail the global programme of gene expression underlying arthritis progression during induction and identified distinct classes of differentially expressed genes during this process in the footpad of these mice.

overall_design:
AIRmax (high inflammation) and AIRmin (low inflammation) mouse footpads were collected for RNA extraction and hybridization on Affymetrix microarrays. We compared control and experimental footpads from male and female AIRmax and AIRmin mice on days 0 and 160, respectively.

Please note that the AIRmax and AIRmin mice were obtained through bidirectional genetic selection, starting with a genetically heterogeneous founder population (F0) produced by intercrossing eight isogenic strains of mice of independent origins (A/J, DBA/2J, P/J, SWR/J, SJL/J, CBA/J, BALB/cJ and C57BL/6J).

first: M


title: Gene expression profiles of induced multipotent germline stem cells and other pluripotent stem cells

status: Public on Oct 21 2013

city: Kyoto

first: Seiji

last: Takashima

address: 53 Kawahara-cho, Shogoin, Sakyo

department: Department of Molecular Genetics

institute: Kyoto University

summary: Spermatogonial stem cells (SSCs) have pluripotent potential. However, frequency of pluripotent cell derivation is low and the mechanism of culture-induced reprogramming remains unknown. Here we report that epigenetic instability of germline stem (GS) cells, cultured SSCs, induces pluripotent cell derivation. GS cells undergo DNA demethylation in H19 differentially methylated region under low-density culture. When H19 demethylation was induced by Dnmt1 depletion, they converted into embryonic stem (ES)-like cells. Dnmt1 depletion downregulated Dmrt1 expression, whose depletion also induced pluripotency. Functional screening of Dmrt1 target gene revealed that Dmrt1 depletion upregulates Sox2, the key molecule responsible for generating induced pluripotent stem cells. Although Sox2 transfection upregulated Oct4 and produced pluripotent cells, this conversion was inhibited by Oct1 overexpression, suggesting that the balance of Oct proteins maintains SSC identity. These results suggest that culture-induced reprogramming is caused by unstable DNA methylation, and that Dmrt1-Sox2 cascade is critical for regulating pluripotency in SSCs.

overall_design: Pluripotent stem-like cells were induced from GS cells by down-regulation of  Dnmt/Dmrt, or up-regulation of Sox2/Oct4 in combination with p53 knock-down and their total RNA samples were subjected to microarray analysis to compare their gene expression profile with other pluripotent stem cells such as ES cells or iPS cells.

first: Takashi

last: Shinohara


title: Analysis of epigenetic changes in survivors of preterm birth reveals the effect of gestational age and evidence for a long term legacy

status: Public on Oct 20 2013

city: NEDLANDS

first: David

last: Martino

state: Western Australia

address: Perth Childrens Hospital, 15 Hospital Avenue

country: Australia

institute: Telethon Kids Institute

summary: Genome-wide DNA methylation profiling of DNA extracted from dried blood spots from preterm and term subjects using longitudinal samples collected at birth and 18 years of age. Infinium HM450 arrays were used to measure methylation at 347,789 autosomal CpGs. DNA was analysed from individuals at birth and 18-years and included 12 preterm and 12 term controls.

overall_design: Bisulphite converted DNA from the 48 samples were hybridised to the Illumina Infinium 450K Human Methylation Beadchip

first: Mark

last: Cruickshank

first: Jeff

last: Craig


title: Distinct Mutational Patterns of Infection and Non-Infection-Related Bile Duct Cancers Revealed by Exome Sequencing

first: Weng Khong

last: Lim

state: Singapore

address: 11 Hospital Drive

department: Department of Medical Sciences

institute: National Cancer Centre Singapore

summary: The impact of different carcinogenic exposures on the specific patterns of somatic mutations in human tumors remains unclear. To clarify this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by liver fluke Opisthorchis viverrini (OV)-infection and 101 cases due to non-OV etiologies. Whole-exome (N = 15) and prevalence screening (N = 194) revealed recurrent somatic mutations in BAP1 and ARID1A, neither of which has been previously reported to be mutated in CCA. Comparisons between intrahepatic OV and non-OV CCAs demonstrated statistically significant different mutation patterns: BAP1 and IDH1/2 were more frequently mutated in non-OV CCAs, while TP53 displayed the reciprocal pattern. Functional studies demonstrated tumor suppressive roles of BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations even within the same tumor type.

overall_design: Illumina 450k methylation array profiling performed on wild-type (n=23) and mutant (n=9) CCA (cholangiocarcinoma) samples, with adjacent normal tissue (n=4)

first: Waraporn

last: Chan-On

first: Bin

last: Teh


title: ERG induced mesenchymal like gene signature

status: Public on Oct 19 2013

first: Claudia

last: Baldus

state: Berlin

address: Hindenburgdamm 30

department: Hematology and Oncology

institute: Charite

summary: ERG overexpression was conducted in stably transfected K562 cell line with a tet-on inducible plasmid habouring ERG3. Prolonged induction of ERG (8 days) produced spindle cell shape changes whereas non-induced cells retained the round morphology. In oder to determine the genes responsible for inducing cell shape changes, a genome wide transcriptional screen was conducted.

overall_design: Three clones that potently induced ERG overexpression (8 days) with the corresponding non-induced cells were hybridized.

first: Liliana

last: Mochmann

first: Martin

last: Neumann

first: Verena

last: Nowak

first: Wolf

middle: K

last: Hofmann


title: Expression data from tumor-associated endothelial cells of hepatocellular carcinoma

city: shanghai

first: ling-qun

last: Kong

address: 180# Fenglin Road, Shanghai

institute: Zhongshan hospital affiliated to fudan university

summary:
Primary uncultured CD31+ and CD105+ tumor endothelial cells (TEC), non-tumor endothelial cells (NEC) ,remnant cells from tumor (TC) and non-tumor liver tissue (NTC)of HCC tissues from patientswere isolated by magnetic-activated cell sorting. Affymetrix Human Gene ST Arrays were used to determine gene expression profiles of HCC cells and matched TEC and NEC cells.
We use the gene expression profiling of the Human Genome U133 Plus 2.0 Arrays (Affymetrix, Santa Clara, CA) to identify distinct genes of TEC and NEC.

overall_design: Patient specimens were collected immediately after removal from patients with pathologically proven HCC and positive alpha-fetoprotein (AFP), then washed 3 times by phosphate buffer solution (PBS). Single cell suspension was obtained from separated tumor and non-tumor liver tissues of surgical specimens following the protocol (http://www.miltenyibiotec.com), then CD31+ cells or CD105+ cells were isolated using CD31 antibody or CD105 antibody conjugated magnetic beads in autoMACSpro (Meltenyi biotec).After the sample preparation, the gene expression profiling was performed using the Human Genome U133 Plus 2.0 Arrays (Affymetrix, Santa Clara, CA) according to manufacturer’s protocols at ShanghaiBio Corporation (Shanghai, China).

first: Hui-Chuan

last: Sun

first: Xin-Wei

last: Wang


title: Global profiling of human hair follicle scalp dermal papilla cells using Affymetrix microarrays

city: New York

first: Claire

last: Higgins

state: NY

address: 1150 St Nicholas Avenue, Russ Berrie 307

department: Department of Dermatology

institute: Columbia University

summary:
Dermal papilla cells isolated from the human hair follicle are capable of inducing hair growth in recipient epithelia.  However, demonstrating disparity from rodent dermal papilla, human cells lose this inductive competance immediately upon growth in culture under normal growth conditions.  We grew dermal papilla cells in hanging drop cultures that are morphologically akin to intact dermal papilla, and found that by enhancing the environment for aggregation, we could restore the inductive capacity of human dermal papilla cells in culture.  The underlying genes that regulate the inductive potential of dermal papilla cells is not well understood, and we sought to use global profiling to identify key genes and pathways related to inductive competance within dermal papilla cells.
We used Affymetrix microarrays to profile human dermal papilla cells in both hair inducing, and non-hair inducing states.

overall_design: Affymetrix microarrays were used to to perform profiling of human dermal papilla cells, both as intact tissues (freshly isolated from scalp), and at several stages in subsequent two dimensional culture; cell explant outgrowths (p0), cells at passage 1 (p1), passage 3 (p3) and passage 5 (p5).  RNA was isolated from cultured cells 72 hours after feeding.  Cells at passage 3 were also grown in hanging drops to form dermal spheroids, that were used for RNA collection 48 hours after establishment.  All experiments were performed using tissue from three biological replicates (#D5, D6, D7),

first: Angela

last: Christiano


title: Effects of Blnk reconstitution in BCR-ABL1 driven pre-B cells

first: Markus

last: Müschen

address: 4650 Sunset Blvd

department: Childrens Hospital Los Angeles

institute: University of Southern California

summary: In order to investigate the function of the adapterprotein Blnk in ALL, we isolated bone marrow cells from Blnk KO mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with Blnk-GFP or empty vector control (GFP) and subjected to gene expression analysis.

overall_design: Five days post transduction, total RNA of GFP positive sorted cells were extracted and subjected to gene expression analysis.

first: Rahul

last: Nahar


title: Blockade of thymic stromal lymphopoietin receptor (TSLPR) reduces allergic inflammation in a cynomolgus monkey model of asthma

status: Public on Oct 22 2013

city: Nutley

first: Donavan

last: Cheng

state: NJ

address: 340 Kingsland Ave

department: Translational Research Sciences

institute: Hoffmann-LaRoche

summary: TSLP pathway blockade is a potential strategy for asthma treatment, as TSLP modulates cytokine production by mast cells and regulates the activation of dendritic cells (DCs), which prime the differentiation of naïve T cells into inflammatory Th2 cells. To assess the effect of TSLPR blockade on the development of allergic inflammation and bronchoconstriction in Cynomolgus monkeys after Ascaris suum allergen challenge. Antibodies against human TSLPR were generated and confirmed to be cross-reactive to cynomolgus. Animals were dosed weekly with either vehicle (n=8) or TSLPR HuMAb (n=8) for 6 weeks and their responses to A.Suum challenge at baseline, week 2 and week 6 were assessed. Antibody-treated animals showed reduced bronchoalveolar lavage (BAL) eosinophil counts (p=0.04), reduced lung resistance (RL) area under the curve (p=0.04), and reduced IL-13 cytokine levels in BAL fluid (p=0.03) in response to challenge at 6 weeks compared to vehicle-treated animals.  To understand the molecular changes underlying these differences, BAL fluid samples pre- and post-challenge were profiled using microarrays. Genes up-regulated by allergen challenge overlapped strongly with 11 genes up-regulated in DCs when stimulated by TSLP (TSLP-DC signature). The number of genes differentially expressed in response to challenge was reduced in aTSLPR-treated animals after 6 weeks relative to vehicle-treated animals.  Expression of the TSLP-DC gene signature was also significantly reduced in aTSLPR-treated animals (p = 0.05). These results demonstrate promising efficacy for TSLPR blockade in an allergen challenge model where TSLP activation of DCs may play a key role.

overall_design: Animals were dosed weekly with either vehicle (n=8) or TSLPR HuMAb (n=8) for 6 weeks and their responses to A.Suum challenge at baseline, week 2 and week 6 were assessed. One monkey in the aTSLPR-treated group expired during the study for reasons not linked to drug safety and tolerability. BAL fluid samples for all animals were subject to gene expression profiling for pre-challenge, 8h and 24h post-challenge timepoints, at baseline, week 2 and week 6. This amounted to a total of 135 microarrays. Data from 8 animals were excluded as outliers, determined by PCA.

first: Cynthia

last: Ma

first: Jens

last: Niewoehner

last: Dahl

last: Tsai

first: Mark

last: Zhang

first: Waldemar

last: Gonsiorek

first: Subbu

last: Apparsundaram

first: Achal

last: Pashine

first: Palanikumar

last: Ravindran

first: Jimmy

last: Jung

first: John

last: Allard

first: Hans

last: Bitter

first: Catherine

last: Tribouley

first: Satwant

last: Narula

first: Stephen

last: Wilson

first: Maria

middle: E

last: Fuentes


title: Investigation of radiosensitivity gene signatures in cancer cell lines

status: Public on Oct 18 2013

city: Manchester

last: Hall

state: Greater Manchester

address: WMIC, 27 Palatine Road

department: Faculty Institute of Cancer Sciences

institute: The University of Manchester

summary:
Commercially available cell lines derived from Head and Neck Squamous cell carcinoma (HNSCC) were cultured and baseline gene expression values were assayed.
We used microarrays to detail the global programme of gene expression underlying differences in radiosensitivity as measured by surviving fraction at 2Gy (SF2)

overall_design: HNSCC Cell lines (n=11) were cultured in standard conditions. RNA was extracted at subconfluence.

middle: J

last: O'Connor


title: Sensitivity to proteasome inhibition and in vivo growth properties of MCL cells

city: Badalona

first: Gael

last: Roue

address: Ctra de Can Ruti, Camí de les Escoles s/n

department: Lymphoma Translational lab

country: Spain

institute: Josep Carreras Leukaemia Research Institute

summary:
MCL cells resistant to bortezomib show distinct tumor growth in vivo when compared to their bortezomib-sensitive counterpart
We used microarrays to detail the factors underlying the increased tumorigenicity of bortezomib-resistant cells in vivo

overall_design: Global RNA expression in tumors harvested from SCID mice and derived from either bortezomib-sensitive or bortezomib-resistant MCL cell lines

first: Alexandra

last: Moros