title: Genome-wide analysis of the therapeutic effect of NeuroD on irradiation-induced intestinal injury

status: Public on Sep 16 2015

city: Suzhou

first: Ming

address: No. 199 Ren'ai Road

institute: Soochow University

summary: The objective was to investigate the therapeutic effect of NeuroD on irradiation-induced intestinal injury at gene expression level. Gene expression profilings between NeuroD and EGFP treated mice which were received 9 Gy total body irradiation were compared.

overall_design: All mice were given 9 Gy radiation and divided into two groups (3 mice per group). After radiation, mice were immediately administered with an intraperitoneal injection of 0.1 mM EGFP or NeuroD-EGFP. EGFP treated mice were served as controls. 12 hours post radiation, mice jejunum tissues were isolated. Total RNA obtained from jejunum tissues and subjected to gene expression profiling assays.

first: Shuyu

last: Zhang


title: Asthma Bronchial Biopsy Gene Expression

status: Public on Sep 08 2015

city: South San Francisco

first: David

middle: Fong

last: Choy

state: CA

address: 1 DNA Way

country: USA

institute: Genentech, Inc.

summary: Transcriptional profiling of lung bronchial biospsy mRNA from asthmatics

overall_design: Two-condition experiment, mRNA from asthma bronchial biopsies for test channel and Stratagene Universal Human Reference RNA for reference channel.

first: D

middle: F


title: Genome wide expression analysis of BET inhibitor resistance

status: Public on Sep 15 2015

city: Melbourne

first: Mark

last: Dawson

state: VIC

address: 305 Grattan Street

country: Australia

institute: Peter MacCallum Cancer Centre

summary: Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. Using primary murine stem and progenitor cells immortalised with MLL-AF9, we have used an innovative approach to generate 20 cell lines derived from single cell clones demonstrating stable resistance, in vitro and in vivo, to the prototypical BET inhibitor, I-BET. Resistance to I-BET confers cross-resistance to chemically distinct BET inhibitors such as JQ1, as well as resistance to genetic knockdown of BET proteins. Resistance is not mediated through increased drug efflux or metabolism but is demonstrated to emerge from leukaemia stem cells (LSC). Resistant clones display a leukaemic granulocyte-macrophage progenitor (L-GMP) phenotype (Lin-, Sca-, cKit+, CD34+, FcγRII/RIII+) and functionally exhibit increased clonogenic capacity in vitro and markedly shorter leukaemia latency in vivo. Chromatin bound BRD4 is globally reduced in resistant cells, however expression of key target genes such as MYC remains unaltered, highlighting the existence of alternative mechanisms to regulate transcription. We demonstrate that resistance to BET inhibitors is in part a consequence of increased Wnt/β-catenin signaling. Negative regulation of this pathway results in differentiation of resistant cells into mature leukaemic blasts, inhibition of MYC expression and restoration of sensitivity to I-BET in vitro and in vivo. Finally, we show that the sensitivity of primary human AML cells to I-BET correlates with the baseline expression of Wnt/β-catenin target genes. Together these findings provide novel insights into the biology of AML, highlight the potential therapeutic limitations of BET inhibitors and identify strategies that may overcome resistance and enhance the clinical utility of these unique targeted therapies.

overall_design: Total RNA obtained from iBET resistant and sensitive cells

first: Chun

last: Fong


title: On the relevance of technical variation due to building pools in microarray experiments [Mouse]

status: Public on Sep 10 2015

city: Bochum

first: Henrik

last: Rudolf

address: Universitätsstr. 150

department: Medical computer science, Biometry and Epidemiology

country: Germany

institute: Ruhr-Universität Bochum

summary:
The objective of the study was to assess the technical error due to blending of individual samples into pools in experimental data.
The blending error variance component corresponds to random effects for inaccuracies, which were modeled on the logarithmic scale of normalized gene expression. It's estimation based on a linear mixed model, fitted for each transcript.

overall_design: Ovaries from 30 animals of line FL1 and of the control line DUKsi were collected at the metestrous stage. They were combined to 6 pools of 5 individuals each and processed for microarray analysis. Additionally, the 10 individuals used for the first two pools of each line were processed.

first: J

last: Vanselow

first: H


title: Paracrine stimulation  effect of human salispheres on mouse salivary  gland

city: Groningen

first: Sarah

last: Pringle

state: Groningen

address: Antonius Deusinglaan 1

department: Cell Biology

country: Netherlands

institute: University Medical Centrum Groningen

summary: Human salispheres, a culture of stem/progenitor cells, represent a potential therapy for radiation induced hyposalivation. Radiation-induced hyposalivation dramatically reduces quality of life of patients. We have demonstrated the potential of human salispheres to engraft and differentiate when transplanted into a mouse model of hyposalivation, in the manuscript associated with these data. We also demonstrate the functional recovery of irradiated salivary glands  (SGs) following human salisphere transplantation, by the measurement of saliva production.  When analyzing human salisphere- transplanted SGs for the presence of human cells,  we noted that the highest proportion of human cells were present 1 week after transplantation. This microarray study was designed to determine if paracrine signaling from transplanted human salisphere cells to recipient mouse SGs accounts for a part of the functional recovery of the recipient SG we observe. We compare the transcriptome from irradiated control SG of immunecompromised  NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG)  mice with that of NSG SGs transplanted with 100,000 human salisphere cells. All mice were sacrificed 1 week following transplantation (or non-transplantation in case of controls) and Illumina array chips used to detect differences in gene expression.

sample_organism:
Homo sapiens
Mus musculus

overall_design: 6 samples were analysed in total. Total RNA from 3 irradiated control SGs (5Gy irradiation) and 3 salivary glands transplanted with 100,000 human salispheres.

first: S

middle: A

first: E

last: Zwart


title: Effect of decitabine, carboplatin and their combination on gene expression in the YB5 colon cancer cell line.

city: Camden

first: Jaroslav

last: Jelinek

state: NJ

address: 403 Haddon Avenue

department: Research Labs

institute: Coriell Institute for Medical Research

summary:
YB5 cell line is a clonal derivative of the SW48 colon cancer cell line that contains a single copy of a green fluorescent protein (GFP) reporter silenced by CpG methylation at its CMV promoter.
We treated the YB5 cells with decitabine (5-aza-2’-deoxycytidine), carboplatin and the combination of decitabine plus carboplatin and analyzed the effects of the drugs on gene expression.

overall_design: YB5 cells in the early log phase of growth were seeded at 3.5 million in 20 ml of culture medium in 10 cm diameter tissue culture plates at day 0.  The cells were treated with 20 microliters of decitabine (final concentration 25 nM), carboplatin (final concentration 20 uM) or both at days 1, 2, 3 and 4. Control cells were treated with 20 microliters of diluent (DMSO). The cells were harvested at day 6. Total RNA was extracted by TRIZOL, labeled with Cy5 (control cells) or Cy3 (treated cells) and hybridized on Agilent Whole Genome Array (G4112F). Raw data from the Agilent scanner were loess normalized using Bioconductor packages limma and agilp.

first: Jiali

last: Si

first: Jean-Pierre

middle: J

last: Issa


title: Paracrine stimulation effect of autologous salispheres and human salispheres on mouse salivary gland

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

overall_design: Refer to individual Series


title: Analysis of the IRE1/XBP1 unfolded protein response (UPR) pathway in Schmid metaphyseal chondrodysplasia hypertrophic chondrocyte endoplasmic reticulum (ER) stress

status: Public on Aug 21 2015

city: Parkville

first: Trevor

middle: L

last: Cameron

address: Royal Children's Hospital, Flemington Road

institute: Murdoch Childrens Research Institute

summary: We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1CartΔEx2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between  Xbp1CartΔEx2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1CartΔEx2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1CartΔEx2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR.

overall_design: Entire growth plate hypertrophic zones were microdissected from one tibia from each of three 2-week old wildtype mice, three 2-week old mice carrying a COL10A1 p.N617K mutation (ColXN617K), three 2-week old mice lacking XBP1 activity in chondrocytes (Xbp1CartΔEx2), and three 2-week old mice resulting from a cross between ColXN617K and Xbp1CartΔEx2 (C/X).

first: Katrina

middle: M

last: Bell

first: Irma

last: Gresshoff

first: Lisa

last: Sampurno

first: Lorna

last: Mullen

first: Joerg

last: Ermann

first: Laurie

middle: H

last: Glimcher

first: Raymond

middle: P

last: Boot-Handford

first: John

last: Bateman


title: Gene expression in human lung cancer cell lines regulated by Bmi-1 gene

status: Public on Aug 15 2015

city: Shanghai

first: Dan

last: Xiong

address: 227 South Chongqing Road

country: China

institute: Shanghai Jiaotong University School of Medicine

summary: This study aimed to understand the role that B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) plays in non-small cell lung cancer (NSCLC) progression. According to fold-change screening between Bmi-1-silencing A549 and the control cells A549, both up-regulated and down-regulated genes were shown.

overall_design: Bmi-1 knockdown in A549 cells were noted as A549-shRNA-Bmi-1 and the respective control cells were named as A549-shRNA-control.

first: Jianhua

last: Wang


title: ERRγ links adaptive neuronal metabolism to spatial learning and memory [Array data]

status: Public on Sep 03 2015

city: La Jolla

first: Ruth

middle: T

last: Yu

address: 10010 N Torrey Pines Rd

department: Gene Expression Lab

institute: Salk Institute

summary: Neurons utilize glucose to generate adenosine triphosphate (ATP) essential for their survival, excitability and synaptic signaling, as well as initiating changes in neuronal structure and function. Defects in oxidative metabolism and mitochondria functions are also associated with aging and diverse human neurological diseases1-4. While neurons are known to adapt their metabolism to meet the increased energy demands of complex behaviors such as learning and memory, the molecular underpinnings regulating this process remain poorly understood4-6. Here we show that the orphan nuclear receptor estrogen related receptor gamma (ERRγ) becomes highly expressed during retinoic-acid induced neurogenesis and is widely expressed in neuronal nuclei throughout the brain. Mechanistically, we show that ERRγ directly orchestrates the expression of networks of genes involved in mitochondrial oxidative phosphorylation and energy generation in neurons. The importance of this regulation is evidenced by decreased adaptive metabolic capacity in cultured neurons lacking ERRγ, and reduced long-term potentiation (LTP) in ERRγ-/- hippocampal slices. Notably, the defect in LTP was rescued by the metabolic intermediate pyruvate, functionally linking the ERRγ knockout metabolic phenotype and memory formation. Consistent with this notion, mice lacking neuronal ERRγ exhibit defects in spatial learning and memory. These findings implicate ERRγ in the metabolic adaptations required for long-term memory formation.

overall_design: We used microarray analysis to compare the genome-wide gene expression changes between wild type (WT) and ERRγ-/- P0 cerebral cortex as it contains mainly neuronal lineage at this stage compared to adult cortex.

first: Liming

last: Pei

first: Ronald

last: Evans


title: Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

status: Public on Sep 05 2015

city: Houston

first: David

middle: Brian

last: Corry

address: One Baylor Plaza

department: Medicine

institute: Baylor College of Medicine

summary:
Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation.  Results provide insight into the biological role and target genes of miR-22.
Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure.  Here we have explored the role of microRNA-22 (miR-22) in emphysema.  MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB.  MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB.  We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4.  Thus, miR-22 is a critical regulator of both emphysema and TH17 responses.

overall_design: Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups.  There were three replicates in each group.

first: Wen

last: Lu

middle: B


title: On the relevance of technical variation due to building pools in microarray experiments

status: Public on Sep 11 2015

first: Henrik

last: Rudolf

sample_organism:
Apis mellifera
Mus musculus

platform_organism:
Apis mellifera
Mus musculus


title: IGF-1 degradation by mast cell chymase promotes delayed cell death in post-ischemic hearts

status: Public on Sep 01 2015

city: Atlanta

first: Gregory

last: Doho

state: GA

address: 1365B Clifton Rd NE

institute: Emory University

summary: Coronary heart disease is the leading cause of death worldwide. After an acute myocardial infarction, early reperfusion reduces infarct size, which correlates with improved clinical outcomes. Paradoxically, reperfusion although relieving ischemia, accelerates apoptosis in injured cardiomyocytes, which has led to the view that myocardial salvage is futile beyond the first few hours of reperfusion. In murine hearts subjected to 90 min of coronary artery occlusion and then 48 h of reperfusion, we show transient activation of intrinsic prosurvival insulin-like growth factor-1 (IGF-1) signaling. In these hearts, acute IGF-1 receptor inhibition decreases the abundance of prosurvival signaling molecules, and markedly activates caspase-3, a potent effector of apoptosis, in infarct border zone cardiomyocytes. We found that mouse mast cell protease-4 (MMCP-4) degraded IGF-1 in vitro by a novel catalytic activity of chymases. In vivo, this degradation, which is triggered by mast cell infiltration into the peri-infarct region and MMCP-4 extravasation, between 48 and 72 h post-ischemia/reperfusion (I/R), attenuates IGF-1 prosurvival signaling. In MMCP-4-deficient mice, while infarct size is not reduced at 24 h post-I/R, at 72 h post-I/R myocardial IGF-1 levels and signaling are increased, resulting in activation of the survival kinases Akt and ERK, inhibition of caspase-3, and reduced myocardial cell death. As a consequence, I/R-mediated loss of viable myocardium, adverse cardiac remodeling and contractile impairment are markedly reduced. Cardiomyocyte survival with consequent myocardial salvage may thus be possible even days after an ischemic insult, making them a novel therapeutic target for delayed cardioprotective therapy.

overall_design: Group 1 is wild type C57Bl6 uninjured hearts. These mice were not undergone any surgery and used as controls.  Group 2 are wild type C57Bl6 72 h post-ischemia reperfusion (IR) injury hearts. These mice for subjected to ischemia reperfusion (IR) involving 90 min of left anterior descending coronary artery occlusion followed by reperfusion for 3 days or 72 h.

first: Ahsan

last: Husain

first: Nawazish

last: Naqvi

first: Thor

last: Tejada

first: Lin

last: Tan


title: Aberrant haematopoiesis in Dnmt2 mutant mice [array]

status: Public on Aug 13 2015

city: Mannheim

first: Francesca

last: Tuorto

address: Ludolf-Krehl-Str. 13-17

department: Division of Biochemistry  Mannheim Institute for Innate Immunoscience (MI3)

institute: Deutsches Krebsforschungszentrum

summary: Bone marrow samples from Dnmt2-/- and wildtype mice were used to identify potential mRNA substrates of Dnmt2

overall_design: Total RNA was extracted from bone marrow of 8 day-old Dnmt2 and wildtype femora mice.The RNAs  were arrayed on Illumina MouseWG-6 v2.0 expression beadchip chips.


title: Pituitary tumors contain a (CD31¯/CD45¯ purified) side population with 'tumor stem cell'-associated characteristics [set 2]

status: Public on Aug 04 2015

city: Leuven

first: Rekin's

last: Janky

address: Herestraat 49 Box 816

department: Nucleomics Core

country: Belgium

institute: VIB

summary: Pituitary adenomas cause significant endocrine and mass-related morbidity. Not much is known about mechanisms underlying pituitary tumor pathogenesis. We searched for a side population (SP) in pituitary tumor, representing cells with high efflux capacity and potentially enriching for cancer/tumor stem cells (CSC/TSC). Human pituitary adenomas contain a SP irrespective of hormonal phenotype. This adenoma SP, as well as the further purified SP (pSP) depleted from endothelial and immune cells, enriches for cells that express ‘tumor stemness’ markers and signaling pathways, including epithelial-mesenchymal transition (EMT)-linked factors. The adenomas were found to contain self-renewing sphere-forming cells, considered a property of TSC. The sphere-initiating cells were retrieved in the pSP. Because benign pituitary adenomas do not grow in vitro and failed to expand in immunodeficient mice, the pituitary tumor cell line AtT20 was further used. We identified a SP in this cell line and found it more tumorigenic than the main population (MP). Of the two EMT-regulatory pathways tested, inhibition of Cxcr4 signaling reduced EMT-linked cell motility in vitro as well as xenograft tumor growth, whereas activation of TGFβ had no effect. The tumor pSP showed upregulated expression of the pituitary stem cell marker SOX2. Pituitaries from dopamine receptor D2 knockout (Drd2-/-) mice bearing prolactinomas, contain more pSP, Sox2+ and colony-forming cells than wildtype glands. In conclusion, we detected a SP in pituitary tumors and identified TSC-associated characteristics. Our study may contribute to a better understanding of pituitary tumor pathogenesis and lead to new therapeutic targets.

overall_design: We determined gene expression profiles for 5 human pituitary adenoma samples (all NF-A type). The samples were obtained immediately after transsphenoidal resection (by the neurosurgeon Dr. van Loon, Division Neurosurgery, University Hospitals Leuven). Informed consent was received from the patients. Hormonal phenotype was determined by the Department of Imaging and Pathology (University Hospitals Leuven). For each sample, CD31¯/CD45¯ SP (purified SP or pSP) and pMP cells were sorted by FACS. Separate assays were run subsequently for the two fractions. As such we present data from 10 microarrays.

first: Freya

last: Mertens

first: Lies

last: Gremeaux

first: Jianghai

last: Chen

first: Qiuli

last: Fu

first: Christophe

last: Willems

first: Heleen

last: Roose

first: Olivier

last: Govaere

first: Tania

last: Roskams

first: Carolina

last: Cristina

first: Damasia

last: Becú-Villalobos

first: Marie

last: Bex

first: Johannes

last: van Loon

first: Hugo

last: Vankelecom


title: Genome-wide analysis of E2F1 dependent gene expression in mouse testicular tissue

city: Turku

first: Emmi

last: Rotgers

address: Kiinamyllynkatu 10

country: Finland

institute: University of Turku

summary: The effect of E2F1 loss on gene expression in testicular tissue was analyzed in 20-day old E2F1-/-, E2F1+/- mice. The hypothesis ws that there would be clear changes in expression of genes related to cell cycle machinery. The results show that E2F1 has wider implications in gene expression dynamics in testicular cell types than merely controlling cell cycle related genes.

overall_design: Total RNA obtained from testis tissue of 20-day-old E2F1-/- (KO), E2F1+/- (HZ) and E2F1+/+ mice (WT).

first: Rotgers

last: Emmi

first: Toppari

last: Jorma


title: Genes altered by miR-634 in three cancer cell lines

status: Public on Aug 06 2015

city: Tokyo

first: Jun

last: Inoue

address: Yushima 1-5-45, Bunkyo-ku

department: Molecular Cytogenetics

country: Japan

institute: Tokyo Medical & dental univ.

summary: To identify genes affected by miR-634 overexpression, we transfected with 20nmol of miR-634 or miR-negative control (NC) in HeLa, KYSE850, or U2OS cells. After 2 days, RNA was extracted, and then expression analysis was performed using agilent microarray.

overall_design: Expression microarray with miR-634 or miR-NC transfected HeLa, KYSE850, or U2OS cells were performed in duplicate.

first: Naoto

last: Fujiwara

first: Johji

last: Inazawa


title: Pituitary tumors contain a side population with 'tumor stem cell'-associated characteristics [set 1]

first: Rekin's

last: Janky

summary: Pituitary adenomas cause significant endocrine and mass-related morbidity. Not much is known about mechanisms underlying pituitary tumor pathogenesis.We searched for a side population (SP) in pituitary tumor, representing cells with high efflux capacity and potentially enriching for cancer/tumor stem cells (CSC/TSC). Human pituitary adenomas contain a SP irrespective of hormonal phenotype. This adenoma SP, as well as the further purified SP (pSP) depleted from endothelial and immune cells, enriches for cells that express ‘tumor stemness’ markers and signaling pathways, including epithelial-mesenchymal transition (EMT)-linked factors. The adenomas were found to contain self-renewing sphere-forming cells, considered a property of TSC. The sphere-initiating cells were retrieved in the pSP.Because benign pituitary adenomas do not grow in vitro and failed to expand in immunodeficient mice, the pituitary tumor cell line AtT20 was further used. We identified a SP in this cell line and found it more tumorigenic than the main population (MP). Of the two EMT-regulatory pathways tested, inhibition of Cxcr4 signaling reduced EMT-linked cell motility in vitro as well as xenograft tumor growth, whereas activation of TGFβ had no effect.The tumor pSP showed upregulated expression of the pituitary stem cell marker SOX2. Pituitaries from dopamine receptor D2 knockout (Drd2-/-) mice bearing prolactinomas, contain more pSP, Sox2+ and colony-forming cells than wildtype glands.In conclusion, we detected a SP in pituitary tumors and identified TSC-associated characteristics. Our study may contribute to a better understanding of pituitary tumor pathogenesis and lead to new therapeutic targets.

overall_design: We determined gene expression profiles for 9 human pituitary adenoma samples (5 x NF-A; 4 x GH-A). The samples were obtained immediately after transsphenoidal resection (by the neurosurgeon Dr. van Loon, Division Neurosurgery, University Hospitals Leuven). Informed consent was received from the patients. Hormonal phenotype was determined by the Department of Imaging and Pathology (University Hospitals Leuven). For each sample, total SP and MP cells were sorted by FACS. Separate assays were run subsequently for the two fractions. As such we present data from 18 microarrays.

first: Freya

last: Mertens

first: Lies

last: Gremeaux

first: Jianghai

last: Chen

last: Becu-Villalobos


title: Pituitary tumors contain a side population with 'tumor stem cell'-associated characteristics.


title: Genome-wide analysis of gene expression in normal and fibrotic mouse kidneys with and without Twist1 or with and without Snai1(Snail) expression in proximal tubular epithelial cells

status: Public on Aug 03 2015

first: Valerie

last: LeBleu

state: TX

address: 1881 East Road

institute: MDACC

summary: In this study mice were engineered to specifically delete Twist1 or Snail expression in proximal tubular epithelial cells of the kidney (ggt-cre+;Twist flox/flox and ggt-cre+;Snail flox/flox ). These mice and control mice (ggtcre-;Twist flox/flox: these express Twist1, and ggtcre-;Snail flox/flox:these express Snail) were subjected to unilaterial ureteric obstruction. This experiment allows for the collection and analysis of expression in contralateral healthy (HK) kidney adn obstructed disease (DK) kidney.

overall_design: Total RNA was isolated from the contralateral healthy (HK) and obstructed disease (DK) kidneys of 3 mice with ggt-cre-;Twist flox/flox genotype (Wildtype like) and 4 mice with ggt-cre+;Twist flox/flox genotype (loss of Twist1 in proximal tubular epithelial cells), 3 mice with ggt-cre-;Snail flox/flox genotype (Wildtype like) and 3 mice with ggt-cre+;Snail flox/flox genotype (loss of Snail in proximal tubular epithelial cells). Total RNA was also isolated from kidneys of completely healthy mice: 3 mice ggt-cre-;WT, 3 mice ggt-cre+;WT, 3 mice ggt-cre+;Twist flox/flox and 3 ggt-cre+;Snail flox/flox

first: Sara

last: Lovisa


title: Different Effects of Tofu (Soybean Curd) and Fish Oil in Serum Lipoproteins and Hepatic Gene Expressions of Rats

city: Akita

first: Tomokazu

last: Konishi

state: Akita

address: Shimoshinjyo Nishi

department: Bioresource Sciences

institute: Akita Prefectural University

summary: Soybean and fish contains various active components that were reported to prevent cardiovasucular diseases. Epidemiological studies indicated that Asian eating patterns, consisting of daily seafood and/or soy consumption, confer protection against cardiovascular diseases. In this context, we expected that simultaneous intake of soybean and fish may be greatly beneficial in a manner different from the ingestion of the individual food. To understand the detailed mechanism for modulating the lipid metabolism by co-ingestion of a soy food (tofu) and fish oil, we investigated the global changes in hepatic mRNA expression in rats by using a microarray analysis. Generally, ingestion of tofu contributed to prevent the mRNA expressions involved in hepatic lipogenesis, whereas fish oil facilitated the mRNA expressions related to the degradation of hepatic fatty acids. In terms of mRNA expression, the interaction of two dietary factors was limited. The expression data was normalized and summarized by using SuperNORM data service (Skylight Biotech Inc.). Significance of expressional change among groups was tested by 2-way ANOVA on the normalized CEL data, which was deposited in a tab-separated ASCII text format. Principal components were identified on the summarized gene data.

overall_design: Rats were divided into four groups each with similar average body weights and assigned experimental diets for 21 days as follows: casein and soybean oil diet (CS); casein and fish oil diet (CF); tofu and soybean oil diet (TS); tofu and fish oil diet (TF). Total protein and fat content of each diet was 200 and 150 g/kg, respectively. Soybean oil diets (CS and TS) contain 150 g/kg diet of soybean-derived fat (i.e. soybean oil and freeze-dried tofu), and 50 g/kg of fish oil was replaced with the same amount of soybean-derived fat for fish oil diets (CF and TF). Animals were allowed free access to food and water.

first: Yoko

last: Takahashi


title: Gene Expression Profile of high grade glioma in Ascl1creERTM driven tumor suppressors knockout mouse model

status: Public on Jul 30 2015

city: New York

first: Daochun

last: Sun

state: New York

department: Cancer Biology and Genetics

institute: Memorial Sloan Kettering Cancer Center

summary: Mouse model with P53f/f;Nf1f/f or P53f/f; Nf1f/- driven by Ascl1creERTM induced at 1 month postnatally forms high grade glioma in the brain. Tumors were harvested and total RNA were extracted for gene expression profile.

overall_design: Ten tumors were harvested from the Ascl1creERTM mouse model with desired genotype when showing neurological symptomes. Eight control brain tissue were harvested at corresponding anatomaical regions in the control mice. Total RNA were extracted from the tumor tissue and control tissue

first: Alcantara

last: Sheila

first: Sun

last: Daochun

first: Parada

last: Luis


title: Expression data from isogenic Pten WT mouse T-ALLs infected with MSCV Myr-AKT-IRES-mCherry or empty vector, treated with DBZ or DMSO

status: Public on Aug 31 2015

first: Alberto

last: Ambesi-Impiombato

state: NY

address: 1130 St. Nicholas Avenue

department: ICG

institute: Columbia University

summary:
To explore the mechanisms downstream of NOTCH1 and PTEN in the control of leukemia cell growth, we performed expression profiling on NOTCH1 induced and Pten-positive T-ALL tumor cells infected with constitutively active AKT (myristoylated-AKT).
Constitutive activation of AKT rescues the transcriptional programs induced by NOTCH1 inhibition in Pten-positive T-ALL cells

overall_design: We performed microarray gene expression analysis of GSI treatment in Pten WT NOTCH1 induced leukemias infected with constitutively active AKT (myristoylated-AKT) or empty vector.

first: Daniel

last: Herranz

first: Jessica

last: Sudderth

first: Marta

last: Sánchez-Martín

first: Laura

last: Belver

first: Valeria

last: Tosello

first: Luyao

last: Xu

first: Agnieszka

last: Wendorff

first: Mireia

last: Castillo

first: J

middle: E

last: Haydu

first: Javier

last: Márquez

first: José

last: Matés

first: Andrew

last: Kung

first: Stephen

last: Rayport

first: Carlos

last: Cordon-Cardo

first: Ralph

last: DeBerardinis

first: Adolfo

last: Ferrando


title: The immunomodulatory effects of soluble receptor of activated nuclear factor kappa ligand (sRANKL) on monocyte-derived macrophages

status: Public on Aug 24 2015

city: Sendai

first: Masayuki

last: Asano

state: Miyagi

address: Seiryo-machi 1-1, Aoba-ku

department: Department of Dermatology

institute: Tohoku University Graduate School of Medicine

summary: To explore the effects of sRANKL on tumor-associated macrophages, we first sorted CD14+ monocytes from peripheral blood mononuclear cells of healthy donors using magnetic-activated cell sorting and then induced their differentiation into macrophages by culture with M-CSF for 5 days. We then stimulated these macrophages with IL-4 (20 ng/ml) together with or without 100 ng/ml of sRANKL for 6 hours and examined gene expression using a cDNA microarray.

overall_design: sRANKL stimulated gene expression on monocyte-derived macrophages was measured at 6 hours after exposure to doses of 100 ng/ml sRANKL.

first: Taku

last: Fujimura

first: Yumi

last: Kambayashi

first: Sadanori

last: Furudate

first: Aya

last: Kakizaki

first: Takanori

last: Hidaka

first: Setsuya

last: Aiba


title: SPINK1 promotes Colorectal Cancer progression by down regulating Metallothioneins expression

status: Public on Jul 21 2015

city: Ann Arbor

first: Chinnaiyan

last: Arul

state: Michigan

address: 5309 Comprehensive Cancer Center, 1400 E. Medical Center Drive

department: Michigan Center for Translational Pathology

institute: University of Michigan

summary: Expression profiling was performed using Agilent Whole Human Genome Oligo Microarray (Santa Clara, CA) according to the manufacturer’s protocol. A total of 3 microarray hybridizations were performed using each stable shSPINK1 cell line samples against control shSCRM cells.

overall_design: SPINK1 gene was knocked down using shRNA in WIDR cells in the experimental group and shScramble cells were used as control.

first: Ritika

last: Tiwari

first: Vipul

last: Bhatia

first: Xiaojun

last: Jing

first: Swaroop

middle: K

last: Pandey

first: Sakshi

last: Goel

first: Sudhanshu

last: Shukla

first: Saravana

last: Dhanasekaran

first: Bushra

last: Ateeq


title: An Artificial Interfering lncRNA Mediated by Oncolytic Adenovirus Competitively Consumes OncomiRs to Exert Antitumor Efficacy in Hepatocellular Carcinoma

first: Changqing

last: Su

address: 225 Changhai Rd.

department: Department of Molecular Oncology

institute: National Center of Liver Cancer

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

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

overall_design: Refer to individual Series


title: Differential miRNA expression profiles betweenHBV-related  HCC tumor versus non-tumor liver tissue

status: Public on Jul 22 2015

city: ChaiYi county

first: Chung-Lin

last: Hung

address: No.2, Minsheng Rd., Dalin Township,

department: Division of Oncology and Hematology, Department of Internal Medicine,

country: Taiwan

institute: Buddhist Dalin Tzu Chi General Hospital

summary: miRNA played an important role in the process of carcinogenesis in HBV related hepatocellular carcinoma. Therefore, we performed miRNA microarray to evaluate the miRNAs that expressed differentially between HCC tumor versus non-tumor liver tissues.

overall_design: RNA was extracted from snap fresh tissue collected from resected HCC tumor and adjacent non-tumor liver tissues. All HCC tumors were HBV-associated HCC.

first: Chia-Jui

last: Yen


title: Genome-wide expression analysis of mouse plasma cell tumors show importance of IL-6 in tumor development

status: Public on Jul 27 2015

city: Iowa City

first: Ramakrishna

last: Sompallae

state: IA

address: 285 Newton Road, 5292 CBRB

department: Iowa Institute of Human Genetics

institute: University of Iowa

summary:
Interleukin 6 (IL-6) is a pro-inflammatory cytokine important for plasmacytomagenesis. Here we showed that the strom cell-derived IL-6 is critical for plasma cell tumors (PCTs).
The gene expression analysis of mouse PCTs showed that adoptive-transfer PCT and spontaneous PCT have similar patterns. Further, the mouse tumors also illustrated resemblance to human multiple myeloma (MM).

overall_design: Twenty-five tumor samples were analyzed, with three normal B cell controls. 14 of the samples are from adoptive transfer of premalignant B cells, while 11 are from spontaneously arising tumors.

first: Timothy

middle: R

last: Rosean

first: Van

middle: S

last: Tompkins

first: Alicia

last: Olivier

first: Lyse

last: Norian

first: Herbert

middle: C

last: Morse III

first: Thomas

last: Waldschmidt

first: Siegfried

last: Janz


title: Genome-wide analysis of gene expression in the cervical spinal cord of a mouse model of atopic dermatitis

status: Public on Jul 17 2015

city: Fukuoka

first: Miho

last: Shiratori-Hayashi

address: 3-1-1 Maidashi, Higashi-ku

department: Department of Life Innovation

institute: Graduate School of Pharmaceutical Science, Kyushu University

summary: Genome-wide analysis of gene expression in the cervical spinal cord of atopic dermatitis model mice was performed. Results provide important information for understanding of molecular mechanisms of the symptoms of atopic dermatitis.

overall_design: Total RNA was odtained from the cervical spinal cord of normal or atopic dermatitis model mice.

first: Makoto

last: Tsuda


title: The immunomodulatory effects of periostin on monocyte-derived macrophages

status: Public on Jul 14 2015

first: Masayuki

last: Asano

summary: To explore the effects of periostin on tumor-associated macrophagess, we first sorted CD14+ monocytes from peripheral blood mononuclear cells of healthy donors using magnetic-activated cell sorting and then induced their differentiation into macrophages by culture with M-CSF for 5 days. In the absence of IL-4 stimulation, these macrophages expressed CD163 and Arg1 (a marker of M2 macrophage activation) but not CD206, suggesting that they were similar to macrophages in the early stage of mycosis fungoides (low frequency of CD206+ cells and low IL-4 expression). We then stimulated these macrophages with or without 100 ng/ml of periostin for 6 hours and examined gene expression using a cDNA microarray.

overall_design: Periostin stimulated gene expression on monocyte-derived macrophages was measured at 6 hours after exposure to doses of 100 ng/ml periostin.

first: Sadanori

last: Furudate

first: Taku

last: Fujimura

first: Aya

last: Kakizaki

first: Yumi

last: Kambayashi

first: Setsuya

last: Aiba


title: Inhibition of the miR-155 target NIAM phenocopies the growth promoting effect of miR-155 in B-cell lymphoma

status: Public on Jul 16 2015

city: Groningen

first: Anke

last: van den Berg

address: Hanzeplein 1

department: Department of Pathology and Medical Biology

institute: University of Groningen, University Medical Center Groningen


title: Inhibition of the miR-155 target NIAM phenocopies the growth promoting effect of miR-155 in B-cell lymphoma [L1236]

summary: Several studies have indicated an important role for miR-155 in the pathogenesis of B-cell lymphoma. Highly elevated levels of miR-155 were indeed observed in most B-cell lymphomas with the exception of Burkitt lymphoma (BL). However, the molecular mechanisms that underlie the oncogenic role of miR-155 in B-cell lymphoma are not well understood. To identify the miR-155 targets relevant for B-cell lymphoma, we performed RNA immunoprecipitation of Argonaute 2 in Hodgkin lymphoma (HL) cells upon miR-155 inhibition and in BL cells upon ectopic expression of miR-155. We identified 54 miR-155-specific target genes in BL cells and confirmed miR-155 targeting of DET1, NIAM, TRIM32, HOMEZ, PSIP1 and JARID2. Five of these targets are also regulated by endogenous miR-155 in HL cells. Both overexpression of miR-155 and inhibition of expression of the novel miR-155 target gene NIAM increased proliferation of BL cells. In primary B-cell lymphoma NIAM-positive cases have significant lower levels of miR-155 as compared to NIAM-negative cases, suggesting that NIAM is also regulated by miR-155 in primary B-cell lymphoma. Thus, our data indicate an oncogenic role for miR-155 in B-cell lymphoma which involves targeting the tumor suppressor NIAM.

overall_design:
Gene expression profiles were performed in L1236 Hodgkin lymphoma cell line in 4 samples: L1236 EV (empty pMSCV-PIG vector) total cell lysate, L1236 miR-155-sp (L1236 with miR-155 sponge) total cell lysate, L1236 EV Ago2-IP, L1236 miR-155-sp Ago2-IP.
Please note that experiments were performed technically as dual channel (eg, Cy3 and Cy5-labeled samples hybridized to the same array) but the results were processed though they are single channel (total 8 sample records for 4 raw data files; Cy3 and Cy5 signals are calculated). Therefore, raw data files for paired samples (e.g. 'L1236 miR-155-sp Total Cy5' and  L1236 miR-155-sp IP Cy3' ) are identical.

first: Izabella

last: Slezak-Prochazka

first: Joost

last: Kluiver

first: Debora

last: de Jong

first: Katarzyna

last: Smigielska-Czepiel

first: Gertrud

last: Kortman

first: Melanie

last: Winkle

first: Bea

last: Rutgers

first: Jasper

last: Koerts

first: Lydia

last: Visser

first: Arjan

last: Diepstra

first: Bart-Jan

last: Kroesen


title: Inhibition of the miR-155 target NIAM phenocopies the growth promoting effect of miR-155 in B-cell lymphoma [KM-H2]

overall_design:
Gene expression profiles were performed in KM-H2 Hodgkin lymphoma cell line in 4 samples: KM-H2 EV (empty pMSCV-PIG vector) total cell lysate, KM-H2 miR-155-sp (KM-H2 with miR-155 sponge) total cell lysate, KM-H2 EV Ago2-IP, KM-H2 miR-155-sp Ago2-IP.
Please note that experiments were performed technically as dual channel (eg, Cy3 and Cy5-labeled samples hybridized to the same array) but the results were processed though they are single channel (total 8 sample records for 4 raw data files; Cy3 and Cy5 signals are calculated). Therefore, the raw data files for paired samples (e.g.KM-H2 EV Total Cy3 and  KM-H2 EV IP Cy5 samples) are identical.


title: Dynamics of gene expression changes in epithelial and mesenchymal HMLER cell lines transitioning from suspension 3D culture to adhesion cultures

status: Public on Jul 10 2015

city: Seattle

first: Anne

last: Grosse-Wilde

state: WA

address: 401 Terry Ave N

institute: Institute for Systems Biology

summary: In order to metastasize, few cells need to detach from the primary tumor, and transition through the circulation to distant sites to establish new solid tumor metastases. The gene expression changes occurring between these transitions are poorly understood, and controversial findings have been reported regarding transitions between epithelial (E) and mesenchymal (M) cell states. To model the metastasis process in vitro, here we examined the dynamics of gene expression changes and respective cell fates that are occurring in cells that are transitioning from adhesion culture to suspension 3D culture (mammospheres) and back to adhesion culture in vitro.   We found that mammosphere and replating cultures of epithelial (E) cell lines (HP cells and E clones) led to enrichment for mesenchymal (M) signatures characteristic of the mesenchymal cell lines, indicative of an epithelial to mesenchymal transition (EMT), but retainment of E-specific signatures (Grosse-Wilde et al., 2015). This co-expression of E and M signatures was stably maintained between the mammosphere state in suspension and in replated cells, indicating a stable E/M gene expression state by partial EMT in E cell lines, which has been associated with a stem-like state (Grosse-Wilde et al., 2015; Jolly et al., 2014; Lu et al., 2014; Zhang et al., 2014). Interestingly, mammosphere suspension culture of mesenchymal M clones also resulted in co-expression of E and M signatures generated by partial mesenchymal to epithelial transition (MET). However, in stark contrast to E clones and HP cells, immediately upon replating M cell-derived mammospheres to adhesion lost the intermediate E/M state and converted back to stable expression of M signatures indicative of rapid EMT. This suggests that the intermediate state in M cells is very unstable. Together, these replating data suggest that prolonged detachment of epithelial-derived cells leads to loss of expression of E signatures and EMT.   Life-threatening macrometastases typically recapitulate the gene expression of the primary tumor, which requires expression of E signatures, while the mesenchymal micrometastases are frequent but not-proliferative and harmless. Since all HMLER cell lines independent of their initial E or M state converged to an M state upon expansion in suspension, our data suggest that induction of EMT in suspended HMLER cells may be one reason for the observed benign non-metastatic character of HMLER cells when used in mouse xenograft experiments, and for their metastatic inefficiency. Our datasets of the replating kinetic may be useful to identify which pathways are involved in the processes enabling the mixed HP population to maintain a stable E/M expression signature and a more stem-like state, which we have identified as caused by cell-cell cooperation between phenotypically different E and M cell-types. By contrast, M cells can only transiently assume this E/M gene expression state, and not generate a stable phenotypic heterogeneity and therefore absence of cooperation between E and M cell-types.   Instability of the intermediate stem-like E/M state in M cell-types and rapid conversion to the M state can explain why 1) pure M populations are often phenotypically stable and are not undergoing MET in vitro (Schmidt et al., 2015; Zhang et al., 2014), 2) why pure M populations are less aggressive resulting in less metastases than mixed cooperating E and M cell populations (Ocaña et al., 2012; Tsuji et al., 2008) or 3) why complete EMT results in more benign less metastasizing tumors than incomplete EMT (Tran et al., 2014; Tsai et al., 2012) and finally 4) why expression of M traits in primary tumors are associated with good patient outcomes and less metastases than E signatures (Kim et al., 2011; Mylona et al., 2008; Tan et al., 2014).   Dontu, G., Abdallah, W.M., Foley, J.M., Jackson, K.W., Clarke, M.F., Kawamura, M.J., and Wicha, M.S. (2003). In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. Genes Dev. 17, 1253–1270.  Elenbaas, B., Spirio, L., Koerner, F., Fleming, M.D., Zimonjic, D.B., Donaher, J.L., Popescu, N.C., Hahn, W.C., and Weinberg, R.A. (2001). Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells. Genes Dev 15, 50–65.  Grosse-Wilde, A., Fouquier d’Hérouël, A., McIntosh, E., Ertaylan, G., Skupin, A., Kuestner, R.E., del Sol, A., Walters, K.-A., and Huang, S. (2015). Stemness of the hybrid Epithelial/Mesenchymal State in Breast Cancer and Its Association with Poor Survival. PLOS ONE 10, e0126522.  Jolly, M.K., Huang, B., Lu, M., Mani, S.A., Levine, H., and Ben-Jacob, E. (2014). Towards elucidating the connection between epithelial-mesenchymal transitions and stemness. J. R. Soc. Interface R. Soc. 11, 20140962.  Kim, H.J., Kim, M.-J., Ahn, S.H., Son, B.H., Kim, S.B., Ahn, J.H., Noh, W.C., and Gong, G. (2011). Different prognostic significance of CD24 and CD44 expression in breast cancer according to hormone receptor status. The Breast 20, 78–85.  Lu, M., Jolly, M.K., Onuchic, J., and Ben-Jacob, E. (2014). Toward decoding the principles of cancer metastasis circuits. Cancer Res. 74, 4574–4587.  Mylona, E., Giannopoulou, I., Fasomytakis, E., Nomikos, A., Magkou, C., Bakarakos, P., and Nakopoulou, L. (2008). The clinicopathologic and prognostic significance of CD44+/CD24−/low and CD44−/CD24+ tumor cells in invasive breast carcinomas. Hum. Pathol. 39, 1096–1102.  Ocaña, O.H., Córcoles, R., Fabra, Á., Moreno-Bueno, G., Acloque, H., Vega, S., Barrallo-Gimeno, A., Cano, A., and Nieto, M.A. (2012). Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1. Cancer Cell 22, 709–724.  Schmidt, J.M., Panzilius, E., Bartsch, H.S., Irmler, M., Beckers, J., Kari, V., Linnemann, J.R., Dragoi, D., Hirschi, B., Kloos, U.J., et al. (2015). Stem-Cell-like Properties and Epithelial Plasticity Arise as Stable Traits after Transient Twist1 Activation. Cell Rep. 10, 131–139.  Tan, T.Z., Miow, Q.H., Miki, Y., Noda, T., Mori, S., Huang, R.Y.-J., and Thiery, J.P. (2014). Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients. EMBO Mol. Med. 6, 1279–1293.  Tran, H.D., Luitel, K., Kim, M., Zhang, K., Longmore, G.D., and Tran, D.D. (2014). Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer. Cancer Res. 74, 6330–6340.  Tsai, J.H., Donaher, J.L., Murphy, D.A., Chau, S., and Yang, J. (2012). Spatiotemporal Regulation of Epithelial-Mesenchymal Transition Is Essential for Squamous Cell Carcinoma Metastasis. Cancer Cell 22, 725–736.  Tsuji, T., Ibaragi, S., Shima, K., Hu, M.G., Katsurano, M., Sasaki, A., and Hu, G. -f. (2008). Epithelial-Mesenchymal Transition Induced by Growth Suppressor p12CDK2-AP1 Promotes Tumor Cell Local Invasion but Suppresses Distant Colony Growth. Cancer Res. 68, 10377–10386.  Zhang, J., Tian, X.-J., Zhang, H., Teng, Y., Li, R., Bai, F., Elankumaran, S., and Xing, J. (2014). TGF- -induced epithelial-to-mesenchymal transition proceeds through stepwise activation of multiple feedback loops. Sci. Signal. 7, ra91–ra91.

overall_design:
For these analyses we used the heterogeneous parental HMLER (HP) cell line, with isogenic epithelial (E) and mesenchymal (M) cell-types (Elenbaas et al., 2001), and stable clonal HMLER-derived E and M cell lines, which are normally passaged under adhesion conditions (_adh, GSE66527). We cultured cell lines under 3D suspension conditions resembling mammosphere growth conditions that are typically used to enrich for stem-like cells (Dontu et al., 2003), and examined gene expression of cells under mammosphere conditions (_sus, GSE66527), or after replating (_re) in a kinetic examining gene expression from 6, 24, 96, and 240 hrs after cells were allowed to readhere to normal dishes for the heterogeneous but mostly epithelial (HP) cell lines and mesenchymal (M4) cell lines. To validate our findings we also examined gene expression of cells replated after mammosphere culture for about two weeks from three different E (E3, E4, E5) and M clones (M3, M4, M1). All gene expression samples were taken from biological replicates (at least duplicates) of cells grown in different wells or even at different times.   Gene expression of replated (_re) cells was compared to the respective cell lines grown under adhesion conditions (_adh), as well as to the respective cell line grown under suspension mammosphere condition (_sus) which have been deposited previously under accession number GSE66527.
HP replicates (re): HP_re_AGW120913, HP_re_RK12026, HP_re_AGW1209_5, HP_re_AGW1209_6, HP_re_AGW1209_7, HP_re_AGW1209_8, HP_re_AGW1209_9, HP_re_0607_1, HP_re_0607_2
E3 replicates (re): E3_re_RK1202, E3_re_RK12028; E4 replicates: E4_re_0622, E4_re_0613; E5 replicates: E5_re_0613_1, E5_re_0613_2
M1 replicates (re): M1_re_0607_1, M1_re_0607_2, M2 replicates: M2_re_RK1202, M2_re_RK12029, M2_re_AGW1209_3, M2_re_AGW1209_4, M2_re_AGW1209_5, M3 replicates: M4_re_0607_1, M4_re_0607_2
HP replicates (adh): HP_adh_0629, HP_adh_2210, HP_adh_0607sc, HP_adh_0607c
E3 replicates (adh):  E3_adh_0629, E3_adh, E3_adh_0826. E4 replicates (adh): E4_adh_0607, E4_adh_0210, E5 replicates (adh): E5_adh_0210, E5_adh_0607
M1 replicates (adh): M1_adh_0210, M1_adh_0607, M4 replicates (adh): M4_adh_0607, M4_adh_0210, M3 replicates (adh): M3_adh, M3_adh_2210, M3_adh_2810
HP replating kinetic (adh): HP_adh_0607c (GSE66527), HP_adh_0607sc (GSE66527), HP (mammospheres, suspension): HP_sus_0603_2 (GSE66527), HP_sus_0603_1 (GSE66527), HP (replated 6 hrs): HP_re_6_0603_1, HP_re_6_0603_2, HP (replated 24hrs): HP_re_24_0607_1, HP_re_24_0607_2, HP (replated 96 hrs): HP_re_96_0607_1, HP_re_96_0607_2, HP (replated 240hrs): HP_re_0607_1, HP_re_0607_2,
M4 replating kinetic (adh): M4_adh_0210 (GSE66527), M4_adh_0607 (GSE66527), M4 (mammospheres, suspension): M4_sus_0603_2 (GSE66527), M4_sus_0603_1 (GSE66527), M4 (replated 24 hrs): M4_re_24_0603_1, M4_re_24_0603_2, M4 (replated 96 hrs), M4_re_96_0607_1, M4_re_96_0607_2, M4 replated 240hrs): M4_re_0607_1, M4_re_0607_2

first: Adrian

last: Ozinsky

first: Rolf

last: Kuestner


title: ITGA11 expression of CAF promotes tumorigenicity and metastasis in NSCLC

status: Public on Jul 15 2015

city: Toronto

first: Ming

last: Tsao

state: Ontario

address: 610 University Avenue

department: Ontario Cancer Institute

country: Canada

institute: University of Toronto

summary: Integrin alpha-11-beta-1 is stroma specific receptor for fibrillar collagen, as it is mainly over-expressed in carcinoma-associated fibroblasts (CAFs). However, its direct role in cancer progression remains unclear. We have investigated this role by generating severe combined immune deficient (SCID) mice deficient in integrin alpha-11 (alpha-11) expression. The growth of A549 lung adenocarcinoma cells in integrin alpha-11 knockout animals (alpha-11-/-) was significantly impeded, as compared to wild type (alpha-11+/+) SCID mice. Orthotopic implantation of a spontaneously metastatic NCI-H460SM cells into the lungs of alpha-11-/- and alpha-11+/+ mice showed significant reduction in the metastatic potential of these cells in the alpha-11 deficient mice.  Our data support an important role for alpha-11 signaling pathway in CAFs, promoting tumor growth and metastatic potential of non-small cell lung cancer (NSCLC) cells by regulating the expression of alpha-SMA and stromal collagen-cross linking genes as the latter affects the organization and stiffness of fibrillar collagen.

platform_organism:
Homo sapiens
Mus musculus

overall_design: Lung cancer cell line A549 was subcutaneously implanted into integrin alpha 11 +/+, +/-, and -/- SCID mice. Each group had 8 mice. RNA from tumors from the 8 mice was pooled and splited into 2, one for human chip for the profiling gene expression of the tumor and the other for mouse chip for the profiling of stromal gene expression. 2 replicates for each group.

first: Ming-Sound

first: Roya

last: Navab

first: ChangQi

last: Zhu


title: cDNA microarray data after influenza A virus infection in mouse lung tissue

status: Public on Jul 08 2015

city: Seoul

first: Hyun Jik

last: Kim

address: 101 Daehak-ro, Jongno-gu

department: Department of otorhinolaryngology

country: South Korea

institute: Seoul National University

summary:
The defense mechanisms that are provided by the innate immune system are a formidable barrier to influenza virus and a special immune system exists at distinct respiratory epithelium to combat invasion by influenza virus.
Innate immune mechanisms for antiviral resistance are mediated by an increase of interferons’ secretion and type I and III IFNs represent the prototypical resistance mechanism as they induce diverse of Interferon stimulated genes that serve as effectors to limit viral replication.

overall_design: To evaluate the change of gene expressions after IAV infection, we performed gene expression analysis using the Illumina MouseWG-6 v2 Expression BeadChip (Illumina, Inc., San Diego, CA)made by Affimetrix, which comprised of more than 770,000 unique 25-mer oligonucleotide features constituting more than 28,000 genes, and each gene is represented on the array by 45,281 probes. The data were processed using the robust multi-array analysis algorithm, which performs a background correction, a normalization step, and a probe-level summary.

first: Hyun

first: Sujin


title: Gene expression profiling of Human ES cell line (hESC) derived embryoid body (EB) treated with H3R17methylation inhibitor TBBD

status: Public on Jul 01 2015

city: Bangalore

first: Genotypic

last: technology

state: Karnataka

address: 259, Apoorva 4th cross,80 feet Road,RMV 2ND STAGE

country: India

institute: Genotypic Technology

summary: H3R17 methylation inhibitor TBBD associated differential gene expression in embryoid bodies was assessed by microarray analysis treated with 10uM TBBD for 48 hours compared to DMSO control treated Ebs

overall_design: Affymetrix one-color experiment,Organism: Homo sapiens[HuGene-1_0-st] Affymetrix Human Gene 1.0 ST Array

first: Ruthrotha

last: Selvi

first: Tapas

last: Kundu


title: Gene and miRNA expression profiling of Human ES cell line (hESC) derived embryoid body (EB) treated with H3R17methylation inhibitor TBBD


title: CaMKII inhibition in smooth muscle cells controls Ang-II-induced gene transcription in the aorta

first: Thomas

last: Bair

address: 335 EMRB

summary:
The Ca2+/calmodulin-dependent kinase II is expressed in smooth muscle and believed to mediate intracellular calcium handling and calcium-dependent gene transcription. CaMKII is activated by Angiotensin-II.
The multifunctional calcium/calmodulin-dependent kinase II (CaMKII) is activated by Angiotensin-II (Ang-II) in vascular smooth muscle cells (VSMC), but its impact on hypertension remains unknown. In our transgenic mice that express the inhibitor peptide CaMKIIN in smooth muscle (TG SM-CaMKIIN), the blood pressure response to chronic Ang-II infusion was significantly reduced as compared to littermate controls. Surprisingly, examination of blood pressure and heart rate under ganglionic blockade revealed a key role for VSMC CaMKII in efferent sympathetic outflow in response to Ang II hypertension. Consistently, the efferent splanchnic nerve activity and plasma phenylephrine concentrations were significantly lower in TG SM-CaMKIIN mice as compared to littermates. Moreover, the aortic depressor nerve activity was reset in hypertensive wild type animals, but not in TG SM-CaMKIIN mice, suggesting that changes in baroreceptor wall activity may be responsible for the blood pressure difference in Ang-II hypertension. The pulse wave velocity, a measure of vascular wall stiffness in vivo, was increased in aortas of hypertensive compared to normotensive WT animals. However, Ang-II infusion did not alter the pulse wave velocity in transgenic mice, suggesting that CaMKII in VSMC controls structural smooth muscle genes. Accordingly, analysis of gene expression changes in aortas from wild type and TG SM-CaMKIIN hypertensive mice demonstrated that CaMKII inhibition mainly altered the expression of muscle contractile proteins. In contrast, TG SM-CaMKIIN aortas were protected from the Ang-II induced upregulation of genes linked to proliferation, suggesting that CaMKII inhibition prevents the Ang-II-induced reprogramming of smooth muscle cell gene expression towards a proliferative phenotype.

overall_design: 5 WT C57Bl/6 and 5 mice that express the  Ca2+/calmodulin-dependent kinase II peptide inhibitor CaMKIIN in smooth muscle only (TG SM-CaMKIIN) were infused with 1.25 ug/kg/min Angiotensin-II by osmotic minipump for 14 days. 5 WT and 5 transgenic mice infused with normal saline served as controls. The mice were sacrificed on day 14 and the thoracic aortas isolated. RNA was isolated and pooled for the following groups: WT (wild type), C (TG SM-CaMKIIN), WT-A (WT with Angiotensin-II), C-A (TG SM-CaMKIIN + Angiotensin-II)

first: Anand

last: Prasad

first: Donald

last: Morgan

first: Daniel

middle: W

last: Nuno

first: Pimonrat

last: Ketsawatsomkron

first: Ashlee

middle: N

last: Venema

first: Megan

last: Dibbern

first: Kathryn

middle: G

last: Lamping

first: Mark

last: Chapleau

first: Curt

middle: D

last: Sigmund

first: Kamal

last: Rahmouni

first: Isabella

last: Grumbach


title: High-fat diet decreases expression of genes controlling lipid metabolism, mitochondrial function and skeletal system development in adipose tissue, along with increased expression of extracellular matrix remodeling- and inflammation-related genes

city: Daegu

first: Un Ju

last: Jung

address: 1370, Sankyuk-dong, Buk-gu

department: Center for Food & Nutritional Genomics

institute: Kyungpook National University

summary: We identified differentially expressed genes in epididymal white adipose tissue of high fat diet(HFD)-fed mice compared to low fat diet-fed mice using microarray analysis. Microarray analysis revealed that genes related to lipolysis, fatty acid metabolism, mitochondrial energy transduction, oxidation-reduction, insulin sensitivity, and skeletal system development were downregulated in HFD-fed mice, and genes associated with extracellular matrix (ECM) components, ECM remodeling, and inflammation were upregulated. The top 10 up- or downregulated genes include Acsm3, mt-Nd6, Fam13a, Cyp2e1, Rgs1, and Gpnmb, whose roles in obesity-associated adipose tissue deterioration are poorly understood.

overall_design: Total RNA of epididymal white adipose tissue was obtained from low fat diet (10 kcal% fat)- and high fat diet(45 kcal% fat)-fed mice and mRNA expression was measured using microarray analysis.

first: Un

middle: J

first: Myung-Sook

last: Choi


title: Transcriptomic analysis of gastric cancer SGC-7901 cells in response to stable over-expression of intelectin 1

city: Wuhan

first: Qiangsong

last: Tong

state: Hubei

address: 1277 Jiefang Avenue

department: Department of Surgery

institute: Union Hospital of Tongji Medical College

summary: Gastric cancer is one of the most common cancers worldwide, with approximately 1 million patients being diagnosed annually. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of gastric cancer. Since our previous studies indicate that intelectin 1 (ITLN1) is aberrantly expressed in gastric cancer and serves as a prognostic factor for predicting the outcomes of gastric cancer patients, we hypothesized that ITLN1 might participate in the progression and aggressiveness of gastric cancer. We employed the human whole genome microarray expression profiling as a discovery platform to analyze the transcriptome profiling changes of human gastric cancer SGC-7901 cells in response to stable over-expression of ITLN1. The results showed that stable over-expression of ITLN1 led to altered expression of 1592 human mRNAs, including 547 up-regulated genes and 1045 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the microarray results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to ITLN1 over-expression in human gastric cancer cells, and these findings will help us understand the pathogenesis of gastric cancer.

overall_design: Total RNA of cells stably transfected with empty vector or ITLN1 was extracted using the TRIZOL Reagent according to the manufacturer's instructions. Gene expression profiling was performed for each RNA sample separately on the Agilent Whole Human Genome Oligo Microarray 4×44K at Shanghai Technology Corporation (Shanghai, China), in which GeneChip microarray service was certificated by Agilent.

first: Liduan

last: Zheng


title: An Artificial Interfering lncRNA Mediated by Oncolytic Adenovirus Competitively Consumes OncomiRs to Exert Antitumor Efficacy in Hepatocellular Carcinoma (mRNA)

city: Shanghai

first: Changqing

last: Su

summary: The study generated an artificially-designed interfering long non-coding RNA (lncRNAi). The adenovirus-expressed lncRNAi with high level in hepatocellular carcinoma (HCC) cells competes with OncomiR target genes to bind to and consume OncomiRs, thereby achieving the targeted anti-HCC efficacy.

overall_design: High expression of an artificially-designed lncRNAi mediated by oncolytic adenovirus can compete with the mRNAs of OncomiR target genes to bind to and consume OncomiRs, thereby achieving the targeted anticancer effect of HCC.

first: Xiaoya

last: Li

first: Yinghan


title: Genome-wide cardiac gene expression analysis of mice with cardiomyocyte-specific deletion of Dnmt3a and Dnmt3b

status: Public on Jun 30 2015

city: Bad Krozingen

first: Thomas

last: Nuehrenberg

state: Baden-Württemberg

address: Südring 15

department: Klinik für Kardiologie II

institute: Universitäts-Herzzentrum Freiburg • Bad Krozingen

summary:
Cardiomyocyte-specific double knockout (DKO) mice lacking the catalytic domains of Dnmt3a (exon 18) and Dnmt3b (exon 19) were obtained by mating Dnmt3aflox and Dnmt3bflox mice [PMID 15757890] with mice expressing a cre recombinase under control of the cardiac atrial myosin light chain promoter (Myl7) [11689889]. Mice with the genotype Dnmt3aflox/flox, Dnmt3bflox/flox without expressing cre recombinase were used as control mice (CTL).
Transcriptome analyses identified upregulation of 44 and downregulation of 9 genes in DKO as compared with control sham mice. TAC mice showed similar changes with substantial overlap of regulated genes compared to sham.

overall_design: Cardiac tissue from sham CTL (n=4) and DKO mice (n=4) as well as TAC-operated CTL (n=6) and DKO mice (n=6) was analysed.

last: Nührenberg

first: Lutz

last: Hein


title: Pharyngeal Satellite Cell Expression Profile

status: Public on Jun 02 2015

city: Atlanta

first: Viren

last: Patel

address: 101 Woodruff Circle

department: EICC

institute: Emory University School of Medicine

summary: To compare the differential gene expression between sorted satellite cells collected from pharyngeal verses limb muscle.

overall_design: Myogenic cells from pharyngeal and limb (gastrocnemius and quadriceps) muscles were isolated, sorted using FACS, and pooled into samples numbering 150,000-200,000 cells collected from 10-30 mice per experiment.  Samples were sent to the Emory University Integrated Genomics Core facility for total RNA isolation using Qiagen miRNEAsy kit with on-column DNAse treatment followed by one round of amplification using NuGEN’s WT-Ovation Pico amplification kit. Analysis of genomic gene expression was performed using an Illumina Mouse WG-6 v2.0 Expression BeadChip. Data was extracted using the Illumina HiScan Scanner and iScan control software. Illumina Genome Studio 2011.1 software suite was used to normalize probe level intensity data with background correction using manifest MouseWG-6_V2_0_R1_11278593_A.txt. Detection p-values were calculated as the proportion of negative control probes with expression greater than the regular probe in question using Partek Genome Studio. Data were further analyzed using both MetaCore Genego (https://portal.genego.com; Thomson Reuters) and Gene Set Enrichment Analysis (www.broadinstitute.org/gsea/index.jsp; Broad Institute).

first: Matthew

last: Randolph

first: Grace

last: Pavlath


title: Genome-wide analysis of adipose tissue from cytoskeletal tropomyosin transgenic mice

status: Public on Jun 21 2015

city: Kensington

first: Anthony

middle: John

last: Kee

state: New South Wales

address: University of New South Wales

department: School of Medical Sciences

institute: University of New South Wales

summary: Analysis of the effect on global gene regulation in epididymal adipose tissue of overexpressing the cytoskeletal tropomyosin, Tm5NM1 to help understand the transcriptional events that lead to increased fat mass in transgenic mice.

overall_design: Total RNA obtained from epididymal adipose tissue for 3 month old transgenic and non-transgenic control mice.

first: Edna

last: Hardeman

first: Peter

last: Gunning


title: Proton Irradiation Impacts Age Driven Modulations of Cancer Progression Influenced by Immune System Transcriptome Modifications from Splenic Tissue

status: Public on Jun 22 2015

city: Mountain View

first: Afshin

last: Beheshti

state: CA

address: Moffett Blvd

institute: NASA Ames Research Center

summary: Age plays a crucial role in the interplay between tumor and host; with further perturbations induced by irradiation. Proton irradiation on tumors induces biological modulations including inhibition of angiogenic and immune factors critical to “hallmark” processes impacting tumor development, in addition to physical targeting advantages. These advantages have provided promising results for proton therapy in cancer. Additionally, protons have implications for carcinogenesis risk of space travel (due to the high proportion of high energy protons in space radiation). Through a systems biology approach, we investigated how host tissue (i.e. splenic tissue) of tumor-bearing mice is altered with age, with or without whole-body proton exposure. Transcriptome analysis was performed on splenic tissue from adolescent (68 day) versus old (736 day) C57BL/6 male mice injected with Lewis lung carcinoma cells with or without three fractionations of 0.5Gy (1GeV) proton irradiation. Global transcriptome analysis indicated that proton irradiation of adolescent hosts caused significant signaling changes within splenic tissues that support carcinogenesis within the mice, as compared to old subjects. Increases in cell cycling and immunosuppression in irradiated adolescent hosts with CDK2, MCM7, CD74, and RUVBL2 as the key players were involved in the regulatory changes in host environment response (i.e. spleen). These results suggest a significant biological component to proton irradiation, operative through host age, that would indicate a modulation of host’s ability to support carcinogenesis in adolescence and the bestowal of resistance to immunosuppression, carcinogenesis, and genetic perturbation by old age.

overall_design: For genome-wide expression profiling of tumor tissue, Mouse WG-6 BeadArray chips (Illumina, San Diego, CA) were used. Total RNA was amplified with the Ambion Illumina TotalPrep Amplification Kit (Ambion, Austin, TX) and labeled from all replicate biological samples for each condition. For spleen replicates, 9 spleen samples from adolescent with 0Gy , 10 from adolescent with 0.5Gyx3 protons, 9 from old from old with 0Gy, and 10 from old mice with 0.5Gyx3 protons, were used. All replicate samples were run individually. Total RNA was isolated and purified using TRIzol (Invitrogen) and quantified using an Agilent Bioanalyzer. Samples were deemed suitable for amplification and hybridization if they had 28s/18s = 2:1, RIN >7. Total RNA of 500ng per sample was amplified using AmbionTotalPrep, and 1.5ug of the product was loaded onto the chips. Following hybridization at 55C, the chips were washed and then scanned using the Illumina iScan System. The data was checked with GenomeStudio (Illumina) for quality control. Data were corrected through COMBAT correction, quantile normalized, collapsed to genes from probes, then imported into MultiExperiment Viewer, MeV for analysis. Statistically significant genes were determined by applying a one-way ANOVA with an adjusted Bonferroni correction and false discovery rate (FDR) < 0.001 that resulted in a list of significant genes.

first: Justin

last: Wage

first: Lili

last: Ma

first: Michael

last: Peluso

first: Clare

last: Lamont

first: Philip

last: Hahnfeldt

first: Lynn

last: Hlatky


title: Gata6 potently initiates reprogramming of pluripotent and differentiated cells to extraembryonic endoderm stem cells [time-course microarray]

city: London

first: Kathy

last: Niakan

address: Mill Hill

country: United Kingdom

institute: The Francis Crick Institute

summary: Transcription factor-mediated reprogramming is a powerful method to study cell fate changes. In this work, we demonstrate that the transcription factor Gata6 can initiate reprograming of multiple cell types to induced extraembryonic endoderm (iXEN) cells. Intriguingly, Gata6 is sufficient to drive iXEN cells from mouse pluripotent cells and differentiated neural cells. Furthermore, GATA6 induction in human ES (hES) cells also downregulates pluripotency gene expression and upregulates extraembryonic endoderm genes, revealing a conserved function in mediating this cell fate switch. Profiling transcriptional changes following Gata6 induction in mES cells reveals step-wise pluripotency factor disengagement, with initial repression of Nanog and Esrrb, then Sox2 and finally Oct4, alongside step-wise activation of extraembryonic endoderm genes. Chromatin immunoprecipitation and subsequent high-throughput sequencing analysis shows Gata6 enrichment near both pluripotency and endoderm genes, suggesting that Gata6 functions as both a direct repressor and activator. Together this demonstrates that Gata6 is a versatile and potent reprogramming factor that can act alone to drive a cell fate switch from diverse cell types.

overall_design: Time-course microarray analysis of Gata6-mediated reprogramming from 12 to 144 hours of doxycycline treatment in mouse embryonic stem (mES) cells compared to uninduced mES cells, embryo-derived extraembryonic endoderm (XEN) cells and Sox7 overexpressing mES cells after 144 hours of doxycycline treatment.

first: Sissy

last: Wamaitha

first: Ignacio

last: del Valle

first: Lily

last: Cho

first: Yingying

last: Wei

first: Norah

middle: M

last: Fogarty

first: Paul

last: Blakeley

first: Richard

middle: I

last: Sherwood

first: Hongkai

last: Ji


title: Primary hepatocytes with glucagon treatment expression profiling

city: South San Francisco

first: Matthew

last: Brauer

state: California

address: 1 DNA Way

department: Bioinformatics

institute: Genentech, Inc.

summary:
Primary human hepatocyte response to stimulation with glucagon.
Fig S3 in Solloway et al.

overall_design: Primary human hepatocytes will be treated with Vehicle and then stimulated with glucagon.

first: Mark

middle: A

last: Solloway


title: Glucagon Couples Hepatic Amino Acid Catabolism to mTOR-dependent Regulation of α-cell Mass

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

overall_design: Refer to individual Series


title: Early dendritic cell molecular signature modelling predicts late vaccine-induced adaptive T-cell responses (Illumina)

city: Paris

first: Nicolas

last: Dérian

address: Bâtiment CERVI, 83 bvd de l'Hôpital

country: France

institute: UPMC

summary: Mice were vaccinated with different Lentivirus vector-plaforms or PBS. Transcriptomes of sorted dendritic cells 6 hours after vaccination were used to build a model predictive of the vector-platform efficacy measured as the antigen-specific response 5, 7 and 10 days after the vaccination

overall_design: Groups of 7-week-old female C57BL/6 mice (Charles River, France and Germany) were immunized either intravenously or sub-cutaneously with a controlled quantity of vector particles as defined in CompuVac assay protocols (www.compuvac.eu). Control mice were injected with 100 µL of phosphate buffered saline solution (PBS).

first: Bertrand

last: Bellier

first: Hang-Phuong

last: Pham

first: Eliza

last: Tsitoura

first: Dorothea

last: Kazazi

first: Christope

last: Huret

first: Penelope

last: Mavromara

first: David

last: Klatzmann

first: Adrien

last: Six


title: Genome wide analysis of SOCS2 dependent gene expression profile in bone marrow LSK following 5-Fluorouracil treatment

status: Public on Jun 01 2015

city: Milan

first: Matteo

last: Dugo

address: via Olgettina 60

department: Department of Medical Oncology

country: Italy

institute: IRCCS Ospedale San Raffaele

summary: Hematopoietic stem cells (HSC) promptly adapt hematopoiesis to stress conditions, such as infection and cancer, by replenishing bone marrow (BM)-derived circulating populations while preserving the stem cell reservoir. SOCS2, a feedback inhibitor of JAK/STAT pathways is expressed in most primitive HSC and is upregulated in response to STAT5-inducing cytokines. We demonstrate that Socs2 deficiency unleashes HSC proliferation in vitro sustaining STAT5 phosphorylation in response to the hematopoietic cytokines IL-3, thrombopoietin (TPO) and GM-CSF. In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil and, in turn, induces exhaustion of long-term HSC function along serial BM transplantations. These findings unveiled a new regulatory role for SOCS2 in normalizing HSC functions under hematopoietic stress and prompted its investigation for involvement in malignant hematopoiesis. Indeed, in acute myeloid and lymphoblastic leukemias high levels of SOCS2 characterize unfavorable subclasses with MLL and BCR/ABL abnormalities. Analysis of gene expression profiles showed that high SOCS2 positively correlates with a pool of genes that are significatively enriched of members of the stemness signature described in acute myeloid leukemia. Unexpectedly, in acute leukemias, SOCS2 and its related genes are not controlled by STAT5 signaling, they are rather part of regulatory networks fronted by IKZF1/Ikaros and MEF2C, two key hematopoietic stemness-related transcriptional factors that, independently, have been described in leukemias but never linked together in controlling SOCS2 expression and unfavorable leukemia outcome.

overall_design: Total RNA  obtained from LSK isolated from bone marrow of wt or Socs2-/- mice 6 days after administration of 5-fluorouracil

first: Caterina

last: Vitali

first: Mario

middle: P

last: Colombo


status: Public on Jul 07 2015

city: Xiamen

first: Shubin

last: Gao

address: Chengzhi building 110,Xiang'an South Road

department: Basic Medical Sciences

institute: Medical College,Xiamen University

summary:
Menin, the product of the MEN1 gene in humans (Men1 in mice), is responsible for the inherited tumor syndrome, multiple endocrine neoplasia type 1 (MEN1). menin interacts with the trithorax group (trxG) proteins (Drosophila) and the mixed-lineage leukemia (MLL) (humans) histone methyltransferase (HMTase) complex, and it alters histone tail modifications and the transcription of target genes. To explore a potential functional implication of menin in HCC, we stably transfected HepG2 or L-02 cells with either vectors or constructs expressing MEN1. A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1.
To obtain a broader understanding of the molecular network of menin in HCC, the whole genome microarray expression profiling was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1.

overall_design: Comparison of gene expression results from HepG2 or L-02 cells with either vectors or constructs expressing MEN1.

first: Bin

last: Xu


title: Expression data from livers from mice receiving high-fat (HF) diets supplemented with different berries

city: Lund

first: Petter

last: Storm

address: Sölvegatan 19, BMC A11

department: Developmental and Regenerative Neurobiology

country: Sweden

institute: Lund University

summary: DNA microarray analysis was employed to analyze hepatic gene expression in mice that were protected against HF-induced obesity and liver steatosis (ie HF diets supplemented with lingonberries, blackcurrants or bilberries) and compare to mice who were not protected (HF control) or even experienced increased obesity and fatty liver (HF diet with açai). The study was done to increase understanding of underlying mechanisms of the observed effects.

overall_design: Livers were taken from male C57BL/6JBomTac mice receiving low-fat diet (10% kcal fat), HF diet (45% kcal fat) or HF diets supplemented with 20% w/w of freeze-dried berries (lingoberries, blackcurrants, bilberries or açai) for 13 weeks (n=6). The microarrays were performed using MouseWG-6 v2.0 Whole-Genome Expression Beadchips according to Illuminas standard protocol.

first: Lovisa

last: Heyman


title: Human 46BR.1G1 fibroblasts vs the derivative cell line 7A3

first: Paolo

last: Cremaschi

state: Non-US

address: 72 Huntley Street

department: Oncology

institute: UCL Cancer Institute

summary: Transcription Profile of human 46BR.1G1 fibroblasts (European Collection of Cell Cultures # CB2577) compared with the 46BR.1G1 derivative cell line 7A3 expressing wild type LigI (Soza et al., Mol Cell Biol , 2009, 29: 2032-2041)

overall_design: One-condition experiment 46BR.1G1 vs. 7A3 cells with dye-swap.

first: Alessandra

last: Montecucco


title: Vaccine-platforms study from spleen-sorted dendritic cell transcriptomes

first: Nicolas

last: Dérian


title: Mechanisms of pparγ activation by non-steroidal anti-inflammatory drugs and GQ16.

city: Houston

first: Paul

last: Webb

address: 6670 Bertner Ave

department: Genomic Medicine

institute: Houston Methodist Research Institute

summary:
This study was undertaken to assess the similarities (or differences) between the well-established PPARγ agonist Rosiglitazone and Non-steroidal anti-inflammatory drugs (NSAIDs) diclofenac, indomethacin and ibuprofen, as well as the partial agonist GQ16 at the transcriptome level.
Assessment of NSAID and GQ16 activities in PPARγ-dependent 3T3-L1 cells reveals that NSAIDs and GQ16 display similar effects toward PPARγ-dependent target genes in a manner similar to that of Rosiglitazone.

overall_design: Murine 3T3-L1 preadipocytes were differentiated into adipocytes (7 days), then treated with DMSO (control), 100nM rosiglitazone, 25μM sodium diclofenac, 10μM indomethacin, 75μM ibuprofen, or 10μM GQ16 for 24 hours, after which total RNA was isolated.

first: Douglas

middle: H

last: Sieglaff


title: FSH and Testosterone treated Infant Monkey Sertoli cells vs FSH and Testosterone treated  pubertal Monkey Sertoli cell

city: New Delhi

first: Sayon

last: Basu

state: Delhi

address: Aruna Asaf Ali Marg

institute: National Institute of Immunology

summary: Transcriptional profiling of Sertoli cells of Monkey origin comparing infant Sertoli cells with pubertal Sertoli cells, isolated from Monkeys in which puberty was induced by extrinsic GnRH administration. Both Infant and pubertal cells were treated with FSH and Testosterone in vitro.

overall_design: Two condition experiment, infant Sertoli cells vs Pubertal Sertoli cells. 2 biological replicates infant sertoli cells, 2 biological replicates pubertal sertoli cells. Dye  swap was performed. In experiment #1 Infant sample is labelled with Cy3 and Pubertal sample with Cy5. Vice versa in Experiment #2

first: Subeer

last: Majumdar

first: Kanchan

last: Sarda


title: Genome-wide analysis of gene expression in partial Dnmt3a deleted colon mucosa cells of APC(Min/+) mice

city: Heidelberg

first: Heinz

last: Linhart

address: Im Neuenheimer Feld 581

department: Translational Oncology

institute: DKFZ

summary: Analysis of gene expression in partial Dnmt3a deleted colon mucosa cells of APC(Min/+) mice. In the present study the influence of Dnmt3a deletion on colonic tumorigenesis, gene expression and DNA methylation was analyzed. Results provide important information about the role of Dnmt3a in colonic tumorigenesis.

overall_design: Total RNA obtained from colonic mucosa cells of APC(Min/+), Dnmt3a(2lox/2lox), Fabp-Cre+ mice (Dnmt3a deletion in 30-50% of mucosa cells) compared to APC(Min/+), Dnmt3a(2lox/2lox), Fabp-Cre- control mice


title: Comparative gene expression analysis of Nrf2 activators, CDDO-Im, CDDO-Me and dimethyl fumarate (DMF) in VC1 lung cancer cells

status: Public on May 31 2015

city: Hanover

first: Karen

middle: T

last: Liby

state: NH

address: Remsen Building, Room 524

institute: Dartmouth Medical School

summary:
Nrf2 is an important therapeutic target as activation of this pathway detoxifies harmful insults and reduces oxidative stress. However, the role of Nrf2 in cancer biology is controversial.  Protection against oxidative stress and inflammation can confer a survival advantage to tumor cells, leading to a poor prognosis, and constitutive activation of Nrf2 has been detected in numerous tumors. In our study, we examined the role of two clinically relevant classes of Nrf2 activators, the synthetic triterpenoids (CDDO-Im and CDDO-Me) and dimethyl fumarate (DMF) in lung cancer.
Using microarrays, we attempt to examine whether these Nrf2 activators have an effect on the same subset of Nrf2 genes.

overall_design: VC1 lung cancer cells were treated with either DMSO, 0.05 uM of CDDO-Im, 0.1 uM of CDDO-Im or 15 uM of DMF for 6 hours before RNA was extracted by Qiagen RNeasy kit and analyzed using Illumina Micorarrays.

first: Ciric

last: To

first: Carol

last: Ringelberg

first: Darlene

middle: B

last: Royce

first: Charlotte

last: Williams

first: Renee

last: Risingsong

first: Michael

last: Sporn


title: The network of genes regulated by Ago1 in metastatic prostate cancer PC3

status: Public on May 22 2015

city: Biella

first: giovanna

last: chiorino

address: via malta 3

department: Cancer Genomics

institute: Fondo Edo Tempia

summary: The objective of this study was to evaluate the consequences of Ago1 knockdown in metastatic prostate cancer cells PC3. To this end we profiled RNA from PC3 cells 72 hours following the transfection with a scramble siRNA (siGL3) and a siRNA targeting Ago1 (siAgo1).

overall_design: We profiled RNA from PC3 cells 72 hours following the transfection with a scramble siRNA (siGL3) and a siRNA targeting Ago1 (siAgo1). siAgo1 vs siGL3 gene expression profiling, two technical replicates with dye swap labeling scheme.

first: Marco

last: Magistri

first: Chiara

last: Pastori

first: Maurizia

last: Mello-Grand

first: Giovanna

last: Chiorino

first: Giuseppina

last: Carbone

first: Carlo

middle: V

last: Catapano


title: Systems-based identification of temporal processing pathways during bone cell mechanotransduction

city: Seattle

first: Ronald

last: Kwon

address: 325 Ninth Ave. Box 359798

department: Orthopaedics and Sports Medicine

institute: University of Washington

summary: In this study, our goal was to characterize transcriptomic perturbations arising from the insertion of intermittent rest periods in bone cells subjected to fluid flow, and assess the utility of these perturbations to identify signaling pathways that are differentially activated by this temporal variation.

overall_design: Total RNA was obtained from MC3T3-E1 osteoblastic cells subjected to no flow, one hour of continuous flow, or one hour of rest-inserted flow (4x bouts of 5min of flow followed by 10min of rest). RNA was isolated in cells immediately following cessation of the one hour flow period, or one hour post-flow (6 samples in total). Each sample contains RNA pooled from three independent experiments.

middle: Y


title: Identification of subset-specific dendritic cell progenitors reveals early commitment in the bone marrow [Microarray Expression]

city: Singapore

first: jinmiao

last: chen

address: 8A Biomedical Grove, #04-06 Immunos

country: Singapore

institute: Singapore Immunology Network

summary: Dendritic cells (DCs) are antigen sensing and presenting cells that are essential for effective immunity. Existing as a multi-subset population, divided by distinct developmental and functional characteristics1,2, DC subsets play important and unique roles in responses to pathogens, vaccines and cancer therapies, as well as during immune-pathologies. Therefore therapeutic manipulation of the DC compartment is an attractive strategy. However, our incomplete knowledge of the inter-relationship between DC subsets and how they develop from progenitors in the bone marrow (BM) has so far limited the realization of their therapeutic potential. DCs arise from a cascade of progenitors that gradually differentiate in the BM; first, the macrophage DC progenitor (MDP), then common DC progenitor (CDP), and lastly the Pre-DC, which will leave the BM to seed peripheral tissues before differentiating into mature DCs3,4. While the basic outline of this process is known, how subset commitment and development is regulated at the molecular level remains poorly understood. Here we reveal that the Pre-DC population in mice is heterogeneous, containing uncommitted Ly6c+/-Siglec-H+ cells as well as Ly6c+Siglec-H- and Ly6c-Siglec-H- sub-populations that are developmentally fated to become Th2/17-inducing CD11b+ DCs and Th1-inducing CD8α+ DCs, respectively. Using single cell analysis by microfluidic RNA sequencing, we found that DC subset imprinting occurred at the mRNA level from the CDP stage, revealing that subset fate is defined in the BM and not in peripheral tissues. Single cell transcriptome analysis allowed identification of the molecular checkpoints between progenitor stages and revealed new regulators of DC-poiesis, shedding light on the role of cell cycle control and specific transcription factors in DC lineage development. These data advance our knowledge of the steady-state regulation of DC populations and open promising new avenues for investigation of the therapeutic potential of DC subset-specific targeting in vivo to improve vaccine-based and immunotherapeutic strategies.

overall_design: Total RNA obtained from either total BM Pre-DCs, CDPs, or 4 different BM Pre-DC subpopulations (Ly6c+Siglec-H+; Ly6c-Siglec-H-; Ly6c+Siglec-H-; Ly6c-Siglec-H+); splenic CD11b+ DC; splenic CD8a+ DC to compare exression of bulk mRNA transcript levels between the populations.

first: Andreas

last: Schlitzer

first: Jinmiao

last: Chen

first: Francesca

last: Zolezzi

last: Poidinger

first: Florent

last: Ginhoux


title: Expression data from Hes1 conditional knock-out NOTCH1-induced leukemias

status: Public on May 07 2015

city: New York

first: Alberto

last: Ambesi-Impiombato

address: 1130 St. Nicholas Avenue

department: ICG

country: USA

institute: Columbia University

summary:
To formally address the biological activity of Hes1 in vivo, we tested the interaction between oncogenic NOTCH1 and acute Hes1 loss in a retroviral-transduction bone marrow transplantation model of NOTCH-induced T-ALL
Forced expression of activated NOTCH1 in this model typically results in full leukemia transformation 5-10 weeks later.

overall_design: We performed microarray gene expression analysis of Hes1 wild type and Hes1-/- NOTCH1 induced leukemias

first: Stephanie

last: Schnell

first: Luyao

last: Xu

first: Yue

last: Qin

first: Ryoichiro

last: Kageyama

first: Adolfo

last: Ferrando


title: The gene expression profile of peripheral blood mononuclear cells (PBMCs) of infants (6 to 11 months) immunized with an inactivated EV71 vaccine or placebo

status: Public on May 06 2015

city: Kunming

first: Jie

last: Song

state: Yunnan

address: Number 935 Jiaoling Load

institute: Institute of Medical Biology, Chinese Academy of Medicine Science and Peking Union Medical College

summary: To study the gene expression after administrating an inactivated EV71 vaccine, we have employed whole human genome microarray expression profiling to emphasize the gene expression profile of the immune system in response to an inactivated EV71 vaccine in humans and confirmed that such an immune response was generated as the result of the positive mobilization of the immune system. Human peripheral blood from this vaccine or placebo was isolated, extracted the RNA and screened by microarray. The results showed significantly greater neutralizing antibody and specific T cell responses in vaccine group after two inoculations on days 0 and 28. Additionally, more than 600 functional genes that were up- or down-regulated in PBMCs were identified by the microarray assay, and these genes included 68 genes associated with the immune response in vaccine group.

overall_design: The vaccine inoculation group and the placebo control group, originated from the cohort of phase II clinical trial, consisted of 20 subjects (aged from 6-11 months, average: 9.6 months). The trial was randomized, double-blinded and placebo-controlled, and all of the parents or guardians of the subjects were required to sign an informed consent explaining the experiment.

first: Liu

last: Long-Ding

first: Zhang

last: Ying

first: Qihan

last: Li


title: The transcription factor SOX6 contributes to the developmental origins of obesity by promoting adipogenesis through inhibition of Wnt signaling

status: Public on Jun 26 2015

first: Walter

last: Stunkel

address: 30 Medical Drive

department: Growth Development Metabolism

institute: Singapore Institute for Clinical Sciences

summary:
The developmental transcription factor SOX6 was found to regulate serum, as well as liver triglycerides in BL6 mice treated with SOX6 antisense gapmers compared to control gapmers.
SOX6 was initially discovered as a gene over-expressed in mesenchymal stem cells derived from small for gestational age newborns. We characterized its metabolic function in BL6 mice using the above antisense knockdown approach.

overall_design: BL6 mice were treated with either SOX6 specific or control gapmer oligonucleotides for 48h. Knockdown efficiency was measured in liver and epididymal white adipose tissues and serum levels of triglycerides and cholesterol quantified.

first: Shi

last: Leow

first: Jeremie

last: Poschmann

first: Roy

last: Joseph

first: Shaillay

last: Dogra

first: Peh

last: Too

first: Shyam

last: Prabhakar

first: Yap

middle: S

last: Chong

first: Peter

last: Gluckman


title: Gene expression in M. tuberculosis and M. africanum infected tuberculosis patients prior to and following treatment

status: Public on Jun 05 2015

city: Berlin

first: Jeroen

last: Maertzdorf

address: Chariteplatz 1

institute: MPIIB

summary: Differential gene expression in M. tuberculosis and M. africanum patients under TB treatment

overall_design: Gene expression analysis of whole blood RNA from tuberculosis patients prior to and following treatment

first: Leopold

last: Tientcheu

first: Martin

last: Ota

first: Hans

last: Mollenkopf

first: Stefan

last: Kaufmann


title: Gene expression profiling of miR27a over-expressing RH36 cell lines.

status: Public on May 04 2015

city: Padova

first: Gerolamo

last: Lanfranchi

address: Via U. Bassi, 58/B

department: CRIBI - Biotechnology Center and Biology Department

institute: University of Padova

summary: In order to identify direct or indirect miR-27a modulated genes, RH36 cells transfected with miR-27a precursors (pre-miR-27a or pre-control), analyzed 48h post-transfection,  were used to perform microarray analysis.

overall_design: Gene expression profiling was carried out in ERMS cell line (RH36) transfected with miR-27a or with a negative pre-control. We performed the experiments in triplicate. We used the ‘‘Whole Human Genome Oligo Microarray’’ (Agilent), consisting of 41.000 (60-mer) oligonucleotide probes, which span conserved exons across the transcripts of the targeted full-length genes.

first: Lucia

last: Tombolan

first: Silvia

last: Casara

first: Matteo

last: Zampini

first: Angelica

last: Zin

first: Chiara

last: Romualdi

first: Angelo

last: Rosolen

first: Cristiano

last: De Pittà


title: Gene expression in male and female smokers

status: Public on May 01 2015

first: Sally

last: Amundson

department: Center for Radiological Research

summary: Smoking is the second leading cause of preventable death in the United States.  Cohort epidemiological studies have demonstrated that women are more vulnerable to cigarette-smoking induced diseases than their male counterparts, however, the molecular basis of these differences has been remained unknown to date.  In this study, we explored if there were differences in the gene expression patterns between male and female smokers, and how these patterns might reflect different gender-specific responses to the stress of smoking.

overall_design: Global gene expression was measured in the peripheral blood cells of 12 each male and female smokers and non-smokers using the Agilent one-color workflow and human whole genome microarrays.

first: Sunirmal

last: Paul


title: Compound mouse mutants of bZIP transcription factors MafG and MafK reveal a regulatory network of non-crystallin genes linled to cataract

city: Newark

first: Deepti

last: Anand

state: Delaware

address: 351 Wolf Hall, University of Delaware

department: Biological Sciences

institute: University of Delaware

summary: Although majority of the genes linked to pediatric cataract exhibit lens fiber cell-enriched expression, our understanding of gene regulation in these cells is limited to function of just eight transcription factors and largely in the context of crystallins. Here, we identify small Maf transcription factors MafG and MafK as regulators of several non-crystallin human cataract genes in fiber cells and establish their significance to cataract. We applied a bioinformatics tool for cataract gene discovery iSyTE to identify MafG and its co-regulators in the lens, and generated various null-allelic combinations of MafG:MafK mouse mutants for phenotypic and molecular analysis. By age 4-months, MafG-/-:MafK+/- mutants exhibit lens defects that progressively develop into cataract. High-resolution phenotypic characterization of MafG-/-:MafK+/- lens reveals severe defects in fiber cells, while microarrays-based expression profiling identifies 97 differentially regulated genes (DRGs). Integrative analysis of MafG-/-:MafK+/- lens-DRGs with 1) binding-motifs and genomic targets of small Mafs and their regulatory partners, 2) iSyTE lens-expression data, and 3) interactions between DRGs in the String database, unravels a detailed small Maf regulatory network in the lens, several nodes of which are linked to human cataract. This analysis prioritizes 36 highly promising candidates from the original 97 DRGs. Significantly, 8/36 (22%) DRGs are associated with cataracts in human (GSTO1, MGST1, SC4MOL, UCHL1) or mouse (Aldh3a1, Crygf, Hspb1, Pcbd1), suggesting a multifactorial etiology that includes elevation of oxidative stress. These data identify MafG and MafK as new cataract-associated candidates and define their function in regulating largely non-crystallin genes linked to mouse and human cataract.

overall_design: Microarray comparision of lenses from mixed background (129Sv/J, C57BL/6J, and ICR) control (MafG+/-:MafK+/-; no-cataract) and compound (MafG-/-:MafK+/-; cataract) mouse mutants

first: Salil

last: Lachke

first: Hozumi

last: Motohashi

first: Masayuki

last: Yamamoto

first: Atul

last: Kakrana