title: eIF4E hypersensitive mRNA translation is characterized by long and structured untranslated regions

city: Minneaplois

first: Matthew

last: Parker

state: MINNESOTA

address: 420 Delaware St. SE

department: Department of Medicine

institute: University of Minnesota

summary: Combining a genetic and pharmacological approach, we modulated eIF4E activity across its physiological activity range and identified subsets of genes whose translation was either hypo- or hyper- sensitive to eIF4E activity changes. eIF4E hypersensitive genes had longer 5'UTRs with higher GC content; and longer 3'UTRs with lower GC content and a higher density of unique microRNA target sites. Proliferation related genes were enriched among eIF4E hypersensitive genes; and consistent with this, decreasing eIF4E activity inhibited cell cycle transit. Our findings provide genome wide insights into the properties of mRNAs under translational control across the physiological range of eIF4E activity.

overall_design: NIH 3T3 derivatives genetically altered to induce eIF4E when treated with mifepristone and a non-inducible control NIH 3T3 derivative were cultured with or without treatment with mifepristone and varying doses of a pharmacological eIF4E inhibiting agent, 4Ei-1 (0 μM, 10 μM, 50 μM, 100 μM, 200 μM). Total RNA and polyribosome RNA were isolated after 4h of treatment. Three replicates of each experimental group were completed. In addition, three replicates of the inducible cell line treated with less potent analog to the inhibiting agent, 4Ei-4, were completed to probe for non-specific drug effects.

first: Jeff

last: Braziunas

middle: W

first: Mark

last: Peterson

first: Karen

last: Smith

first: Aniekan

last: Okon

first: J

last: Underwood

first: Carston

middle: R

last: Wagner

first: Ola

last: Larsson

first: Peter

last: Bitterman


title: The homing receptor CD44 is involved in the progression of precancerous gastric lesions in patients infected with Helicobacter pylori and in development of mucous metaplasia in mice (mouse)

status: Public on Dec 17 2015

city: New Orleans

first: Jovanny

last: Zabaleta

state: LA

address: 1700 Tulane Ave

department: Interdisciplinary Oncology

country: USA

institute: LSUHSC

summary: Gastric cancer continues to be one of the most common cancers, with the third highest cancer-related mortality in the world. After infection with Helicobacter pylori, a cascade of inflammatory events that can lead to gastric cancer is triggered. This inflammatory response to the infection is characterized by the infiltration of mononuclear and polymorphonuclear cells into the infected mucosa. The transition of these cells from the circulation to the tissues is mediated through the interaction of receptors on the immune cells and their ligands in the endothelial compartment. CD44 is the receptor for hyaluronan, but it also interacts with osteopontin and collagen, among other molecules. Previous reports have shown that CD44 expression is increased in advanced gastric lesions. However, the association of this molecule with the progression of these lesions over time has not been investigated. In addition, there is a lack of understanding of the CD44-dependent cellular processes that lead to gastritis, and possibly to gastric cancer. Here we studied a subset of subjects from a cohort of individuals with various degrees of gastric inflammation to determine gene expression changes associated with disease progression over a period of six years. We report that CD44 expression is significantly increased in individuals whose gastric lesions progressed over time (from multifocal atrophic gastritis to intestinal metaplasia or from intestinal metaplasia to dysplasia) along the gastric precancerous cascade. We also show that CD44-/- mice develop less severe and less extensive Helicobacter pylori-induced metaplasia, and show fewer infiltrating Gr1+ cells compared to wild type mice. Thus, we present data suggesting that CD44 is associated with disease progression. Mechanisms associated with these effects include induction of interferon gamma responses.

overall_design: A cohort of individuals having at least  Multifocal Atrophic Gastritis (MAG) was follwed for 6 six years to study the evolution of the gastric lesions over time. The gene CD44 was found to be significantly different between the baseline and follow-up samples of individuals with progression to more advanced gastric lesion. Mouse models of H. pylori infection in wild type and CD44-/- mice showed that the KO mice had reduced levels of gastric itestinal metaplasia than their wild type counterparts after infection. The lesions were associated with differential immune responses and infiltration of GR1 positive cells

first: Jone

last: Garay

first: M

middle: B

last: Piazuelo

first: Sumana

last: Majumdar

first: Li

last: Li

first: Jimena

last: Trillo-Tinoco

first: Luis

last: del Valle

first: Barbara

middle: G

last: Schneider

first: Alberto

last: Delgado

first: Keith

middle: T

last: Wilson

first: Pelayo

last: Correa


title: Human skeletal muscle gene expression analysis on Lean, obese insulin sensitive, obese insulin resistant and obese Type II diabetic subjects

status: Public on Dec 15 2015

city: Camperdown, Sydney

first: Rima

last: Chaudhuri

state: NSW

address: D17 Johns Hopkins Drive

department: Charles Perkins Center

country: Australia

institute: University of Sydney

summary:
The obese people with abnormal BMI are predisposed to insulin resistance and diabetes. At the same time, human subjects with obesity and high BMI that are otherwise insulin sensitive are an interesting group to study the underlying gene expression patterns which provide them with such protective phenotype.
Objective: Insulin resistance (IR) is one of the earliest predictors of type 2 diabetes. However, diagnosis of IR is limited. High fat fed mouse models provide key insights into IR. We hypothesized that early features of IR are associated with persistent changes in gene expression (GE) and endeavoured to (a) develop novel methods for improving signal:noise in analysis of human GE using mouse models; (b) identify a GE motif that accurately diagnoses IR in humans; and (c) identify novel biology associated with IR in humans. Methods: We integrated human muscle GE data with longitudinal mouse GE data and developed an unbiased three-level cross-species analysis platform (single-gene, gene-set and networks) to generate a gene expression motif (GEM) indicative of IR. A logistic regression classification model validated GEM in 3 independent human datasets (n =115). Results: This GEM of 93 genes substantially improved diagnosis of IR compared to routine clinical measures across multiple independent datasets. Individuals misclassified by GEM possessed other metabolic features raising the possibility that they represent a separate metabolic subclass. The GEM was enriched in pathways previously implicated in insulin action and revealed novel associations between β-catenin and Jak1 and IR. Functional analyses using small molecule inhibitors showed an important role for these proteins in insulin action. Conclusions: This study shows that systems approaches for identifying molecular signatures provides a powerful way to stratify individuals into discrete metabolic groups. Moreover, we speculate that the β-catenin pathway may represent a novel biomarker for IR in humans that warrant future investigation.

overall_design: Gene expression from muscle biopsies of Lean, Obese insulin sensitive (OIS), Obese insulin resistant (OIR) and obese T2D patients (T2D) were compared for differential expression between the groups (n=7 in each group)

first: Zora

last: Modrusan


title: Systems analysis of uterine  microenvironment 4, 6, 8, 10, 11 or 12 days after fertilization

status: Public on Dec 10 2015

city: Farmington

first: Djamel

last: Nehar-Belaid

state: CONNECTICUT

address: 10 discovery drive

institute: THE JACKSON LABORATORY

summary: Analysis of uterine microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchestrated the immune reponse triggered in presence of embryo

overall_design: Total RNA obtained from uterine microenvironment tissues (4, 6, 8, 10, 11 or 12 days after fertilization) compared to control tissues (uterus from non pregnant mice).

last: NEHAR-BEALID

first: Tristan

last: COURAU

first: Nicolas

last: Dérian

first: Laura

last: FLOREZ

first: Maria

last: RUOCCO

first: David

last: KLATZMANN


title: The immunomodulatory effects of IL-4 on monocyte-derived macrophages

city: Sendai

first: Masayuki

last: Asano

state: Miyagi

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

department: Department of Dermatology

country: Japan

institute: Tohoku University Graduate School of Medicine

summary: To explore the effects of IL-4 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. We then stimulated these macrophages with or without IL-4 (20 ng/ml) for 6 hours and examined gene expression using a cDNA microarray.

overall_design: IL-4 stimulated gene expression on monocyte-derived macrophages was measured at 6 hours after exposure to doses of 20 ng/ml IL-4.

first: Sadanori

last: Furudate

first: Taku

last: Fujimura

first: Aya

last: Kakizaki

first: Takanori

last: Hidaka

first: Setsuya

last: Aiba


title: CFTR is a tumor suppressor gene in murine and human intestinal cancer [microarray]

city: Minneapolis

first: Ying

last: Zhang

state: MN

address: 117 Pleasant St S.E.

department: Minnesota Supercomputing Institute

summary: Analysis of the cystic fibrosis gene Cftr in the colon and small intestine of Cftr-deficient murine model. The hypothesis was loss of Cftr altered expression of genes important in intestinal homeostasis and oncogenic signaling pathways. The results identified potential roles of Cftr in up- or down-regulating major gene clusters that belong to groups of immune response, ion channel, intestinal stem cell and other growth regulators.

overall_design: Total RNA was isolated from the normal intestine of three Apc wildtype Cftr wildtype and three Apc Cftr-deficient mice. For the colon intestinal epithelia from the same region of the distal colon of each mouse was separated from the rest of the intestine prior to RNA isolation. Therefore RNA was obtained from only epithelial cells. For the small intestine, a section of the mid-duodenum from each mouse was sheared of villi prior to RNA isolation. Therefore RNA was obtained from whole duodenum (minus villi), containing epithelia cells but also stromal and other cells. RNA Seq was then conducted on all samples, with at least two replicates for each biological sample.

first: B

middle: L

last: Than

first: J

middle: F

last: Linnekamp

first: T

middle: K

last: Starr

first: D

middle: A

last: Largaespada

first: A

last: Rod

first: Y

first: V

last: Bruner

last: Abrahante

last: Schumann

last: Luczak

last: Niemczyk

first: M

last: O’Sullivan

middle: P

last: Medema

first: R

middle: J

last: Fijneman

first: G

last: Meijer

first: E

last: Van den Broek

first: C

last: Hodges

first: P

middle: M

last: Scott

first: L

last: Vermeulen

last: Cormier


title: Molecular characterization of chronic antibody mediated rejection in kidney transplantation (mRNA CD4)

city: Bari

first: Paola

last: Pontrelli

address: Piazza G.Cesare 11

department: Dept. of Precision and Regenerative Medicine and Ionian Area (DIMEPRE-J)

country: Italy

institute: University of Bari

summary:
Chronic antibody-mediated rejection (CAMR) represents the main cause of kidney graft loss, but its pathogenesis is unclear. In order to uncover the molecular mechanisms underlying this condition, we characterized the molecular signature of circulating peripheral blood mononuclear cells and, separately, of CD4+ T lymphocytes isolated from CAMR patients compared to kidney transplant recipients with normal graft function and histology.
In total peripheral lympho-monocytes, forty-five genes resulted differentially expressed between the two groups, most of them were up-regulated in CAMR and were involved in type I interferon signaling. In addition, in the same set of patients, 16 microRNAs resulted down-regulated in CAMR subjects compared to controls: 4 were predicted modulators of 6 mRNAs identified in the transcriptional analysis. In silico functional analysis supported the involvement of type I interferon signaling. To further confirm this hypothesis, we investigated the transcriptomic profiles of CD4+ T lymphocytes in an independent group of patients and we observed that the activation of type I interferon signaling was a specific hallmark of CAMR. In addition, in CAMR patients we detected a reduction of circulating BDCA2+ dendritic cells, the natural type I interferon- producing cells and their recruitment into the graft along with an increased expression of MXA, a type I interferon-induced protein, at tubulointerstitial and vascular level.
In conclusion, our data suggest that type I interferon signaling may represent the molecular signature of CAMR.

overall_design: We performed microarray experiments in CD4+ T cells isolated from a small independent group of 5 patients included into the control-group and 5 included into the study group. The control group was represented by renal transplant recipients undergoing protocol graft biopsies, with normal renal function and histology, in the absence of circulating anti-HLA antibodies. Study group patients showed clinical and histological evidence of CAMR according to Banff 2011 criteria.

first: Rascio

last: Federica

first: Pontrelli

last: Paola

first: Accetturo

last: Matteo

first: Oranger

last: Annarita

first: Gigante

last: Margherita

first: Castellano

last: Giuseppe

last: Maddalena

first: Zito

last: Anna

first: Zaza

last: Gianluigi

first: Lupo

last: Antonio

first: Ranieri

last: Elena

first: Stallone

last: Giovanni

first: Gesualdo

last: Loreto

first: Grandaliano


title: Systems analysis of uterine  microenvironment  in Treg depleted pregnant mice at 12 days after fertilization

first: Djamel

last: Nehar-Belaid

summary: Analysis of uterine microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchestrated the immune reponse triggered in presence of embryo.

overall_design: Total RNA obtained from uterine microenvironment tissues of Treg depleted pregnant mice (12 days after fertilization) compared to control tissues (uterus from PBS treated pregnant mice).

last: NEHAR-BEALID

first: Tristan

last: COURAU

first: Nicolas

last: Dérian

first: Laura

last: FLOREZ

first: Maria

last: RUOCCO

first: David

last: KLATZMANN


title: Genome-wide analysis of high glucose and DZNep (EZH2 inhibitor) induced gene expression by mouse podocytes

status: Public on Dec 09 2015

city: Toronto

first: Andrew

last: Advani

state: Ontario

address: 6-151 61 Queen Street East

department: Medicine

country: Canada

institute: St. Michael's Hospital

summary: Analysis of DZNep-induced gene expression changes in cultured podocytes. The hypothesis tested in the present study was that DZnep ultimately augments Txnip expression, increasing oxidative stress in podocytes. These results provide important information on the response of podocytes to histone methyltransferase inhibition and a possible mechanism for DZNep action in podocytes.

overall_design: Total RNA obtained from cultured podocytes subjected to 48 hours in vitro, with or without DZNep.

first: Moustafa

last: Abdalla

first: Ferhan

last: Siddiqi


title: Systems analysis of B16 tumor microenvironment 4 or 14 days after tumor inoculation

summary: Analysis of B16 tumor microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchastrated the immune reponse triggered in presence of tumors

overall_design: Total RNA obtained from tumor microenvironment tissues (at Day 4 and Day 14 after tumor inoculation) compared to control tissues.


title: Systems analysis of uterine and tumor microenvironments

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

overall_design: Refer to individual Series


title: Genome-wide analysis of differential gene expression after treatment of the PLCε inhibitor U73122 in colorectal CD110+TICs

status: Public on Dec 01 2015

city: Shanghai

first: Li

last: Qingquan

address: No.138，Yixueyuan Rd.

country: China

institute: fudan university

summary: Analysis of PLCε-regulation of tyrosine metabolism at gene expression level. The hypothesis tested in the present study was that the PLCε pathway-directed transcriptional control play a key role for metabolic reprogramming in CD110+TICs after Kras extinction. Results provide important information of the response of colorectal CD110+TICs to inhibition of the PLCε pathway, such as specific stress-responsive genes, up- or down-regulated specific anabolic/catabolic cellular functions.

overall_design: Total RNA obtained from isolated CD110+TICs subjected to 24 hours in vitro U73122 (1μM) treatment compared to untreated control cells.

first: Qingquan

last: Li

first: Wenchao

last: Gao


title: The homing receptor CD44 is involved in the progression of precancerous gastric lesions in patients infected with Helicobacter pylori and in development of mucous metaplasia in mice

first: Jovanny

last: Zabaleta

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Gene expression analysis of B cell lymphomas from representative IµHABcl6, IµHABcl6 Ung-/- Msh2-/-, and IµHABcl6 Msh2-/- mouse models.

status: Public on Dec 08 2015

city: New Haven

first: Matthew

middle: P.

last: Strout

state: CT

address: 300 George St

department: Yale Cancer Center Section of Hematology

institute: Yale University

summary: Somatic hypermutation (SHM) and class switch recombination (CSR) of immunoglobulin (Ig) genes are genomic modification events that occur in germinal center (GC) B cells and are initiated through deamination of cytidine to uracil by activation induced cytidine deaminase (AID).  Resulting uracil-guanine (U-G) mismatches are subsequently processed by low-fidelity base-excision (BER) and mismatch repair (MMR) pathways to yield mutations and DNA strand lesions.  Although off-target AID activity also contributes to oncogenic point mutations and chromosome translocations associated with B cell lymphomas, the role of downstream AID-associated DNA repair pathways in the pathogenesis of these lymphomas is unknown.  Here, we show that simultaneous BER and MMR deficiency causes genomic instability and a shorter latency to the development of a BCL6-driven GC B cell lymphoma.  In contrast, loss of BER alone is highly protective against B cell transformation while loss of MMR fosters the development of a variety of malignancies.  These findings lend insight into a complex interplay between AID-associated BER and MMR pathways that produces a net protective effect against GC B cell lymphomagenesis.

overall_design: Representative B cell lymphomas from 3 IµHABcl6, 6 IµHABcl6 Ung-/- Msh2-/-, and 5 IµHABcl6 Msh2-/- mice were analyzed in this study. Total RNA was extracted from frozen tumor cells and processed according to Illumina standard protocols.

first: Xiwen

last: Gu


title: Identification of a selective G1-phase benzimidazolone inhibitor by a senescence-targeted virtual screen using artificial neural networks

city: Glasgow

first: W. Nicol

last: Keith

address: Wolfson Wohl Translational Cancer Research Centre

department: Institute of Cancer Science

country: United Kingdom

institute: University of Glasgow

summary: Cellular senescence is a barrier to tumorigenesis in normal cells and tumour cells undergo senescence responses to genotoxic stimuli, which is a potential target phenotype for cancer therapy. However, in this setting, mixed-mode responses are common with apoptosis the dominant effect. Hence, more selective senescence inducers are required. Here we report a machine learning-based in silico screen to identify potential senescence agonists. We built profiles of differentially affected biological process networks from expression data obtained under induced telomere dysfunction conditions in colorectal cancer cells and matched these to a panel of 17 protein targets with confirmatory screening data in PubChem. We trained a neural network using 3517 compounds identified as active or inactive against these targets. The resulting classification model was used to screen a virtual library of ~2M lead-like compounds. 147 virtual hits were acquired for validation in growth inhibition and senescence-associated b-galactosidase (SA-β-gal) assays. Among the found hits a benzimidazolone compound, CB-20903630, had low micromolar IC50 for growth inhibition of HCT116 cells and selectively induced SA-β-gal activity in the entire treated cell population without cytotoxicity or apoptosis induction. Growth suppression was mediated by G1 blockade involving increased p21 expression and suppressed cyclin B1, CDK1 and CDC25C. Additionally, the compound inhibited growth of multicellular spheroids and caused severe retardation of population kinetics in long term treatments. Preliminary structure-activity and structure clustering analyses are reported and expression profiling of CB-20903630 against other cell cycle suppressor compounds suggests that distinct pathways are affected.

overall_design: Treatment of IMR90 with 13 kinase inhibitors and novel compound CB20903630 or DMSO control performed in duplicate.

first: Alan

middle: E

last: Bilsland

first: Angelo

last: Pugliese

first: Yu

last: Liu

first: John

last: Revie

first: Sharon

last: Burns

first: Carol

last: McCormick

first: Claire

last: Cairney

first: Justin

last: Bower

first: Martin

last: Drysdale

first: Masashi

last: Narita

first: Mahito

last: Sadaie

first: W

middle: N


title: Genome-wide ChIP-seq binding profiles and linked gene expression arrays [array]

city: Cambridge

first: Evangelia

last: Diamanti

address: Wellcome Trust / MRC Building, Hills Road

department: Haematology

institute: University of Cambridge

summary: Pu.1-mutated murine AML cell line X18.1.1 transfected with inducible Pu.1 (PuER) or empty vector (EV) and clonal lines selected. Cells were induced with OHT for 2 hours prior to collection for ChIPSeq and expression arrays.

overall_design: Examination of RNA expression profile by array

first: Jonathan

last: Sive


title: Gbx2 is essential for maintaining thalamic neuron identity and repressing habenular characters in the developing thalamus

first: James

middle: YH

last: Li

address: 263 Farmington Ave

department: Genetics and Genome Sciences

institute: UCHC

summary: Using microarray, we compared the transcriptome of the wild-type and Gbx2-KO thalamus at E12.5. We show that Gbx2 promotes thalamic but inhibits habenular molecular characters.

overall_design: Total RNA obtained from microdissected thalamus of wild-type and Gbx2-KO embryos at E12.5.


title: Comparing gene expression profiles of pigmented and amelanotic (MPNST-like) melanomas arising in the genetically engineered BRAF(V600E)-Cdk4(R24C) mouse melanoma model

city: Bonn

first: Michael

last: Holzel

address: Sigmund-Freud Str. 25

department: Institute of Clinical Chemistry and Clinical Pharmacology

country: Germany

institute: University Hospital Bonn

summary:
We found that pigmented and amelanotic (MPNST-like) melanomas arise in the genetically engineered BRAF(V600E)-Cdk4(R24C) mouse melanoma model and even in the same animal.
To explore the molecular differences between the two type of melanomas in this model  we performed global gene expression profiling and pathway analysis to compare the underlying mechanisms. This information was used to identify human melanomas that resemble each type of the mouse melanomas found in the in the genetically engineered BRAF(V600E)-Cdk4(R24C) mouse melanoma model.

overall_design: Total RNA was isolated from excised and liquid nitrogen frozen tumors and global gene expression was performed using the Illumina Mouse WG6 v2.0 platform.

first: Thomas

last: Tüting

first: Jennifer

last: Landsberg

last: Hölzel


title: Thymic Epithelial Cells  with Human T cell Leukemia Virus type 1 (HTLV-1) Infected T cell supernatant (with or without supernatant)

status: Public on Nov 30 2015

city: Rio de Janeiro

first: Leandra

middle: Linhares

last: Lacerda

state: RJ

address: Av. Brasil 4365 pav 26 sala 506 Manguinhos

department: Oswaldo Cruz Institution

country: Brazil

institute: Oswaldo Cruz Foundation

summary: The human T-lymphotropic virus type-1 (HTLV-1) is the cause of adult T cell leukemia/lymphoma (ATL) and HTLV-1 associated myelopathy/tropical spatic paraparesis (HAM/TSP). Both diseases have a late onset, although ATL has a medium survivor of 7.7 months after the onset despise aggressive treatment. T CD4+ cells are the main target of HTLV-1, but other cells types are known to be infected as T CD8+, CD34+ progenitor, dendritic cells and immature lymphocytes. The thymus gland is a primary lymphoid organ, in which the lymphocytes undergo differentiation, where selected T cell ultimately being exported from the organ and going to peripheral lymphoid organs. This process occurs along with immature lymphocyte migration and interaction with thymic microenvironment. Thymic epithelial cells (TECs) are the main component of the thymic stroma and are responsible for the process of intrathymic T cell maturation. This process are dependent of T cell receptor (TCR)-mediated recognition of antigenic peptide fragments presented by major histocompatibility complex (MHC) molecules in TEC and culminate in TCR repertoire formation. In this study, we show that TECs have the receptors for HTLV-1 entry and can be infected by cell-cell contact and cell-free virus. These cells change gene expression of anti-apoptosis, chemokine and adhesion molecules genes; however, there is no difference in antigen presentation molecules. Furthermore, HTLV-1 infected TECs can transmit the virus to a CD4 T cell lineage and CD4 T cells derived from peripheral blood of healthy donors after in vitro co-cultivation. Conjointly, our data points to the possibility that the human thymic epithelial cells must favor the HTLV-1 infection as a reservoir, transmitting the virus to maturing lymphocytes that cause the disease in the periphery.

overall_design: We used non-treated Thymic Epithelial Cell (TEC) and TEC treated with non-infected T cell supernatant (CEM). We analyze three independent samples (biological replicates) for each conditions (total 2 conditions) and also technical replicates using dye-swap. In total we use 1.5 slides with 4 array in each.

first: Luciana

last: Carvalho

first: Klaysa

last: Moreira-Ramos

first: Natalia

last: Santucci

last: Linhares-Lacerda

first: Marcelo

last: Ribeiro-Alves

first: Dumith

middle: C

last: Bou-Habib

first: Wilson

last: Savino


title: Transcriptome analysis of a novel mouse model of osteosarcoma and soft tissue sarcoma

first: Yuning

middle: Jackie

last: Tang

address: 686 Bay Street

department: Program in Developmental Biology

institute: Hospital for Sick Children

summary: Analysis of differential gene expression between mouse sarcoma and normal tissue

overall_design: Total RNA is isolated from mouse tumor tissue and compared to normal bone marrow and muscle tissue.

first: Shingo

last: Sato


title: Thymic Epithelial Cells  with Human T cell Leukemia Virus type 1 (HTLV-1) Infected T cell supernatant (CEM, CIB, C91PL)

overall_design: We used  thymic epithelial cell (TEC) treated with non-infected T cell supernatant (CEM) and TEC treated with infected T cell supernatant (CIB or C91PL). We analyze three independent samples (biological replicates) for each conditions (total 3 conditions) and also technical replicates using dye-swap. In total we use 4.5 slides with 4 array in each.

middle: R


title: Detection of lower levels of SNAP25 using multiple microarray systems and its functional significance in medulloblastoma

status: Public on Nov 13 2015

city: New Taipei

first: Chih-Cheng

last: Chien

address: No 2, Ln 59, Jian-Cheng Rd, Sijhih Dist

country: Taiwan

institute: Sijhih Cathay General Hospital

summary: Medulloblastoma (MB) is the most common pediatric malignant brain tumor and patients with a high-risk or recurrent MB respond poorly to current therapies, with higher related mortality. Potential molecules related to MB must be identified to develop targets for therapeutic development. In the present study, we compared MB microarray data obtained using different microarray systems and significant targets were selected by gene annotation and enrichment analysis. Genes for soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) annotated with the function “vesicle” were identified and one of these proteins, synaptosomal-associated protein 25 (SNAP25), had significantly lower expression levels in MB. In addition, SNAP25 was detected in a very low number of MB cells according to western blot analysis and immunohistochemical analyses of archived and formalin-fixed/paraffin-embedded human MB specimens. We found that SNAP25 could change the morphology and the chemotherapeutic effect of arabinofuranosyl cytidine (Ara-C) on SNAP25-expressing MB cells. In conclusion, the expression of SNAP25 is crucial for the dendrite formation and correlate to the targeted chemotherapy. The detection of SNAP25 expression in MB cells may be essential for the chemotherapeutic application of Ara-C.

overall_design: In the present study, various MB microarray data were extracted and compared. Significant genes that had similar expression patterns in MB according to different microarray systems were selected following gene annotation. Enrichment analysis of the gene set was also performed to elucidate the biological pathways and processes that are affected in patients with MB. Archived and formalin-fixed/paraffin-embedded human MB specimens were also used to validate the significant candidates. A crucial molecular pathway related to MB was identified by this whole-genome survey.

first: Chi-jung

last: Huang

first: Chia-long

last: Lee

first: Chih-yi

last: Liu

first: Shih-hung

first: Jia-woei

last: Hou

first: Yi-hou

last: Chen

first: Chih-cheng

first: Chih-ming

last: Ho

first: Wen-cheng

last: Lo

first: Kun-long

last: Hung


title: porcine T cells : colostral T cells vs blood T cells

city: Kyoto

first: Ryo

last: Inoue

address: 1-5, Hangi-cho, shimogamo

institute: Kyoto Prefectural University

summary: CD8 single positive T cells and CD4/CD8 double positive T cells were sorted from porcine colosrum and blood by using a cell sorter. Transcriptional profiles was compared between colostral and blood T cells.

overall_design: Two comparisons: colostral CD8 single postive T cells vs blood CD8 single positive T cells, and colostral double positive T cells vs blood double T cells. Biological replicates;  colostrum and blood from two sows

first: R

first: S

last: Ogawa


title: Microbiota regulate the ability of lung dendritic cells to induce IgA class switch recombination and generate protective GI immune responses

city: New York

first: Gaurav

last: Pandey

state: New York

address: 1 Gustave L. Levy Place, Box 1498

department: Genetics and Genomic Sciences

institute: Icahn School of Medicine at Mount Sinai

summary: Analyses of gene expression between CD103+ lung DCs, CD24+ lung DCs and CD64+ lung macrophages in Specific pathogen free (SPF) and germ free (GF) mice. Hypothesis tested was that the IgA class switching function of lung DCs is regulated by genes differentially expressed in GF mice compared to SPF mice. Results obtained provide important insights into the mechanisms of IgA induction by lung DCs

overall_design: Total RNA was obtained from flow sorted, lung CD103+ DCs, CD24+ lung DCs and CD64+ lung macrophages from SPF and GF mice

first: Saurabh

last: Mehandru


title: Comparasion between MCF7-NIK overexpressing cells, MCF7-control cells and MCF7-NIK depleted cells

city: México

first: Vilma

middle: Araceli

last: Maldonado

state: Distrito Federal

address: Periferico  4809

department: Investigacion

country: Mexico

institute: INMEGEN

summary:
Analysis of differentially expressed genes in MCF7 cancer cells transfected with an expression vector containing the ORF of NIK,  a shRNA of NIK  and a control shRNA.  Transient transfections were performed in triplicates .
We use micorarrays to elucidate the machanisms by which NIK regulates stem cells biology

overall_design: Three groups were analyzed in triplicate each. The First  group was MCF7 group· transfected with an expression vector that overexpress NIK, other group was MCF7 cells transfected with a shRNA to inhibit NIK and the last group was transfected with a shRNA to inhibit luciferase expression.

first: Karla

middle: I

last: Vázquez

first: Jorge

last: Meléndez

first: Patricia

last: Piña

first: Gustavo

last: Martínez

first: Luis

last: Jiménez

first: Laura

last: Muñoz

first: Javier

last: Torres

first: Carolina

last: González

first: Marco

last: Velasco-Velázquez

first: Sonia

last: Pérez-Tapia

first: Eduardo

last: Arreola

first: Federico

last: Ávila


title: Gene expression analysis of hematopoietic stem progenitor cells from AGO2 knock out mice.

first: Chozha Vendan

last: Rathinam

state: NY

address: 701 W 168th street

department: Genetics & Development

institute: Columbia University Medical Center

summary: Hematopoietic stem cells (HSCs) are capable of both self-renewing throughout the lifetime of an organism and differentiating into all lineages of the blood system. A proper balance between quiescence and proliferation is critical for the self-renewal and functions of HSCs.  To identify the functions of the slicer endonuclease Argonaute (Ago) 2 in the physiology of HSCs, we generated Ago2Hem-KO mice, that are deficient for Ago2 in HSCs and in their progeny. Our analysis indicated that Ago2 deficient HSCs show increased quiescence and reduced entry to proliferation. To understand molecular mechanisms that are deregulated in Ago2 deficient hematopoietic stem and progenitor cells (HSPCs), we isolated Lin-Sca1+c-Kit+ (LSK) cells from control and Ago2 deficient mice and performed microarray analysis using the Illumina's MouseWG-6 v2.0 Expression BeadChip platform.

overall_design: Total RNA was obtained from lineage- Sca1+ c-Kit+ (LSK) cells of control and Ago2 deficient mice.

first: Chozha

middle: V

first: Masahiro

last: Nakagawa


title: Topaz1, a germ cell specific factor essential for male meiotic progression.

status: Public on Nov 10 2015

city: Jouy-en-Josas

first: Jouneau

last: Luc

address: Domaine de Vilvert

country: France

institute: INRA

summary: Testicular gene expression changes with loss of Topaz1

overall_design: Total RNA was extracted from 15 or 20 dpp of WT or Topaz1-/- (KO) mouse testis (C57Bl6), There were 3 biological repeats by conditions.

first: Alix

last: Luangpraseuth-Prosper

first: Elodie

last: Lesueur

first: Luc

last: Jouneau

first: Eric

last: Pailhoux

first: Corinne

last: Cotinot

first: Beatrice

last: Mandon-Pepin


title: Gene expression profiling of E18.5 FoxD1 Cre;Dicer and control embryonic kidneys

status: Public on Nov 04 2015

city: New York City

first: Dr. Yu Leng

last: Phua

address: 1 Gustave L. Levy Pl

summary: The aim of this study is to address the functional role of miRNAs in the FoxD1+ renal stroma progenitors and derivatives during embryonic kidney development. To achieve this, we generated transgenic mice that lack miRNAs in the renal stroma lineage (FoxD1 Cre;Dicer), and performed a microarray analysis on E18.5 whole kidneys to determine the transcriptional changes.

overall_design: 3 litters of E18.5 FoxD1 Cre;Dicer and control littermate kidneys were used for the microarray analysis. Each litter consists of kidneys pooled from 2 embryos per genotype for the RNA extraction.

first: Yu

middle: L

first: Jacqueline

last: Ho


title: Gene expression profiling of E15.5 FoxD1 Cre;Dicer and control embryonic kidneys

summary: The aim of this study is to address the functional role of miRNAs in the FoxD1+ renal stroma progenitors and derivatives during embryonic kidney development. To achieve this, we generated transgenic mice that lack miRNAs in the renal stroma lineage (FoxD1 Cre;Dicer), and performed a microarray analysis on E15.5 whole kidneys to determine the transcriptional changes.

overall_design: 3 litters of E15.5 FoxD1 Cre;Dicer and control littermate kidneys were used for the microarray analysis. Each litter consists of kidneys pooled from 2 embryos per genotype for the RNA extraction.


title: Genome-wide analysis of gene expression in mouse pancreas tumors

status: Public on Nov 20 2015

city: Houston

first: Valerie

last: LeBleu

state: TX

address: 1881 East Road

institute: MDACC

summary: Genetically engineered mice developed spontaneous pancreas cancer (Pdx-Cre;LSL-KRASG12D;P53Mut). Mice were also engineered to develop similar spontaneous pancreas cancer without Twist or Snail (conditional gene knockout). The pancreas tumors were harvested and analysed for gene expression profiles comparisons.

overall_design: Total RNA was isolated from the pancreas tumors of 2 mice with wild-type Twist and Snail, from 2 mice without Twist expression in the pancreas, and from 2 mice without Snail expression in the pancreas.


title: Molecular function of Lhx1 in early mouse development (BeadChip)

status: Public on Oct 19 2015

city: Oxford

first: Arne

middle: Wyndham

last: Mould

state: Oxfordshire

address: Warneford Hospital

department: Psychiatry

institute: Oxford University

summary:
Expression profiling of wild-type and Lhx1 null mouse definitive endoderm cultures using Illumina whole genome mouse V2 arrays.
The hypothesis tested was that Lhx1 regulates gene expression of definitive endoderm and anterior mesendoderm genes

overall_design: Lhx1 null and littermate control wild-type embryonic stem cells were generated from blastocyst outgrowths.  Total RNA was obtained from four wild-type ES cell clones and four Lhx1 null ES cell clones differenitated for five and six days with  Activin-A to enrich for defintive endoderm cells and hybridized to Illumina WG6_V2 arrays

first: I

last: Costello

first: S

last: Nowotschin

first: X

last: Sun

first: A

last: Hadjantonakis

first: E

last: Bikoff

last: Robertson


title: Variation in the immune and inflammatory responses during pneumonia, an important role of the host and pathogen genetic background

status: Public on Oct 28 2015

city: Leicester

first: Peter

middle: W

last: Andrew

address: University Rd

department: Infection, Immunity and Inflammation

institute: University of Leicester

summary: Analysis of the pulmonary gene expression in two mouse strains BALB/cOlaHsd (BALB/c) and CBA/CaOlaHsd (CBA/Ca) after infection with various serotypes of Streptococcus pneumoniae. BALB/c mice show high resistance to infection with S. pneumoniae strain D39 (serotype 2), while CBA/Ca mice are highly susceptible. The lung samples of BALB/c and CBA/Ca were collected at 6h post-infection with one of the tested pneumococcal serotypes (2, 3, 6B and 19F) and for control animals (PBS-treated). Additionally lung samples from both mouse strains were collected at 12h and 24h post-infection with pneumococcal strain D39. The lists of differentially expressed genes were created by the comparison of infected versus PBS-treated animals and infected BALB/c versus infected CBA/Ca for each pneumococcal strain. The tested hypotheses were: 1) infection with S. pneumoniae will change the pulmonary transcriptomes of both mouse strains 2) The pulmonary gene expression will be specific for mouse strains and for the pneumococcal serotype and 3) The change in the pulmonary gene expression will associate with future clinical outcome of infection or with the type of observed inflammatory responses.

overall_design: Total RNA obtained from lung tissue from BALB/cOlaHsd and CBA/CaOlaHsd mouse strains (Harlan) post intranasal infection with Streptococcus pneumoniae of various serotypes (2, 3, 6B and 19F) dose 5.0E06 CFU or PBS-treated animals

first: Magda

middle: S

last: Jonczyk

first: Nicolas

last: Sylvius

first: Vitor

last: Fernandes

first: Laura

last: Escudero


title: Hypoxia-induced miR-210 modulates gene expression in response to acute peripheral ischemia.

status: Public on Oct 23 2015

city: Milan

first: Fabio

last: Martelli

address: via morandi 30

institute: IRCCS-Policlinico San Donato

summary: Peripheral Artery Disease is caused by the restriction or occlusion of arteries supplying the leg. Better understanding of the molecular mechanisms underpinning tissue response to acute and chronic ischemia is urgently needed to improve therapeutic options. The aim of this study is understanding miR-210 regulation and role in a mouse model of hindlimb ischemia.

overall_design: To investigate miR-210 function, mice were injected with a miR-210 complementary LNA-oligonucleotide (anti-miR-210). Then, the left femoral artery was dissected in order to induce unilateral hindlimb ischemia. Mice were sacrified 3 days later and gene expression profiles of gastrocnemius muscles were obatained.

first: Germana

last: Zaccagnini

first: Pasquale

last: Fasanaro

first: Biagina

last: Maimone


title: Gene expression profiling of FOXP1-silenced diffuse large B-cell lymphoma (DLBCL) cell lines

status: Public on Oct 27 2015

city: Kubang Kerian

first: Kah Keng

last: Wong

state: Kelantan

address: School of Medical Sciences, Health Campus

department: Department of Immunology

country: Malaysia

institute: Universiti Sains Malaysia

summary: To identify differentially expressed genes regulated by FOXP1 in DLBCL cells via gene expression profiling of GCB-DLBCL (DB, K422) and ABC-DLBCL (OCI-Ly3, HBL-1) cell lines treated with siRNA targeting FOXP1 or non-silencing siRNA control.

overall_design: Two GCB-DLBCL (DB, K422) and two ABC-DLBCL (OCI-Ly3, HBL-1) cell lines were each treated separately with two independent siRNA oligonucleotides targeting FOXP1 (siFOXP1_308, siFOXP1_309) or non-silencing siRNA (siCtrl). Biological replicates derived from three independent experiments were obtained, RNA-extracted and subsequently hybridized into a human microarray platform for gene expression profiling.

first: Philip

middle: J

last: Brown

first: Kah

middle: K

first: Suet

last: Felce

first: Linden

last: Lyne

first: Hayley

last: Spearman

first: Elizabeth

last: Soilleux

first: Lars

last: Pedersen

first: Michael

middle: B

last: Møller

first: Tina

last: Green

first: Duncan

last: Gascoyne

first: Alison

middle: H

last: Banham


title: Molecular characterization of systemic sclerosis esophageal pathology identifies inflammatory and proliferative signatures

city: Lebanon

first: Tammara

last: Wood

state: NH

address: WTRB 674

department: Biomedical Data Science

institute: Dartmouth Medical School

summary: Esophageal involvement in patients with systemic sclerosis (SSc) is common, but tissue-specific pathological mechanisms are poorly understood. Fibrosis in the esophagus is thought to disrupt smooth muscle function and lead to esophageal dilatation, but autopsy studies demonstrate esophageal smooth muscle atrophy and the absence of fibrosis in the majority of SSc cases. Molecular characterization of SSc esophageal pathology is lacking. Herein, we perform a detailed characterization of SSc esophageal histopathology and molecular signatures at the level of gene expression. Esophageal biopsies were prospectively obtained during esophagogastroduodenoscopy in 16 consecutive SSc patients and 7 subjects without SSc. Upper and lower esophageal biopsies were evaluated for histopathology and gene expression. Individual patient’s upper and lower esophageal biopsies showed nearly identical patterns of gene expression. Similar to skin, inflammatory and proliferative gene expression signatures were identified suggesting that molecular subsets are a universal feature of SSc end-target organ pathology. The inflammatory signature was present in biopsies without high numbers of infiltrating lymphocytes. Molecular classification of esophageal biopsies was independent of SSc skin subtype, serum autoantibodies and esophagitis. Proliferative and inflammatory molecular gene expression subsets in tissues from patients with SSc may be a conserved, reproducible component of SSc pathogenesis. The inflammatory signature is observed in biopsies that lack large inflammatory infiltrates suggesting that immune activation is a major driver of SSc esophageal pathogenesis.

overall_design: Gene expression was measured in upper and lower esophageal biopsies from 16 patients with and 7 subjects without SSc.

first: Monique

last: Hinchcliff

first: Guang

middle: Y

last: Yang

first: Viktor

last: Martyanov

middle: A

first: Barbara

last: Jung

last: Whitfield

first: Darren

last: Brenner

first: John

last: Varga

first: Rowland

last: Chang

first: Ikuo

last: Hirano

first: Mary

last: Carns

first: Matthew

last: Mahoney

first: Sofia

last: Podlusky


title: Gene expression profiling of colorectal normal mucosa, adenoma and adenocarcinoma tissues

status: Public on Oct 16 2015

city: Beijing

first: Xiaoyu

last: Shi

address: Chao Yang District Pan Jia Yuan Nan Li No.17

department: Cancer Institute (Hospital)

institute: Peking Union Medical College and Chinese Academy of Medical Sciences

summary: Approximately two decades ago, Vogelstein and Fearon proposed the adenoma-carcinoma sequence of sporadic CRC development and illustrated the accumulation of genetic alterations during the stepwise progression, thereby providing a guideline for clinical practice. Although the detection and excision of precancerous lesions could prevent colorectal cancer and reduce mortality, 6% of adenomas will ultimately develop into colorectal cancer. Thus, this genetic model for colorectal tumorigenesis may not completely reflect the complex essence of the disease and whether the mode of initiation of the events in the multistep progression affects the outcome of CRC is still unknown. In this study, mRNA and miRNA expression profiling was performed with human colorectal tissues, including normal mucosa, adenoma and adenocarcinoma. Then, an integrated approach was adopted to establish the regulatory interaction networks that were correlated with colorectal carcinogenesis. Finally, a 55-gene signature whose expression was down-regulated in precancerous lesions compared to normal tissue was identified as a potential early indicator of CRC survival. The results suggested that genes related to immunity and homeostasis played a critical role in protection against adenoma initiation and that the altered molecular events that influence colorectal cancer prognosis may be set in an early, precancerous stage.

overall_design: Four types of human colorectal tissues were selected by colonoscopic resection or colorectal surgery, including 12 normal mucosae, 21 low-grade adenomas (mild or moderate atypical hyperplasia), 30 high-grade adenomas (severe atypical hyperplasia or carcinoma in situ) and 25 adenocarcinomas. Gene expression profiling analysis of these samples was performed using Agilent 4x44K human whole genome gene expression microarray (G4112F).

first: Yueming

last: Zhang

first: Bangrong

last: Cao

first: Ning

last: Lu

first: Lin

last: Feng

first: Xuebing

last: Di

first: Naijun

last: Han

first: Chenghua

last: Luo

first: Guiqi

last: Wang

first: Shujun

last: Cheng

first: Kaitai


title: Global gene expression changes associated with miR-375 overexpression

status: Public on Oct 21 2015

city: Toronto

first: Victor

last: Tron

state: ON

address: 30 Bond St.,Rm 2-040b CC Wing

department: Laboratory Medicine and Pathobiology

institute: St. Michael's Hospital, University of Toronto

summary: To determine gene expression changes assoicated with miR-375 overexpression, MCC26 (merkel cell carcinoma cell line) were transfected with 5nM of miR-375 mimics. RNA was isolated 72 hours post-transfection and subjected to gene expression analysis using Agilent human 4X44 whole genome microarrays. Analysis was performed on microarray data corresponding to two independent experiments (n=2)

overall_design: 5nM of mirVana miR-375 or neg cntrl mimics (Invitrogen) was transfected into MCC26 cells using lipofectamine 2000. Cells apporimately 30% confluence when transfected and RNA was collected 72 hours post-transfection. miR-375 overexpression was confirmed, and then RNA was subjected to whole genome microarray analysis using Agilent human 4x44 chip. Experiment was repeated (n=2).

first: Karan

last: Abraham


title: Opposing roles of JNK and p38 in regulating lymphangiogenesis and invasiveness in melanoma

status: Public on Oct 01 2015

city: vienna

first: Peter

last: Petzelbauer

address: Währinger Gürtel

department: Dermatology

country: Austria

institute: Medical University Vienna

summary: In primary melanoma, the amount of VEGF-C expression and lymphangiogenesis predict the probability of metastasis to sentinel nodes, but conditions boosting VEGF-C expression in melanoma are poorly characterized. By comparative mRNA expression analysis of a set of 22 human melanoma cell lines, we found a striking negative correlation between VEGF-C and MITF expression, which was confirmed by data mining in GEO databases of human melanoma Affymetrix arrays. Moreover, in human patients, high VEGF-C, and low MITF levels in primary melanoma significantly correlated with the chance of metastasis. Pathway analysis disclosed the respective JNK- and p38/MAPK activities as being responsible for the inverse regulation of VEGF-C and MITF. Predominant JNK signaling results in a VEGF-Clow/MITFhigh phenotype, these melanoma cells are highly proliferative, show low mobility and are poorly lymphangiogenic. Predominant p38 signaling results in a VEGF-Chigh/MITFlow phenotype, corresponding to a slowly cycling, highly mobile, lymphangiogenic and metastatic melanoma.

overall_design: Comparative mRNA expression analysis of a set of 22 human melanoma cell lines

first: Emmi

last: Puujalka


title: Tumor-Host Signaling Interaction Reveals a Systemic, Age-Dependent Splenic Immune Influence on Tumor Development [LLC tumor bearing mice]

status: Public on Oct 12 2015

city: Mountain View

first: Afshin

last: Beheshti

state: CA

address: Moffett Blvd

institute: NASA Ames Research Center

summary: The concept of age-dependent host control of cancer development raises the natural question of how these effects manifest across the host tissue/organ types with which a tumor interacts, one important component of which is the aging immune system. To investigate this, changes in the spleen, an immune nexus in the mouse, was examined for its age-dependent interactive influence on the carcinogenesis process. The model is the C57BL/6 male mice (adolescent, young adult, middle-aged, and old or 68, 143, 551 and 736 days old respectively) with and without a syngeneic murine tumor implant. Through global transcriptome analysis, immune-related functions were found to be key regulators in the spleen associated with tumor progression as a function of age with CD2, CD3, CCL19, and CCL5 being the key molecules involved. Surprisingly, other than CCL5, all key factors and immune-related functions were not active in spleens from non-tumor bearing old mice. Our findings of age-dependent tumor-spleen signaling interaction suggest the existence of a global role of the aging host in carcinogenesis. Suggested is a new avenue for therapeutic improvement that capitalizes on the pervasive role of host aging in dictating the course of this disease.

overall_design: For genome-wide expression profiling of spleen tissue from Lewis lung carcinoma (LLC) tumor bearing mice, 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 mice, 7 from young adult mice , 6 from middle-aged mice, and 10 from old mice 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) < 0.05 that resulted in a list of significant genes.

first: Justin

last: Wage

first: J

middle: T

last: McDonald

first: Clare

last: Lamont

first: Michael

last: Peluso

first: Philip

last: Hahnfeldt

first: Lynn

last: Hlatky


title: Tumor-Host Signaling Interaction Reveals a Systemic, Age-Dependent Splenic Immune Influence on Tumor Development [control mice]

overall_design: For genome-wide expression profiling of spleen tissue from wild-type non-tumor bearing C57BL/6 mice, 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, 10 spleen samples from adolescent mice, 10 from young adult mice , 10 from middle-aged mice, and 10 from old mice 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) < 0.05 that resulted in a list of significant genes.


title: Tumor-Host Signaling Interaction Reveals a Systemic, Age-Dependent Splenic Immune Influence on Tumor Development

status: Public on Oct 13 2015

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

overall_design: Refer to individual Series


title: Effects of residual metals contained in single-wall carbon nanotubes on cellular response in rat alveolar macrophages and human alveolar epithelial cell line

status: Public on Oct 02 2015

city: Tsukuba

first: Makiko

last: Fukuda

state: Ibaraki

address: West,16-1 onogawa, Tsukuba, Ibaraki,305-8569,JAPAN

institute: Technology Research Association for Single Wall Carbon Nanotubes

summary: Gene expression profiling of the rat alveolar macrophages (NR8383) and human alveolar epithelial cell line (A549) exposure to iron-enriched pristine single-wall carbon nanotubes (SWCNTs) or their purified SWCNTs were employed to gain insights at the transcriptional level.

sample_organism:
Homo sapiens
Rattus norvegicus

platform_organism:
Homo sapiens
Rattus norvegicus

overall_design: Two kinds of singlewall carbon nanotubes (SWCNTs), CNT-1 or CNT-2 induced gene expression in rat alveolar macrophages and human alveolar epithelial cell line were measured at 24 hours exposure to doses of 0.1mg/mL. The experiments were performed using control for each experiment (n=4).

first: Katsuhide

last: Fujita


title: Thymic Epithelial Cells with Human T cell Leukemia Virus type 1 (HTLV-1) Infected T cell supernatant

city: Rio de Janeiro

first: Leandra

middle: Linhares

last: Lacerda

address: Av. Brasil 4365 pav 26 sala 506 Manguinhos

institute: Oswaldo Cruz Foundation


title: Prenatal ethanol exposure alters adult hippocampal VGLUT2 expression with concomitant changes in promoter DNA methylation, H3K4 trimethylation and miR-467b-5p levels

status: Public on Oct 09 2015

city: Woolloongabba

first: Suyinn

last: Chong

state: QLD

address: 37 Kent St

institute: Mater Research Institute - The University of Queensland

summary:
Background
Maternal consumption of alcohol during pregnancy is associated with a range of physical, cognitive and behavioural outcomes in the offspring which are collectively called fetal alcohol spectrum disorders. We and others have proposed that epigenetic modifications, such as DNA methylation and post-translational histone modifications, mediate the effects of prenatal alcohol exposure on gene expression and, ultimately, phenotype. Here we use an inbred C57BL/6J mouse model of early gestational ethanol exposure equivalent, developmentally, to the first 3-4 weeks of pregnancy in humans to examine the long-term effects on gene expression and epigenetic state in the hippocampus.

Results
Gene expression analysis in the hippocampus revealed sex- and age-specific up-regulation of solute carrier family 17 member 6 (Slc17a6), which encodes vesicular glutamate transporter 2 (VGLUT2). Transcriptional up-regulation correlated with decreased DNA methylation and enrichment of histone H3 lysine 4 trimethylation, an active chromatin mark, at the Slc17a6 promoter. In contrast to Slc17a6 mRNA levels, hippocampal VGLUT2 protein levels were significantly decreased in adult ethanol-exposed offspring, suggesting an additional level of post-transcriptional control. MicroRNA expression profiling in the hippocampus identified four ethanol-sensitive microRNAs, of which miR-467b-5p was predicted to target Slc17a6. In vitro reporter assays showed that miR-467b-5p specifically interacted with the 3’ UTR of Slc17a6, suggesting that it contributes to the reduction of hippocampal VGLUT2 in vivo. A significant correlation between microRNA expression in the hippocampus and serum of ethanol-exposed offspring was also observed.

Conclusions
Prenatal ethanol exposure has complex transcriptional and post-transcriptional effects on Slc17a6 (VGLUT2) expression in the mouse hippocampus. These effects are observed following a relatively moderate exposure that is restricted to early pregnancy, modelling human consumption of alcohol before pregnancy is confirmed, and are only apparent in male offspring in adulthood. We propose that altered epigenetic and microRNA-mediated regulation of glutamate neurotransmission in the hippocampus contributes to the cognitive and behavioural phenotypes observed in fetal alcohol spectrum disorders. Our findings also support the idea that circulating microRNAs could be used as biomarkers of early gestational ethanol exposure and/or hippocampal dysfunction.

overall_design:
Hippocampus, male, 12 weeks old.
Two groups, ethanol-exposed (EtOH) and Control, with 6 replicates per group.

first: Christine

last: Zhang


title: Transcriptional regulation of hepatic target genes during thyrotoxicosis and recovery

city: Singapore

first: Paul

middle: Michael

last: Yen

address: 8 College Road

department: Cardiovascular & Metabolic disorder Program

country: Singapore

institute: Duke-NUS Graduate Medical School Singapore

summary: Transcriptome analysis showed that most positively- and negatively-regulated T3 target genes were altered by either acute or chronic stimulation, with few regulated both acutely and chronically. In addition, several target genes showed differential temporal expression patterns not only between acute vs. chronic stimulation, but also after T3 withdrawal.

overall_design: Mice received daily intraperitoneal injection of L-T3 (liothyronine; Sigma) for 14 days, and were sacrificed 6 hours after a single L-T3 injection (acute T3) as well as 6 hours after multiple L-T3 injections (chronic T3). In parallel groups, mice treated with L-T3 for 14 days were maintained untreated for another 10 days and sacrificed on days 10 after the last (14th) L-T3 injection (T3 withdrawal). Animal experiments were performed as two subsets, with two baseline groups. Acute T3 effect was evaluated relative to “Baseline A”, whereas chronic T3 and its withdrawal were compared to “Baseline B”.

middle: M

first: Kenji

last: Ohba

first: Khee-Shing

last: Leow

first: Chia

middle: G

last: Sng

first: Sujoy

last: Ghosh


title: Mesenchymal cancer cell-stromal crosstalk promotes niche activation, epithelial reversion and metastatic colonization

status: Public on Nov 21 2015

city: London

first: Ilaria

last: Malanchi

address: 1 Midland Rd,

institute: The Francis Crick Institute

summary: The experiment was design to address the intrinsic differences between metastatic cancer stem cells in the primary tumour and during metastatic colonization in the mouse mammary gland tumour model MMTV-pyMT.

overall_design: Total RNA was prepared from the  indicated cancer cells freshly isolated, stained and  FACS sorted either from primary tumours or from lungs upon intravenous injection of cancer cells.

first: Yaiza

last: del Pozo Martin

first: Danielle

last: Park

first: Erik

last: Sahai


title: Identification of genes characteristic of Zfp423-expressing perivascular cells in mouse epididymal adipose tissue

city: Durham

first: Rana

last: Gupta

state: North Carolina

address: Carmichael Building, 300 North Duke St.

department: Duke Molecular Physiology Institute

institute: Duke University

summary: Committed perivascular preadipocytes were genetically labelled in transgenic mice expressing GFP under the control of the locus (BAC) for Zfp423, a gene controlling preadipocyte determination.  The overall goal was to identify genes differentially expressed between perivascular (PDGFRbeta+) GFP+ cells and perivascualar (PDGFRbeta+) GFP-  cells from mouse epididymal adipose tissue.

overall_design: Adipose stromal vascular fraction from epididymal fat of 5 week-old male Zfp423-GFP mice was labeled with fluorophore-conjugated antibodies recognizing PDGFRbeta, CD31, and CD45.  Pdgfrbeta+; CD45/CD31- (herein Lin-) cells were then separated on the basis of GFP expression. GFP+ and GFP- from the PDGFRbeta+ Lin- perivascular population were collected by FACS into separate tubes. Triplicate biological samples were collected for RNA extraction and  Illumina analysis.

first: Karen

last: MacPherson

first: Lavanya

last: Vishvanath


title: FOXO1 regulates a subset of thyroid hormone target genes

first: Brijesh

middle: Kumar

last: Singh

address: CVMD Level-8, 8 College Road

department: Cardiovascular and Metabolic Disorders Program

institute: Duke-NUS Gradiate Medical School

summary: Transcriptome analysis of thyroid hormone activated genes in euthyroid, hyperthyroid and FOXO1 knockdown hyperthyroid mouse liver tissues showed that FOXO1 regulates transcription of thyroid hormone-induced genes. FOXO1 and THRB1-ChIP-seq analysis suggested that the regulation required binding of either FOXO1 or THRB1 or both in a genes subset specific manner.

overall_design: Total RNA obtained from liver tissues of euthyroid, hyperthyroid and FOXO1 knockdown hyperthyroid mouse. Mouse were treated with triiodothyronine (T3) for 3 days to make them hyperthyroid. FOXO1 was knocked down in liver using hydrodynamic tail vein injection of FOXO1 siRNA as previously described (Singh et al. J Biol Chem. 2013;288(42):30365-72).

first: Madhulika

last: Tripathi


title: Expression profiling of murine inner-ear hair cells

city: Tel Aviv

first: Ran

last: Elkon

address: Ramat Aviv

department: Human Genetics

country: Israel

institute: Tel Aviv University

summary: Murine auditory and vestibular epithelia were separated into hair-cells (HCs), epithelial non-sensory cells (ENSCs) and non-epithelial cells (NECs) by flow cytometry. Gene expression levels were recorded in independent triplicates from the sorted cells using Illumina whole genome expression microarrays

overall_design: Total RNA from 3 cell types (HCs, ENSCs, NECs) isolotaed from 2 inner-ear organs (cochlea and vestibular system)

first: Rani

first: Ronna

last: Hertzano


title: Inter-individual variability in gene expression profiles in human hepatocytes and comparison with HepaRG cells

city: RENNES

first: rogue

last: alexandra

address: 2 av du professeur leon bernard

institute: inserm

summary:
Basal transcriptomic profiling of primary human hepatocytes and HepaRG cells
We have analysed basal gene expression profiles in 6 primary human hepatocytes (2 technical replicates) and in 2 HepaRG cell passages (3 batches, 4 technical replicates)

overall_design: 6 primary human hepatocytes donors and 2 HepaRG cell passages

first: Alexandra

last: Rogue


title: Genome-wide identification and analysis of mRNA and miRNA expression in MEFs, ESCs, and iPSCs

city: Minneapolis

first: Nobuaki Kikyo

email: kikyo001@umn.edu, hiraih@umich.edu

address: 2001 6th St SE

department: Genetics, Cell Biology and Development

institute: University of Minnesota

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


title: The influence of LepR tyrosine site mutations on mouse ovary development and related gene expression changes

status: Public on Sep 30 2015

city: Shanghai

first: Zhaogui

last: Sun

state: Shanghai

address: Road Xietu 2140

institute: Shanghai Institute of Planned Parenthood Research

summary:
The mRNA profile in ovaries of mouse strain (denoted Y123F) with artificially mutated leptin receptors (LepR), with phenylalanine (F) substitution for all 3 tyrosine (Y) residues within exon 18 of LepR of Tyr985, Tyr1077 and Tyr1138 with wild types of the same litter as the control. Y123F mice also manifested obesity, hyperphagia, hyperleptinemia, hyperinsulinemia and impairment in glucose tolerance, but less pronounced than in db/db mice.

Leptin exerts many biological actions, such as on metabolism, reproduction, etc., through binding to and activating LepR, which is expressed mainly in many brain regions. To better understand different roles of downstream signaling pathways, Y123F mice, which expressed mutant leptin receptors with phenylalanine (F) substitution for 3 tyrosines (Y) ---Tyr985, Tyr1077 and Tyr1138, was generated. The body weight and abdominal fat depots of Y123F homozygous mice (HOM) were higher than that of wild mice (WT), and HOM ovaries were atrophic and the follicles developed abnormally, though HOM ovaries did not exhibit polycystic phenotypes. Moreover, Y123F HOM adult had no estrous cycle and blood estrogen concentration remained stable at a low level below detection limit of 5 pg/ml. LepR expression in HOM ovaries was higher than in WT ovaries. Scanned through cDNA microarrays, 41 genes were increased, and 100 genes were decreased in mRNA levels, in HOM vs. WT ovaries; and many signaling pathways were evaluated to be involved significantly. The data of 19 genes were validated by real-time quantitative PCR, most of which were consistent. So Y123F HOM mice were suggested as a new animal model of PCOS when research mainly emphasizes on metabolism disorders and anovulation, but not on the polycystic phenotype. Meanwhile, through the model, we found that JAK-STAT and hormone biosynthesis pathways were involved in the follicular development and ovulation disorders caused by LepR deficiency in ovaries, though not having excluded its indirect actions from brain.

overall_design: To compare the mRNA expression differences of ovaries between LepR mutant Y123F mice and wild type mice from the same litter.

first: Zhichao

last: Kuang

first: Xiaoyu

last: Tu


title: Patients with Chronic Kidney Disease with Acute Exercise Before and After Kidney Transplant

city: Tucson

first: Dawn

last: Coletta

state: AZ

address: 1501 N. Campbell Ave

department: Medicine

institute: UNIVERSITY OF ARIZONA

summary: The post kidney transplant period is associated with insulin resistance partly due to corticosteroids. Patients on minimal corticosteroid therapy receiving tacrolimus (FK506) for immunosuppression also are affected. FK506 inhibits calcineurin in immune cells. Skeletal muscle calcineurin, which also might be inhibited, mediates exercise-induced transcription leading to more insulin-sensitive muscle. This study was performed to determine if gene transcription responses to exercise are lower in patients awaiting kidney transplant or 3 months post-transplant on a low-steroid, FK506 protocol.

overall_design: Transplant patients (n=5, age 52±2) had glucose clamps (Rd) and an exercise bout with muscle biopsies (Bx) pre- and 30 minutes post-exercise for gene expression analysis (Agilent-014850 4x44K Whole Human Genome Microarrays) before and after kidney transplant.

first: Lawrence

last: Mandarino

first: Harini

last: Chakkera


title: Genome-wide gene expression analysis on remote non-infarcted myocardium after treatment with Valsartan in a mouse model of myocardial infarction

city: Milano

first: Gualtiero

middle: Ivanoe

last: Colombo

address: Via Carlo Parea, 4

institute: Centro Cardiologico Monzino IRCCS

summary:
To find which genes were significantly modulated by Valsartan in non-infarcted left ventricle, 4 weeks after coronary artery ligation, and to correlate emerging modulated pathways with histology and cardiac magnetic resonance (CMR) imaging. The goal was to validate the estimation of the systolic dysfunction and of the regions preserved by pharmacological treatment performed with a CMR index.
Title of the associated submitted paper: Evaluation of left ventricle function by regional fractional area change (RFAC) in a mouse model of myocardial infarction secondary to Valsartan treatment.  Abstract:  Purpose: Left ventricle (LV) regional fractional area change (RFAC) measured by cardiac magnetic resonance (CMR) allows the non-invasive localization and quantification of the extent of myocardial infarction (MI), and could be applied to assess the effectiveness of pharmacological or regenerative therapies. Here we investigate the ability of RFAC to identify regional dysfunction and discriminate the effect of pharmacological treatment with valsartan, a selective antagonist of angiotensin II type 1 receptor, in a model of MI.  Methods: C57BL/6N mice, undergoing coronary artery ligation, were divided into two groups: untreated (MI) or treated with Valsartan (MI+Val). Sham-operated mice were used as a control. Cardiac dimensions and function were assessed at baseline, 24 hours, 1 and 4 weeks post surgery by CMR and echocardiography. At sacrifice histology and whole-genome gene expression profiling were performed.  Results: RFAC was able to detect significant differences between treatment groups whereas the global ejection fraction was not. RFAC showed greater loss of contractility in remote non-infarcted myocardium in MI group than in MI+Val group. Consistently, in the same region MI+Val mice showed reduced myocyte hypertrophy, fibroblast proliferation, and fibrosis and modulation of target genes; in addition, left atrium volumes, appendage length and duct contractility were preserved.  Conclusion: In this study, RFAC effectively estimated the degree of systolic dysfunction and discriminated the regions preserved by pharmacological treatment. RFAC index is a promising tool to monitor changes in LV contractility and to assess the effectiveness of therapeutic regimens in clinical settings.

overall_design: MI was induced by left anterior descending (LAD) coronary artery ligation. Mice were randomized to 2 experimental groups: infarcted only animals (MI, n=6) and treated animals with Valsartan 1 mg/Kg/die in drinking water (MI+Val, n=5). As control of surgery procedure, sham operated mice underwent thoracotomy without LAD coronary artery ligation (n=6). For transcriptome analysis,  4 weeks after surgery hearts were perfused with PBS and the portion of the non-infarcted wall corresponding to the posterior and inferior sectors was collected in RNAlater (Life Technologies) and stored at -80°C.

first: Elisa

last: Bono

first: Luca

last: Piacentini

middle: I


title: Multi-platform assessment of transcriptional profiling technologies utilizing a precise probe mapping methodology (Affymetrix_Gene1.0) (exon analysis)

status: Public on Sep 28 2015

city: St. Louis

first: Jinsheng

last: Yu

state: MO

address: 660 S. Euclid Ave.

department: Genetics

institute: Washington University School of Medicine

summary: We present a more extensive and yet precise assessment to elucidate differences and similarities in performance at numerous aspects including signal range, sensitivity to fold-change, and fidelity with TaqMan qRT-PCR. There were three levels of data examined: entire data sets, data derived from gene name annotation oriented subset of 15442 RefSeq genes, and data derived from transcript pattern defined subset of 7034 RefSeq genes.  Our results showed a fair degree of overall correlation between all 6 platforms evaluated; but, to varying degrees, two RNA-seq protocols outperformed three of the microarray platforms in most categories.  Notably, a fourth microarray platform, Agilent, was comparable, or marginally superior, to the RNA-seq protocols within these same assessments.  Furthermore, 3 platforms (Agilent and two RNA-seq methods) demonstrated over 80% concordance with the gold standard TaqMan assay in terms of fold-change accuracy.  Our study suggests that the use of transcript patterns can enhance a number of the observed cross-platform correlations, indicating a potential usefulness for similar evaluations.

overall_design: The study assessed differences and similarities in performance at numerous aspects including signal range, sensitivity to fold-change, and fidelity with TaqMan qRT-PCR. There were three levels of data examined: entire data sets, data derived from gene name annotation oriented subset of 15442 RefSeq genes, and data derived from transcript pattern defined subset of 7034 RefSeq genes.

first: Richard

middle: D

last: Head


title: mRNA profiling at various time points during adipocyte differentiation of human Multipotent Adipose-Derived Stem (hMADS) cells

city: Vienna

first: Michael

last: Karbiener

address: Benatzkygasse 2-6 / G

department: Global Pathogen Safety

institute: Takeda

summary: human Multipotent Adipose-Derived Stem (hMADS) cells constitute a highly interesting in vitro model to study adipocyte development in vitro. Using a chemically defined medium with several hormonal inducers, these cells can be differentiated into mature adipocytes within ~2 weeks. To gain a global view on transcripts which are induced or downregulated at various stages of adipocyte differentiation, we performed a microarray analysis with samples harvested at the stem cell stage, the terminally differentiated stage, as well as various time points in between.

overall_design: Analysis used proliferating hMADS cells as control sample for comparison to hMADS cells at confluence and at various time points after induction of adipocyte differentiation. Biological replicates: 2, indepently grown and harvested. All hybridizations were repeated with reversed dye assignment (dye-swap) as technical replicates.

first: Marcel

last: Scheideler


title: mRNA profiling of SNEV (PRPF19) knockdown in human adipocyte precursor cells at early stage (day 3) of adipocyte differentiation

summary: Aging and premature aging are both accompanied by loss of subcutaneous adipose tissue mass in human and in mouse model of progeria. This may be due to reduced differentiation or deficiency in DNA damage repair (DDR) factors. Here we investigated the role of SNEV (Senescent Evasion factor; pre-mRNA processing factor 19) which was implicated in DDR and senescence evasion, in adipogenic differentiation of human adipose derived stem cells (ASCs).

overall_design: Two-condition experiment, ASCs at day 3 after induction of adipocyte differentiation, comparison of cells transfected with an siRNA targeting SNEV (siSNEV) to cells transfected with a control siRNA (siC). Biological replicates: 2, indepently grown and harvested. On each array, one biological replicate of siSNEV-transfected cells was directly compared to one biological replicate of siC-transfected cells (serving as reference sample). All hybridizations were repeated with reversed dye assignment (dye-swap) as technical replicates.


title: Translational compensation of genomic instability in neuroblastoma

status: Public on Sep 24 2015

city: Trento

first: Erik

last: Dassi

state: TN

address: Via Sommarive, 9

department: CIBIO

institute: University of Trento

type: Genome variation profiling by genome tiling array


title: Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models

status: Public on Sep 17 2015

city: Newark

first: Antonina

last: Mitrofanova

state: NJ

address: 65 Bergen Street, Rm 923B

institute: Rutgers University


title: Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (II)

summary: Analysis of the transcriptome of allografted mouse tumors after treatment with rapamycin and PD0325901. Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) were induced and their tumors removed to generate allograft lines by implanting a 1.5 mm3 tumor fragment in the subcutaneous space of athymic nude mice. Allografted NPK tumors were allowed to grow until they reached a volume of 1 cm3, at which moment they were randomly assigned to either vehicle (Veh) or combination therapy using rapamycin and PD0325901 (RAPPD). Allografted mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) during five consecutive days (Allo SHORT). Mice were euthanized in the fifth day 6 hours after having received the last treatment and the tumors were harvested and snap frozen for subsequent molecular analysis.

overall_design: Total RNA obtained from prostate tumors/tissues. Prostate tumors/tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion). Total RNA was amplified and labelled for subsequent microarrays hybridization using the Illumina TotalPrep RNA Amplification Kit.

first: Alvaro

last: Aytes

first: Cory

last: Abate-Shen

first: Andrea

last: Califano


title: Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (I)

summary: Analysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and  PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis.


title: Genome-wide identification and analysis of mRNA expression in  MEFs, ESCs, and iPSCs

first: Nobuaki Kikyo

state: MN

summary: Microarray analysis of mRNA—RNA was prepared from ESCs (CGR8 and CJ7), MEFs, and iPSCs with a PureLink RNA Mini Kit (Life Technologies). Initial sample quality control was performed with a Nanodrop 8000 (Thermo Scientific). RNA samples with an optical density (OD) 260/280 ratio and an OD 260/230 ratio of 1.8 or higher were used. Samples with an RNA Integrity Number of 7.5 or greater measured with a LabChip Caliper GX (Perkin Elmer) were applied to an Illumina TotalPrep-96 RNA Amplification Kit (Life Technologies) to generate biotinylated and amplified RNA. With this kit, 300 ng of total RNA was first processed in a reverse transcription reaction. The cDNA then underwent second-strand synthesis and cleanup to serve as a template for in vitro transcription, which generated biotinylated antisense RNA copies of each mRNA. Samples went through another round of quality control with the Nanodrop 8000 and were applied to Illumina MouseWG-6 v2.0 Beadchips (#BD-201-0202). After overnight hybridization, the Beadchips were washed, stained, and scanned using an Illumina iScan Beadarray Reader. The obtained data were analyzed with an Illumina Genome Studio.

overall_design: In the study presented here, compared the genome-wide expression patterns of mRNAs in MEFs, ESCs, and various iPSCs to identify mRNAs that were potentially involved in the LIF-independence. iPSCs in this study: O-retro-iPSCs-LIF(+), O-lenti-iPSCs-LIF(+), M3O-lenti-iPSCs-LIF(+), and M3O-lenti-iPSCs-LIF(-). O-retro-iPSCs-LIF(+) was established by transduction of the OSKM genes into MEFs with the pMXs-IP retroviral vector and maintained with LIF. O-lenti-iPSCs-LIF(+) was prepared with lentiviral Oct4 and retroviral Sox2, Klf4, and c-Myc (SKM) to maintain the expression of the Oct4 transgene in iPSCs as a control for the two M3O-based iPSC types. M3O-lenti-iPSCs-LIF(+) was the same as O-lenti-iPSCs-LIF(+) except that M3O was used instead of Oct4. M3O-lenti-iPSCs-LIF(-) was the same as M3O-lenti-iPSCs-LIF(+) except that LIF was omitted during establishment and maintenance.

first: Hiroyuki

last: Hirai

first: Nobuaki

last: Kikyo


title: Effects of Sorcin (SRI) overexpression on mouse pancreatic beta cells transcriptome

status: Public on Sep 09 2015

first: Alice

last: Marmugi

address: Du cane Road

institute: Imperial College London

summary: Pancreatic beta cells use electrical signals to couple changes in blood glucose concentration to insulin release via extracellular calcium (Ca2+) influx. Sorcin (SRI) is a Ca2+-binding protein whose overexpression in cardiomyocytes rescues the abnormal contractile function of the diabetic heart.

overall_design: In order to investigate the role of sorcin in regulating mouse pancreatic beta cell transcriptome, transgenic mice were generated on a C56BL/6 background permitting inducible overexpression of SRI cDNA with the TetOn-system specifically in beta cells. Animals bearing ten copies of the SRI transgene (SRI-tg10), and littermate controls, were fed a high fat diet (60% fat, HFD) and exposed to doxycycline in the drinking water (500mg/L) from 4 weeks onwards. Microarray analysis were performed using total RNA from isolated pancreatic islets of 8-week-old mice.

first: Marmugi

last: Alice

first: Guy

last: Rutter

first: Isabelle

last: Leclerc

first: Dilair

last: Baban

first: Helen

last: Lockstone


title: ATF3 is a central regulator of interferon-beta and interferon-stimulated genes during the innate immune response

status: Public on Sep 07 2015

city: Bonn

first: Joachim

last: Schultze

state: NRW

address: Carl-Troll-Strasse 31

department: Genomics and Immunoregulation

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

summary: This study shows that in the absence of Atf3, primary mouse macrophages display significantly greater basal and PRR-inducible IFNβ expression. This regulation appears to be directly on the level of Ifnb1 transcription mediated by ATF3 binding proximal to the Ifnb1 promoter under basal condition. The ATF3 expression was demonstrated to be type I IFN-inducible in both human and mouse immune cells. A subset of 36 genes downstream of IFNAR signalling were modulated in an ATF3-dependent manner.The regulation of IFN responses by ATF3 had significant relevance on in vitro viral infection. Together these findings demonstrate that ATF3 is an important regulatory handbrake that limits the magnitude of IFN responses on multiple levels; basal Ifnb1 expression; PRR-inducible IFNβ; and the expression of specific ISGs.

overall_design: 12 samples

first: L

last: Labzin

first: S

middle: V

last: Schmidt

middle: L

last: Masters

first: R

last: Stahl

first: D

last: Lütjohann

first: J

first: E

last: Latz

last: De Nardo


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

status: Public on Sep 10 2015

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. We previously employed Illumina microarrays to determine if transplanted human salisphere cells exert a paracrine stimulatory effect on recipient mouse SGs. Results of this array unveiled a large cohort of immuneresponse genes unregulated following human salisphere transplantation. In order to negate this immune response and unveil any true paracrein stimulatory effects, we performed autologous transplantation of salispheres from NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) mice, the same model employed in our first microarray study, in the irradiated SGs of NSG mice.

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 NSG salispheres.

last: Zwart


title: Sixty-nine samples obtained from surgical excision with overall survival.

status: Public on Sep 25 2015

city: Beijing

first: Ning

last: An

address: NO.17 Pan Jiayuan Nan Li, Chao Yang District

institute: Chinese academy of medical sciences

summary: To further development of our gene expression signature for survival prediction, we conducted expression profiles of lung squamous carcinoma samples with overall survival information as the training cohort.

overall_design: Sixty-nine LSQC samples with OS information were obtained from patients at the Cancer Institute and Hospital, Chinese Academy of Medical Sciences

first: An

last: Ning

first: Tong

last: run


title: Total and polysomal gene expression profiling of MYCN-amplified Neuroblastoma cell lines

first: Erik

last: Dassi

summary: Total and polysomal mRNA expression levels have been profiled on 13 MYCN-amplified Neuroblastoma cell lines

overall_design: Extracted mRNA for each cell lines has been hybridized on Agilent Whole Human Genome Microarray 4x44K

first: Viktoryia

last: Sidarovich

first: Paola

last: Scaruffi

first: Gianpaolo

last: Tonini

first: Alessandro

last: Quattrone


title: Genome-wide analysis of blood, spleen and lung expression of C57BL/6 mice subjected to Burkholderia pseudomallei infection

status: Public on Sep 02 2015

first: Krzysztof

last: Potempa

address: The Ridgeway

institute: National Institute for Medical Research (NIMR)

summary: Melioidosis, a severe human disease caused by the bacterium Burkholderia pseudomallei, has a wide spectrum of clinical manifestations ranging from acute septicaemia to chronic localized illness or latent infection. Mice were intranasally infected with either high or low doses of B. pseudomallei to generate either acute, chronic or latent infection and host blood and tissue transcriptional profiles were generated. Acute infection was accompanied by a homogeneous signature associated with induction of multiple innate immune response pathways, such as IL10, TREM1 and IFN-signaling, largely found in both blood and tissue. The transcriptional profile in blood reflected the heterogeneity of chronic infection and quantitatively reflected the severity of disease. Comparison of these mouse blood datasets by pathway and modular analysis with the blood transcriptional signature of patients with melioidosis showed that many genes were similarly perturbed, including IL10, TREM1 and IFNsignaling, revealing the common immune response occurring in both mice and humans.

overall_design: Total RNA obtained from isolated blood, lung and spleen of C57BL/6 mice subjected to either acute or chronic infection by Burkolderia compared to uninfected controls.

first: Anne

last: O'Garra

first: Greg

last: Bancroft

first: Laura

last: Conejero

first: Christine

last: Graham

first: Natasha

last: Spink

first: Simon

last: Blankley

first: Rugnapa

last: Pankla

first: Prasong

last: Khaenan

first: Jacques

last: Banchereau

first: Virginia

last: Pascual

first: Damien

last: Chaussabel

first: Ganjana

last: Lertmenongkolchai


title: Analysis of the effects of Bmx deficiency on Angiotensin II -induced cardiac hypertrophy

status: Public on Sep 21 2015

city: Helsinki

first: Riikka

last: Kivelä

address: Haartmaninkatu 8

country: Finland

institute: University of Helsinki and Wihuri Research Institute

summary: We show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression

overall_design: Angiotensin II or NaCl were infuced for two weeks into wild-type and Bmx-deficient mice to induce cardiac hypertrophy

first: Tanja

last: Holopainen

first: Kari

last: Alitalo


title: Deciphering Cell-Specific Responses to Oncogenic Stress in the Liver

status: Public on Sep 20 2015

city: Houston

first: Brian

last: York

state: Texas

address: One Baylor Plaza

department: Molecular and Cellular Biology

country: USA

institute: Baylor College of Medicine

summary: Each cell type responds uniquely to stress and fractionally contributes to global and tissue-specific stress responses. Hepatocytes, liver macrophages (MΦ), and sinusoidal endothelial cells (SEC) play functionally important and interdependent roles in adaptive processes such as wound healing, obesity, and tumor growth. Although these cell types demonstrate significant phenotypic and functional heterogeneity, their distinctions enabling disease-specific responses remain understudied. To address this, we developed a strategy for simultaneous isolation and quantification of these liver cell types based on antigenic cell surface marker expression in response to DEN and found that while there was only a marginal increase in hepatocyte number, MΦ and SEC populations were quantitatively increased. Global gene expression profiling of hepatocytes, MΦ and SEC identified characteristic gene “fingerprints” that define each cell type and their distinct physiological or oncogenic stress signatures. Integration of these cell-specific gene fingerprints with available hepatocellular carcinoma (HCC) patient microarray data demonstrates that the hepatocyte-specific response strongly correlates with the human HCC gene expression profile. Liver-specific MΦ and SEC gene signatures demonstrate significant alterations in inflammatory and angiogenic gene regulatory pathways, which may impact the hepatocyte response to oncogenic stress. Further validation confirms alterations in components of two key pathways, AP-1 and p53, that have been previously associated with HCC onset and progression. Our data reveal unique gene expression patterns that serve as molecular “fingerprints” for the cell-centric responses to pathologic stimuli in the distinct microenvironment of the liver. The technical advance highlighted in this study provides an essential resource for assessing hepatic cell-specific contributions to oncogenic stress, information that could unveil previously unappreciated molecular mechanisms for the cellular crosstalk that underlies the development of hepatic cancer.

overall_design: Total RNA isolated from each specific cell type (Hepatocyte (PH), Sinusoidal Endothelial Cell (SEC), and Macrophage (MP)) pooled from 3-4 DEN-treated mice and compared to their untreated counterparts.

first: Kathrina

last: Marcelo

first: Fumin

last: Lin

first: Kimal

last: Rajapakshe

first: Erin

last: Stashi

first: Adam

last: Dean

first: Naomi

last: Gonzales

first: Cristian

last: Coarfa

first: Anthony

middle: R

last: Means

first: Lauren

middle: C

last: Goldie


title: Genetic profiling of HNC cell lines

status: Public on Sep 01 2015

city: chicago

first: Tanguy

last: Seiwert

state: IL

address: 900 E. 57th street

institute: University of Chicago

summary: We performed gene expression profiling of 39 head and neck cancer cell lines and 1 hela cell line, and classified them based on previous classification of head and neck squamous cell tumors from patients

overall_design: We performed gene expression profiling of 39 head and neck cancer cell lines and 1 hela cell line.

first: Zhixiang

last: Zuo

first: Michaela-Kristina

last: Keck

first: Arun

last: Khattri


title: Imatinib induces mesenchymal stem cell-mediated drug resistance in BCR-ABL–positive acute lymphoblastic leukemia

first: Xiaoping

last: Sun

address: 2130 Westholcombe Blvd, LSP12.3014

department: Laboratory Medicine

institute: The University of Texas MD Anderson Cancer Center

summary:
One of the main objective of this study is to characterize Imatinib induced MSCs-mediated resistance evolution in BCR-ABL+ ALL.
Tyrosine kinase inhibitor (TKI) Imatinib (IM) is used as a frontline therapy for BCR-ABL–positive (BCR-ABL+) acute lymphoblastic leukemia (ALL). However, resistance to IM therapy develops rapidly in a substantial proportion of treated patients, and the molecular mechanisms underlying the resistance are poorly understood. In this study, we identified a novel cascade of consequential events that are initiated by IM, which traverse through mesenchymal stem/stromal cells (MSCs) to leukemic cells, and lead to IM resistance. Our data showed that MSCs exposed to IM were decreased in their stemness and acquired a new functional status that enabled the formation of leukemic cell niches. These MSCs had increased expression of genes encoding chemo-attractants, adhesion molecules, and pro-survival stimulant growth factors. We found that BCR-ABL+ leukemic cells persistently exposed to IM were able to switch from BCR-ABL–driven signaling to growth factor–driven signaling for survival, and this switch was reversible. Blocking both the BCR-ABL–driven pathway and the growth factor–driven JAK pathway effectively eradicated the leukemic cell niches. Our findings illustrate TKI-induced, MSC-mediated drug resistance, suggesting an effective way to eliminate this type of drug resistance in patients with BCR-ABL+ ALL.

overall_design: Gene expression signatures were compared from triplicate samples of MSCs that were either treated with vehicle or imatinib for 32, 64 and 96 hours.

first: Saradhi

last: Mallampati


title: Fatty Acid Amide Hydrolase regulates peripheral B cell receptor revision, polyreactivity and B1 cells in lupus

first: Simanta

last: Pathak

address: 3605 Cullen Blvd

institute: University of Houston

summary: FAAH expresson is induced in Sle2 splenic B cells. Increased peripheral B cell receptor revision, or selective peripheral expansion of BCR-revised B-cells, may lead to systemic autoimmunity, and FAAH is a lupus susceptibility gene that could regulate this process in Sle2 mice.

overall_design:
To determine the gene expression profile in peripheral B cells from Sle2 mice (compared to B6 mice), we isolated splenic B cells from these two strains of mice, extracted the total mRNA and performed the microarray analysis
Please note that Sle2 mouse is a congenic strain that harbors the Sle2 locus from Chromosome 4 of NZM2410 strain in a B6 background and Sle2 is the name of the lupus susceptibility locus.

first: Kirthi

last: Kumar

first: Hasna

last: Kanta

first: Ferdicia

last: Carr-Johnson

first: Jie

last: Han

first: Anna

last: Bashmakov

first: Lionel

last: Faure

first: Huihua

last: Ding

first: Kamala

last: Vanarsa

first: Shaheen

last: Khan

first: Quan-Zhen

last: Li

first: Kent

last: Chapman

first: Edward

middle: K

last: Wakeland

first: Chandra

last: Mohan


title: Decorin and EphA2 mediate Carcinoembryonic Antigen Cell Adhesion Molecule 1-L inhibition of colorectal cancer metastasis

status: Public on Sep 19 2015

city: Montreal

first: Gregory

last: VOISIN

state: Québec

address: 6825 rue Saint Denis

institute: Atelerics

summary: Objective  We have previously shown that expression of the CEACAM1 long isoform (CC1-L) in metastatic colorectal cancer (CRC) cells results in significant inhibition of liver metastasis via Chemokine (C-C motif) Ligand 2 (CCL2) and Signal Transducer and Activator of Transcription 3 (STAT3) signaling.  Yet, despite recent advances in identifying molecules involved in the CC1-L inhibition of metastasis, much remains to be elucidated regarding the molecular mechanisms orchestrating this pathway.   Design We performed an untargeted transcript profiling and a phosphokinase screen between CC1-L-expressing and non-expressing (CT) CRC cells.  Identified targets were validated in vitro and in vivo for their involvement in signaling and invasion or metastasis.  We validated our conclusions in CRC patient cohorts for time to metastasis development and long-term survival.  Results Untargeted transcript profiling revealed high Decorin (Dcn) expression in CC1-L-expressing cells versus CT cells.  Decorin was detected at the peri-endothelial layers of large blood vessels and in liver stellate cells.  In metastatic lesions, it was expressed in pericyte-like cells covering capillary endothelium.  Phosphokinase differential screening revealed reduced Ephrin type-A receptor 2 (EphA2) expression and activity in CC1-L- versus CT-expressing cells.  Treatment of CT cells with recombinant Dcn led to decreased migration and invasion and decreased EphA2-mediated Erk and Akt signaling.  CRC patients exhibiting high CC1 and DCN expression, in combination with low EPHA2 expression, benefit from longer 10-year survival than those with high EPHA2 expression.    Conclusion  CC1-L expression in poorly differentiated CRC inhibits liver metastasis through increased Decorin expression and EphA2-mediated signaling.

overall_design: Quadriplicate samples of each mouse colon cancer cell lines (control cells versus those expressing either short or long isoform of CEACAM1) have been used for RNA extraction

first: Azadeh

last: Arabzadeh

first: Kevin

last: McGregor

first: Sharang

last: Ghavampour

first: Valérie

last: Breton

first: Lauren

last: VanderKraak

first: Uri

last: Akavia

first: Celia

last: T Greenwood

first: Suleyman

last: Ergün

first: Nicole

last: Beauchemin