title: Gene expression changes induced by overexpression of IDH1mut and treatment with 2HG in the sorted mouse bone marrow cells

status: Public on Jun 01 2016

city: Hannover

first: Anuhar

last: Chaturvedi

address: Cral Neuberg Strasse-1

department: Hematology, Hemostasis, Oncology and Stem Cell Transplantation

institute: Hannover Medical School

summary: Mutations in the enzymes IDH1 and IDH2 have been identified in a wide variety of tumors like glioma, chondrosarcoma, thyroid cancer, lymphoma, melanoma, and in acute myeloid leukemia. Mutated IDH1/2 produces the metabolite 2-hydroxyglutarate (2HG), which interferes with epigenetic regulation of gene expression, and thus may promote tumorigenesis.

overall_design: HoxA9 immortalised bone marrow cells from C57BJ/6 mice were tranduced with either empty vector or pSF91-IDH1wt-IRES-EGFP, or pSF91-IDH1mut-IRES-GFP and transplanted in irradiated recipient mice. Alternatively, HoxA9 immortalised cells transduced with empty vector transplanted mice were treated with R-2HG at dose of 1mg/day for four weeks. Four weeks after transplantation/treatment GFP+ cells were sorted from mouse bone marrow, from which total RNA ws extracted and subjected to microarray analysis.

first: Michael

last: Heuser


title: Adverse Health Effects of Cylindrospermopsin in Laboratory Animal (Mouse) Studies in Multi-day Study using Affymetrix Array

status: Public on Jun 24 2016

city: RTP

first: Neil

last: Chernoff

state: NC

address: 109 TW Alexander Dr

country: USA

institute: US EPA

summary: The goal of this project was to determine gene expression changes in the liver at different times post treatment with the common freshwater cyanobacterial toxin, cylindrospermopsin (CYN).  The liver is generally considered to be the primary target of this toxin and all the data has been derived from livers of exposed animals as well as concurrent controls.  Preliminary gene expression effects have been reported (Chernoff et al., 2010) and the current data extend the time course from 1 hour post exposure to 1-day post cessation of a 5-day period dosing period.

overall_design: Gene expression changes were determined in the livers of pregnant mice exposed to toxic levels of the cyanobacterial toxin, cylindrospermopsin.  Animals were exposed to a dose of CYN that elicited significant hepatic toxicity.  This multi-day study used tissue obtained 1-day, 2-days, 4-days, and 5-days after the initiation of a 5 consecutive day dosing regimen.  Toxicity data including gross observations, necropsy findings and clinical chemistry endpoints indicative of hepatic, renal and homeostasis functions were collected at the same time liver tissues for gene expression analysis were obtained.  Gene expression changes were analyzed on the GeneChip® Mouse Genome 430 2.0 Array.


title: Expression data from cultured fetal lung epithelium

status: Public on Jun 16 2016

city: Osaka

first: Katsumi

last: Fumoto

state: State...

country: Japan

institute: Osaka university

summary: Branching morphogenesis in lung development is regulate by growth factor signaling. Wnt signaling is one of the important singnaling pathway that is required for progenitor maintainance. In the presence of CHIR99021, an agonist for the beta-catenin pathway of Wnt signaling, specific group of genes are upregulated in cultured lung epithelium.

overall_design: RNAs were extracted from cultured epithelium and cDNAs were hybridized to Affymetrix microarrays.


title: The transcription factor BACH2 is required to establish immunosuppression within tumors

city: BETHESDA

first: PING

last: JIN

state: MD

address: 9000 ROCKVILLE PIKE

department: DTM

institute: CC/DTM/NIH

summary: Through a diversity of functional lineages, cells of the innate and adaptive immune system either drive or constrain immune reactions within tumors. Thus, while the immune system has a powerful ability to recognize and kill cancer cells, this function is often suppressed preventing clearance of disease. The transcription factor (TF) BACH2 controls the differentiation and function of multiple innate and adaptive immune lineages, but its role in regulating tumor immunity is not known. Here, we demonstrate that BACH2 is required to establish immunosuppression within tumors. We found that growth of subcutaneously implanted tumors was markedly impaired in Bach2-deficient mice and coincided with intratumoral activation of both innate and adaptive immunity but was dependent upon adaptive immunity. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-γ. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression. These findings demonstrate that BACH2 is a key component of the molecular programme of tumor immunosuppression and identify a new target for development of therapies aimed at reversing immunosuppression in cancer.

first: Rahul

last: Roychoudhuri

first: Robert

middle: L

last: Eil

first: David

last: Clever

first: Gautam

last: Mehta

first: Christopher

middle: A

last: Klebanoff

first: Madhusudhanan

last: Sukumar

first: Zhiya

last: Yu

first: Hui

last: Liu

first: Ping

last: Jin

first: Yun

last: Ji

first: Douglas

middle: C

last: Palmer


title: Systematic analysis of time resolved transcriptional signature of the cross-talk between HGF and IL-6 refines the role of Cxcl10 in hepatocyte proliferation control

city: Lübeck

first: Hauke

last: Busch

state: Schleswig-Holstein

address: Ratzeburger Allee 160

department: Lübeck Institute of Experimental Dermatology

country: Germany

institute: University of Lübeck

summary: Liver regeneration is characterized by a scheduled sequence of inner and intra-cellular signaling events. It starts with an initial inflammatory phase, followed by a period of rapidly proliferating hepatocytes and stopping abruptly when the liver mass is restored. The cytokines hepatocellular growth factor (HGF) and interleukin 6 (IL-6) play a pivotal role during this process with the former driving proliferation that is enhanced by the latter. While the individual importance of HGF and IL6 has been studied comprahensively the role of cross-talk in control of hepatic proliferation is jet largely unknown. To this end, we performed time-resolved transcriptional profiling of of murine hepatocytes stimulated with HGF and IL-6 indiviually as well as in combination. Thorough systematic investigation performing statistical analysis, mathematical formalization of cross-talk effects on the transcriptional level as well as gene-regulatory network inference revealed the transcriptional program of the cross-talk initiated by HGF and IL-6. Using the proliferation associated Hepcidin (Hamp) and Amphiregulin  (Areg) as marker genes for liver regeneration we perform exthensive in-silico experiments with the inferred gene-regulatory network for the identification of the most important players in regulation of the proliferation process. Among other genes, this predicted chemokine (C-X-C motif) ligand 10 (Cxcl10) as an important factor in the temporal regulation of proliferation. These predictions were validated by independent in vitro expression data as well as independent in vivo literature data. While Cxcl10 is known to be involved in liver regeneration, our study extend its role towards its temporal orchestration.

overall_design: Cells were stimulated with either 40 ng/ml rmHGF (all R&D Systems) or 40 ng/ml rhIL-6 alone or in combination. Cells were left untreated as unstimulated control. RNA from three biological triplicates was extracted at 0, 0.5, 2, 4, 8, 16, 24 and 32 hours after stimulation using the RNeasy Mini Plus Kit (Qiagen, Hilden, Germany).

first: Andreas

last: Hoppe

first: Sebastian

last: Vlaic

first: Nikola

last: Mueller

first: Svantje

last: Braun

first: Rene

last: Meyer

first: Sandra

last: Bonefas

first: Lorenza

last: D'Allesandro

first: Stephanie

last: Müller

first: Norbert

last: Gretz

first: Ursula

last: Klingmüller

first: Melanie

last: Boerries


title: Bhlha9 deficiency effect in limb bud

status: Public on May 31 2016

city: Tokyo

first: Takahide

last: Matsushima

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

department: Systems BioMedicine

institute: Tokyo Medical and Dental University

summary: Analysis of mouse limb bud (E10.5) lacking the Bhlha9 gene. Bhlha9 knockout mouse shows syndactyly and poliosis in the limb. This microarray results provides insight into the molecular mechanisms underlying Bhlha9 function in the limb development

overall_design: DNA microarray analysis was performed using Affymetrix mouse genome 430 2.0 array. RNA samples were obtained from the whole limb bud of the E10.5 wild-type and Bhlha9 knockout embryos described above. Total RNA (200 ng) was reverse-transcribed and biotinylated using the GeneChip 3′ IVT Express Kit (Affymetrix). The microarray data were summarized using the MAS 5.0 method.

first: K

last: Kataoka

first: T

first: H

last: Asahara


title: Expression profiling of 83 matched pairs of lung adenocarcinomas and non-malignant adjacent tissue

city: Dallas

first: Luc

last: Girard

state: TX

address: 5323 Harry Hines Blvd

department: Hamon Center for Therapeutic Oncology Research

institute: UT Southwestern Medical Center

summary:
Background: Non-small cell lung cancers (NSCLCs) consist of adenocarcinoma (ADC), squamous cell carcinoma (SCC) and other types. Since most NSCLCs are now diagnosed from small biopsies or cytology materials, classification is not always accurate. This is a problem as many therapy regimens and clinical trials are histology-dependent.

Specific Aim: To develop an RNA expression signature as an adjunct test for routine histo-pathological classification of NSCLCs.

Methods: A microarray dataset of resected ADC and SCC cases was used as the learning set for an ADC-SCC signature. The Cancer Genome Atlas (TCGA) lung RNAseq dataset was used as a validation set. Another microarray dataset of ADCs and non-malignant lung was used as the learning set for a Tumor-Nonmalignant signature. The classifiers were selected as the most differentially expressed genes and sample classification was determined by a nearest distance approach.

Results: We developed a 42-gene expression signature that contained many genes used in immunostains for NSCLC typing. Testing of the TCGA and other public datasets resulted in high accuracies (93-95%). We also observed that most non-malignant lung samples were classified as “adenocarcinomas”, so we added 20 genes to differentiate tumor from non-malignant lung. Together, the 62-gene signature can discriminate ADC, SCC, and non-malignant lung. Additionally, a prediction score was derived that correlated both with histologic grading and survival.

Summary and significance: Our histologic classifier provides a non-subjective method to aid in the pathological diagnosis of lung cancer and assist enrollment onto histology-based clinical trials

overall_design: 83 lung adenocarcinomas and 83 matched adjacent non-malignant lung were profiled on Illumina WG6-V3 expression arrays

first: Adi

last: Gazdar

first: Lam

last: Stephen

last: Wan

first: Wei

last: Zhang


title: Developmental nicotine mediated gene expression and epigenetic change effects on neuronal structure and behavior [gene expression]

status: Public on May 30 2016

city: New Haven

first: Marina

last: Picciotto

state: CT

address: 301 Cedar Street Congess place/YPI 4th floor

department: Psychiatry

institute: Yale University

summary:
Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior.
We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine

overall_design: mRNA prepared from dissected cortical tissue from mice that were administered saccharin or nicotine from conception through weaning at postnatal day 21 (pre- & postnatal period), and that were then allowed to remain nicotine-free until 3 months of age

first: Yonwoo

last: Jung

first: Christophe

middle: J

last: Heath

middle: R

last: Piccitto


title: Expression data from V156D matn1 knock-in mouse rib chondrocytes at 5 days

status: Public on May 26 2016

city: Newcastle Upon Tyne

first: Katarzyna

last: Pirog

address: Central Parkway

department: Institute of Genetic Medicine

country: United Kingdom

institute: Newcastle University

summary:
V156D matn1 mutation (homologous to the V194D matn3 mutation causing Multiple Epiphyseal Dysplasia (MED)) was introduced by gene targetting in order to evaluate the potential of matrilin-1 to be a novel chondrodysplasia based on domain homology and aminoacid conservation.
We used microarrays to analyse the differential expression of genes between wild type and mutant animals at day 5 (postnatal)

overall_design: Rib chondrocyes were extracted from 5 littermates of known genotype and RNA was extracted from the pooled smaple using the TriZOL method; the RNA integrity was checked using BioAnalyser, and hybridised to the Affymetrix Mouse Genome 430 2 Array

first: Peter

last: Bell

first: Leo

last: Zeff


title: Multiple levels of transcriptional regulation by PLZF in NKT cell development [Mouse430_2]

status: Public on May 24 2016

city: Chicago

first: Aiping

last: Mao

state: IL

address: 929 East 57th street

department: Pathology

institute: University of Chicago

summary:
To identify genes that require PLZF for their regulation in NKT cells, we compared the developmental stages of thymic NKT cells from wildtype and PLZF-deficient mice
The transcription factor PLZF is induced during the development of innate and innate-like lymphocytes to direct their acquisition of a T helper effector program, but the molecular mechanisms involved are poorly understood. Using biotinylation-based ChIP-seq and microarray analysis of both NKT and PLZF-transgenic thymocytes, we identified several layers of regulation of the innate-like NKT effector program: first, PLZF bound and regulated genes encoding cytokine receptors as well as homing and adhesion receptors; second, PLZF bound and activated T helper-specific transcription factor genes that in turn control T helper specific programs; finally, PLZF bound and suppressed the transcription of Bach2, a potent general repressor of effector differentiation in naive T cells. These findings reveal the architecture of the transcriptional program recruited by PLZF and elucidate how a single transcription factor can drive the developmental acquisition of a broad effector program.

overall_design: FACS-sorted stage 1 NKT (CD1d tetramer+ CD24low CD44- NK1.1-) from the thymi of Valpha14 TCR transgenic mice or PLZF-deficient Luxoid mutant mice that were also Valpha14 TCR transgenic and CD4SP (CD4+ CD8-) thymocytes from wildtype mice. 3 biological replicates of stage 1 NKT from PLZF-deficient Valpha14 transgenic mice, 2 biological replicates of stage 1 NKT from PLZF-sufficient Valpha14 transgenic mice and 2 biological replicates of CD4SP thymocytes from wildtype mice were compared using Mouse Genome 430 2.0 microarrays.

first: Albert

last: Bendelac

first: Michael

middle: G

last: Constantinides


title: Cross-talk of Il6 and HGF in the inflammation and proliferation response of primary murine hepatocytes

first: Hauke

last: Busch

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

overall_design: Refer to individual Series


title: Cancer associated-mesenchymal stem cells accelerate hepatocellular carcinoma progression though lncRNA-MUF-miR-34a-Snail1 axis

status: Public on Aug 30 2016

city: Beijing

first: Runsheng

last: Chen

address: 15 Datun Road, Chaoyang District

department: CAS Key Laboratory of RNA Biology

country: China

institute: Institute of Biophysics, Chinsese Academy of Sciences

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

summary: Recently, long noncoding RNAs (lncRNAs) have been implicated in diverse processes of hepatocarcinogenesis. However, the involvement of lncRNAs in the crosstalk between LC-MSCs microenvironment and HCC progression is still unknown. In this study, for the first time, we investigated the role of lncRNAs in the crosstalk between HCC cells and LC-MSCs. We found that LC-MSCs acted as a pivotal contributor to HCC metastasis, cancer stem cell maintenance and epithelial-mesenchymal transition (EMT).

overall_design: GFP-positive Huh7, SMMC-7721 and HepG2 cells were cocultured with LC-MSCs for 7 days, GFP-positive HCC cells were sorted with BD FACSAria II. Total RNA was extracted with Trizol and hybridized to custom lncRNA microarray

first: Xinlong

last: Yan

first: Dongdong

first: Fang

last: Wu

first: Jiayi

first: Yajing

last: Hao

first: Yinghui

last: Huang

first: Pingping

last: Zhu

first: Benyu

last: Liu

first: Jianjun

last: Luo

first: Guanling

first: Xinling

last: Yang

first: Jingfeng

last: Qian

first: Yanying

last: Wang

first: Xiaomin

first: Ying

last: Du

first: Zusen

last: Fan


city: Camden

first: Xiaoxin

middle: Luke

state: NJ

address: 403 Haddon Ave

institute: Coriell Institute for Medical Research

summary: Determine whether 4NQO treatment may modulate gene expression in mouse tongue. C57BL/6J mice were given 4NQO (100ug/ml in drink) for 8 weeks; Non-treated control samples were used for comparison.

overall_design: Negative control; 8-week 4NQO treated

first: David


title: The effect of antibiotic mediated gut microbiome perturbation on ileal gene expression in NOD mice.

status: Public on May 20 2016

city: New York

first: Thomas

middle: W

last: Battaglia

state: NY

address: 423 E 23rd Street

department: Medicine

institute: NYU School of Medicine

summary: The early life microbiome plays important roles in host immunological and metabolic development. Because type 1 diabetes (T1D) incidence has been increasing substantially in recent decades, we hypothesized that early-life antibiotic use alters gut microbiota that predisposes to disease.  Using NOD mice that are genetically susceptible to T1D, we examined the effects of exposure to either continuous low-dose antibiotics or pulsed therapeutic antibiotics (PAT) early in life, mimicking childhood exposures. We found that in mice receiving PAT, T1D incidence was significantly higher, microbial community composition and structure differed compared with controls. In pre-diabetic male PAT mice, the intestinal lamina propria had lower Th17 and T reg proportions and intestinal SAA expression than in controls, suggesting key roles in transducing the altered microbiota signals. PAT affected microbial lipid metabolism and host cholesterol biosynthetic gene expression. These findings show that early-life antibiotic treatments alter the gut microbiota and its metabolic capacities, intestinal gene expression, and T-cell populations, accelerating T1D onset in NOD mice.

overall_design: Microarray experiment was performed on RNA extracted from the terminal ileum of control; STAT; and PAT mice. (Female n=3/group; Male n=5/group except STAT n=3).

first: Alexandra

middle: E

last: Livanos

middle: U

last: Greiner

first: Pajau

last: Vangay

first: Wimal

last: Pathmasiri

first: Delisha

last: Stewart

first: Susan

last: McRitchie

first: Huilin

last: Li

first: Jennifer

last: Chung

first: Jiho

last: Sohn

first: Sara

last: Kim

first: Zhan

last: Gao

first: Cecily

last: Barber

first: Joanne

first: Sandy

last: Ng

first: Arlin

middle: B

last: Rogers

last: Sumner

first: Xue-Song

last: Zhang

first: Ken

last: Cadwell

first: Dan

last: Knights

first: Alexander

last: Alekseyenko

first: Fredrik

last: Backhed

first: Martin

last: Blaser


title: mRNA expression pattern of KrasG12D mice with acute pancreatitis compared with wild-type mice without acute pancreatitis

status: Public on May 14 2016

city: BEIJING

first: XIAFEI

last: HONG

state: BEIJING

address: DONGDAN SANTIAO

institute: Peking Union Medical College Hospital

summary: Transgenic KrasG12D mice can recapitulate pancreas intra-epithelial neoplasia (PanIN). Caerulein is a cholecystokinin analogue and induces acute pancreatitis when injected intra-abdominally. Caerulein-induced acute pancreatitis will accelerate PanIN progression in KrasG12D mice. We compared mRNA profile changes between KrasG12D mice with acute caerulein-induced pancreatitis and wild-type mice without acute pancreatitis.

overall_design: The experiment had two groups. Experiment group: KrasG12D mice with acute caerulein-induced pancreatitis (N=6). Three mice in experiment group received 1-week caerulein injection, and the other three mice received 2-week caerulein injection. All experiment group mice started to receive caerulein injection at 1-month of age, and were sacrificed at the last day of caerulein injection. Control group: wild-type mice without acute pancreatitis (N=6). The mice were sacrificed at 1.5-month of age. Whole pancreas tissue lysate samples were subjected to mRNA array assay.

first: YP

last: Zhao

first: WM

last: Wu

first: XF

last: Hong

first: J

first: Q

first: WZ

last: Wang

first: AY

last: Ye

first: W

last: Song

first: HM

last: Dai

first: XZ

first: F

first: L

last: You


title: Expression data of normal and under developed testes obtained from sexually mature rats.

status: Public on May 19 2016

city: Winnipeg

first: Alemu

middle: Regassa

last: Hunde

state: Manitoba

address: 12 Dafoe Road

department: Animal Science

country: Canada

institute: University of Manitoba

summary: Zucker (fa/fa) obese rats often have non-identical and different sized paired testes, leaving one testis underdeveloped. Our earlier study found that the underdeveloped testes have a selective decrease in docosapentaenoic acid (DPA, C22:5n-6), a dominant fatty acid in the testes

overall_design: Normal and under developed testes were collected from zuker rats, RNA isolated and gene expression was studied.

first: Jutika

last: Datar

last: Regassa

first: WooKyun

last: Kim

first: Miyoung

last: Suh


title: Modeling the time resolved transcriptional signature of time sequential stimulation with HGF and IL-6 in hepatocyte proliferation

first: Hauke

last: Busch

summary: Liver regeneration is characterized by a scheduled sequence of inner and intra-cellular signaling events. It starts with an initial inflammatory phase, followed by a period of rapidly proliferating hepatocytes and stopping abruptly when the liver mass is restored. The cytokines hepatocellular growth factor (HGF) and interleukin 6 (IL-6) play a pivotal role during this process with the former driving proliferation that is enhanced by the latter. While the individual importance of HGF and IL6 has been studied comprahensively the role of cross-talk in control of hepatic proliferation is jet largely unknown. To this end, we performed time-resolved transcriptional profiling of of murine hepatocytes stimulated with HGF and IL-6 indiviually as well as in combination. Thorough systematic investigation performing statistical analysis, mathematical formalization of cross-talk effects on the transcriptional level as well as gene-regulatory network inference revealed the transcriptional program of the cross-talk initiated by HGF and IL-6. Using the proliferation associated Hepcidin (Hamp) and Amphiregulin (Areg) as marker genes for liver regeneration we perform exthensive in-silico experiments with the inferred gene-regulatory network for the identification of the most important players in regulation of the proliferation process. Among other genes, this predicted chemokine (C-X-C motif) ligand 10 (Cxcl10) as an important factor in the temporal regulation of proliferation. These predictions were validated by independent in vitro expression data as well as independent in vivo literature data. While Cxcl10 is known to be involved in liver regeneration, our study extend its role towards its temporal orchestration.

overall_design: Cells were stimulated with either 40 ng/ml rmHGF (all R&D Systems) and 40 ng/ml rhIL-6 alone or in combination. Cells were left untreated as unstimulated control. RNA was extracted at 1,2,3,4,5,6,7,8,9,10,12,24 hours. Cells were treated with IL6 alone for the first 4 hours and then additionally with HGF from hours 4-24. Controls were taken at -5,0,4,8,12,24 hours.

first: Sebastian

last: Vlaic

first: Lorenza

last: D'Allesandro

first: Norbert

last: Gretz

first: Ursula

last: Klingmüller

first: Melanie

last: Boerries


title: Expression data from cell lines forced expressed PGC7/Stella

status: Public on May 13 2016

city: Setagaya

first: Keisuke

last: Oboki

state: Tokyo

address: 2-1-6 Kamikitazawa

department: Center for Medical Research Cooperation

institute: TOKYO METROPOLITAN INSTITUTE of MEDICAL SCIENCE

summary:
Global DNA hypomethylation and DNA hypermethylation of promoter regions—including tumor suppressor genes—are frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis.
We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression.

overall_design: RNA was extracted from NIH3T3 or B16F10 murine cell lines overexpressed PGC7/Stella and was hybridized on Affymetrix microarrays. We compared gene expression levels between control and PGC7/Stella-overexpressed cells. Microarray analysis was performed in NIH3T3 cells including two independent Stella-expressing NIH3T3 clones and a mixture of Stella-expressing NIH3T3 clones and in B16-F10 cells including three independent Stella-expressing B16-F10 clones.

first: Toshinombu

last: Nakamura

first: Kenji

last: Matsumoto

first: Hirohisa

last: Saito

first: Tohru

last: Nakano


title: MET Amplified Gastric Cancer Cell Lines +/- Crizotinib

city: houston

first: Rebecca

middle: Dunbar

last: Schroeder

state: Texas

address: 4425 stillbrooke dr

institute: MD Anderson Cancer Center

summary: MET amplification has been clinically credentialed as a therapeutic target in gastric cancer, but the molecular mechanisms underlying sensitivity and resistance to MET inhibitors are still not well understood. Using whole-genome mRNA expression profiling, we identified autophagy as a top molecular pathway that was activated by the MET inhibitor crizotinib in drug-sensitive human gastric cancer cells, and functional studies confirmed that crizotinib increased autophagy levels in the drug-sensitive cells in a concentration-dependent manner.  We then used chemical and molecular approaches to inhibit autophagy in order to define its role in cell death.  The clinically available inhibitor of autophagy, chloroquine, or RNAi-mediated knockdown of two obligate components of the autophagy pathway (ATG5 and ATG7) blocked cell death induced by crizotinib or RNAi-mediated knockdown of MET, and  mechanistic studies localized the effects of autophagy to  cytochrome c release from the mitochondria. Overall; the data reveal a novel relationship between autophagy and apoptosis in gastric cancer cells exposed to MET inhibitors. The observations suggest that autophagy inhibitors should not be used to enhance the effects of MET inhibitors in gastric cancer patients.

overall_design: 12 samples triplicate samples of SNU-5 and MKN45 +/- criztonib for 24 hours

middle: D

first: David

last: McConkey

first: Woonyoung

last: Choi


title: Immunization with Attenuated Equine Herpesvirus 1 Strain KyA Induces Innate Immune Responses that Protect Mice from Lethal Challenge

status: Public on May 07 2016

city: Shreveport

first: Seong

middle: K

state: Louisiana

address: 1501 Kings Highway

department: Microbiology and Immunology

institute: LSU Health Sciences Center

summary: Equine herpesvirus 1 (EHV-1) is a major pathogen affecting equines worldwide and causes respiratory disease, abortion, and in some cases, neurological disease. EHV-1 strain KyA is attenuated in the mouse and equine, whereas wild-type strain RacL11 induces severe inflammatory infiltration of the lung, causing infected mice to succumb at 4 to 6 days post-infection. Our previous results showed that EHV-1 KyA immunization protected CBA mice from pathogenic RacL11 challenge at 2 and 4 weeks post-immunization, and that the infection with the attenuated KyA elicits protective humoral and cell-mediated immune responses. To investigate the protective mechanisms of EHV-1 KyA by innate immune responses, CBA mice immunized with live KyA were challenged with RacL11 at various times post-vaccination. KyA immunization effectively protected CBA mice from RacL11 challenge at 1 to 7 days post-immunization. Immunized mice lost less than 10% of their preinfection body weight and rapidly regained body weight. Lung virus titers in EHV-1 KyA-immunized CBA mice were 1,000-fold lower at 2 days post-RacL11 challenge than lungs of non-immunized mice, which was indicative of accelerated virus clearance. Affymetrix microarray analysis revealed that IFN-γ and 16 antiviral interferon-stimulated genes (ISGs) were upregulated 3.1- to 48.2-fold at 8 h post-challenge in the lungs of RacL11-challenged mice that had been immunized with KyA. Murine IFN-γinhibited EHV-1 infection of murine alveolar macrophage MH-S cells and effectively protected mice against lethal EHV-1 challenge, suggesting that IFN-γ expression may be important in mediating protection elicited by KyA immunization. These results suggest that EHV-1 KyA can be used as a live attenuated EHV-1 vaccine as well as a prophylactic agent in horses.

overall_design: Lungs of CBA mice infected with EHV-1 KyA were harvested at 6 (KyA 6hpi), 8 (KyA 8hpi), and 12 (KyA 12hpi) hours post-infection (hpi). Lungs of CBA mice infected with EHV-1 RacL11 were harvested at 8 hpi (L11 8hpi).  CBA mice were immunized with EHV-1 KyA and challenged with RacL11 at 3 days post-immunization. Lungs were harvested at 8 h post-RacL11 challenge (KyA→L11 8hpi). CBA mice were immunized with heat-inactivated KyA (HI-KyA) and challenged with RacL11 at 3 days post-immunization. Lungs were harvested at 8 h post-RacL11 challenge (HI-KyA→L11 8hpi). Affymetrix microarray analyses were performed with infected mice lung RNA. Mock-infected lung RNAs were used as a control.

first: Akhalesh

last: Shakya

first: Dennis

last: O'Callaghan


title: Expression data from MeGRX232-OE and MeGRX360-OE Arabidopsis

status: Public on May 06 2016

city: Haikou

first: Mengbin

last: Ruan

address: Xueyuan Rd 4#

institute: Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Science

summary:
MeGRX232 and MeGRX360 are drought-inducible CC-type glutaredoxins in cassava. Overexpression of them in Arabidopsis caused different effects on plant growth.
We used microarray to identified the different expression genes in MeGRX232-OE and MeGRX360-OE Arabidopsis

overall_design: Experiments were performed as three biological repeats using cDNAs prepared independently from three individual homozygote lines that have been phenotypic analyzed in plant growth. The transgenic Arabidopsis plants that carried the pG1300 vector were used as control.

first: Yiling

last: Yang

first: Xin

last: Guo

first: Xue

last: Wang

first: Bin

first: Xiaoling

last: Yu

first: Peng

last: Zhang

first: Kaimian

last: Li

first: Ming

last: Peng


title: Examination of loss of Selenophosphate Synthetase 1 (SPS1) in mouse tissues and cells

city: Bethesda

first: Bradley

last: Carlson

address: 9000 Rockville Pike

institute: National Cancer Institute

summary: To examine the role of SPS1 in mammals, we generated a Sps1 knockout mouse and found that systemic SPS1 deficiency was embryonic lethal. Embryos were clearly underdeveloped by E8.5 and virtually reabsorbed by E14.5. Removal of Sps1 specifically in hepatocytes using Albumin-cre preserved viability, but significantly affected expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione-S-transferase omega 1. To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma cell line, which recapitulated changes in the glutathione system proteins. We further found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 has a role in supporting and/or sustaining cancer. In addition, the increased ROS levels observed in F9 SPS1/GLRX1 deficient cells were reversed and became more like those in F9 SPS1 sufficient cells by overexpressing mouse or human GLRX1. The results suggest that SPS1 is an essential mammalian enzyme with roles in regulating redox homeostasis and controlling cell growth.

overall_design: Gene expression analysis of liver tissue from 3 control and 3 hepatocyte-specific (Alb-Cre) SPS1 knockout mice taken at 3 months of age. Gene expression analysis of Control and SPS1 knockdown (shSPS1) mouse F9 cells. 3 replicates each.

first: Ryuta

last: Tobe

first: Jang

middle: H

last: Huh

first: Nadia

middle: P

last: Castro

first: Xue-Ming

last: Xu

first: Petra

last: Tsuji

first: Sang--Goo

last: Lee

first: Jeyoung

last: Bang

first: Ji-Woon

first: Young-Yun

last: Kong

first: Daniel

last: Beaglehole

first: Eileen

last: Southon

first: Harold

last: Seifried

first: Lino

last: Tessarollo

middle: S

last: Salomon

first: Ulrich

last: Schweizer

first: Vadim

middle: N

last: Gladyshev

first: Dolph

last: Hatfield

first: Byeong


title: Activation of Inflammation and Metabolic Networks in Age-related Thymic Involution.

city: Stanford

first: Kenneth

last: Weinberg

state: CA

address: 1291 Welch Road, G3040

department: Pediatrics

institute: Stanford University

summary: Genetic modeling of thymic involution has demonstrated the importance of individual inflammatory pathways affecting the thymic microenvironment, particularly thymic epithelial cells (TEC). We studied the pathogenic processes in chronological aging of the murine thymus. We used microarrays to elucidate the global gene expression and to identify a leading edge subset of age-associated genes in TEC. Analyses of the TEC transcriptome demonstrated altered expression associated with inflammatory and fatty acid metabolism.

overall_design: TECs were FACS sorted from different age of mice (6 weeks, 7 months and 15 months old)  for RNA extraction and hybridization on Affymetrix microarrays. Each cohort sample derived from 3-5 mice.

middle: I

first: Dullei

last: Min


title: DGAT1 regulates retinol-dependent regulatory T cell generation and mediates autoimmune encephalomyelitis

status: Public on May 03 2016

city: Atlanta

first: Kareem

last: Graham

state: GA

address: 615 Michael Street, Room 601

department: Physiology

institute: Emory University

summary: This file contains gene microarray data from FACS purified mouse memory phenotype CD4+ T cells (CD44hiCD45RBloCD25-), which were isolated from lymph node and spinal cord tissues of mice with experimental autoimmune encephalomyelitis (EAE), a widely studied model of human multiple sclerosis (MS). Memory phenotype CD4+ T cells infiltrating the CNS during EAE expressed high levels of mRNA for Dgat1 encoding diacylglycerol-O-acyltransferase-1 (DGAT1). We studied the biology of DGAT1 in EAE models and in assays of T cell differentiation and function.

overall_design: We analyzed transcript expression data from memory phenotype CD4+ T cells derived from draining lymph nodes (n=3) and spinal cords (n=3) of mice with acute symptomatic EAE .

middle: L


title: Expression data from mouse intestinal organoids II

status: Public on Apr 30 2016

city: Koto-ku

first: Ryoji

last: Yao

address: 3-8-31 Ariake

institute: The JFCR-Cancer Institute

summary:
APC inactivation is the early process in the tumorigenesis of colorectal cancer. We established organoid cultures from intestines of genetically modifeid mice harboring Apcfl/fl, Tacc3wt/wt or Apcfl/fl, Tacc3fl/fll and R26CreERT2 allele
We used microarrays to determine the alterations in intestinal stem cells in response to Tacc3 disruption.

overall_design: Organoids were treated with 4OHT to induce recombination of APC and Tacc3, and collected at 4 or 6 days after treatment. RNA were extracted and hybridization on Affymetrix microarrays.


title: DREAM in pain mechanisms in the trigeminal ganglia

status: Public on Apr 22 2016

city: Cantoblanco

first: Juan

middle: Carlos

last: Oliveros

state: Madrid

address: Darwin 3

country: Spain

institute: CNB, CSIC

summary: Expression of DREAM in dorsal root ganglia and spinal cord is related to endogenous control mechanisms of acute and chronic pain. In primary sensory trigeminal neurons high levels of endogenous DREAM protein are preferentially localized in the nucleus, suggesting a major transcriptional role. Here, we show that DREAM participates in the control of trigeminal pain perception through the regulation of prodynorphin and BDNF. Furthermore, genome-wide analysis of trigeminal neurons in daDREAM transgenic mice revealed that cathepsin L (CTSL) and the monoglyceride lipase (MGLL) are new DREAM downstream targets and have a role in the regulation of trigeminal nociception.

overall_design: Four biological replicates were independently hybridized to Affymetrix chips (GeneChip Mouse Genome 430 2.0 Array) for each sample type.

first: Tomaso

last: Benedet

first: Paz

last: González

middle: C

first: José

middle: M

last: Dopazo

first: Kedar

last: Ghimire

first: Malgorzata

last: Palczewska

first: Britt

last: Mellstrom

middle: R

last: Naranjo


title: The genomic responses of mouse liver to diclofenac treatment reveals an immune mediated mechanism of liver injury

status: Public on Aug 09 2016

city: Hannover

first: Juergen

last: Borlak

state: Lower Saxony

address: Feodor-Lynen-Str. 35

department: Centre for Pharmacology and Toxicology

institute: Hannover Medical School

summary: Diclofenac (DCL) is a non-steroidal anti-inflammatory drug. Its use can be associated with serious adverse drug reactions most notable myocardial infarction and drug-induced liver injury (DILI). The molecular causes leading to DILI remains unclear and it seems to be multifactorial. The aims of this study is to identify the molecular mechanisms involving immune mediated inflammatory reactions and its link to DILI through whole genome gene expression profiling. Diclofenac was given to mice at 30 mg/kg for 1, 3 and 14 days. Microarray experiments were performed with RNA extracts from liver samples. The performed gene expression studies showed >600 significantly regulated genes after single and repeated dosing for 3 and 14 days. The functional annotation revealed several genes were regulated in common coding for inflammatory, immune, stress and acute-phase responses. Immunohistochemistry, qRT-PCR as well as Western blotting were performed to evidence the regulation of key molecules in affected livers. In conclusion, the present study provides evidence for a mechanism of diclofenac induced liver injury that involves pro-inflammatory cytokine and acute phase responses.

overall_design: C57BL6- mice (males, 8 weeks old) (n=5) were administered daily by intraperitoneal injection of 30 mg/kg diclofenac sodium for up to 14 days. Control mice (n=5) were treated corresponding quantities of saline. The mice were euthanized at 24h (day 1), 72h (day 3) or 14 days after vehicle or diclofenac administration. The whole genome gene expression profiling studies of liver samples were performed to define the molecular mechanism of diclofenac induced immune mediated liver injury.

first: Eun-Hee

last: Lee

first: Jung-Hwa

last: Oh

first: Saravanakumar

last: Selvaraj

first: Se-Myo

last: Park

first: Mi-Sun

last: Choi

first: Reinhard

last: Spanel

first: Seokjoo

last: Yoon

first: Jürgen


title: Retinal transcriptomes of Plk3-deficient animals

status: Public on Apr 20 2016

city: Ames

first: Jeffrey

last: Trimarchi

state: IA

address: 3188 Molecular Biology Building

department: GDCB

institute: Iowa State University

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

overall_design: Refer to individual Series


title: Expression data from embryonic Plk3 WT and KO animals

summary: These data investigate the transcriptomic differences in the whole retinas of mice resulting from loss of Polo-like Kinase 3 (Plk3) at embryonic day (E)16.

overall_design: To determine transcriptomic differences resulting from Plk3 deficiency during embryonic retinogenesis, microarrays were performed on retinas isolated from Plk3-KO mice and their WT littermates

first: J

last: Goetz


title: Expression data from wild-type or Rb mutant MEFs

status: Public on May 01 2016

city: Louisville

first: Brian

middle: F

last: Clem

state: KY

address: 505 S. Hancock St, CTRB, Rm. 422

department: Biochemistry and Molecular Genetics

institute: University of Louisville

summary:
The retinoblastoma family regulates numerous genes in multiple biochemical processes including cell cycle, apoptosis, and cellular metabolic. We used multiple genetically modified cell lines in order to better understand the contributing role of each pocket protein to gene expression.
Microarray analysis was performed on wild-type, Rb1 knock-out, triple knock-out (TKO: Rb1, p107, p130), or TKO-RasG12D mouse embryonic fibroblasts

overall_design: MEFs from each genetic background were collected during exponential growth to discern the role of the Rb family on gene expression. RNA from biological triplicates from each cell lines was collected for microarray analysis.


title: Comparsion of IGRP reactive CD8 T cell clones

status: Public on May 21 2016

city: Utrecht

first: Bobby

last: Koeleman

address: Universiteitsweg 100

department: Genetics

country: Netherlands

institute: UMC Utrecht

summary: Autoreactive CD8+ T-cells recognizing autoantigens expressed by pancreatic islets lead to the destruction of insulin-producing β-cells in type 1 diabetes, but these T-cell also occur in healthy subjects. We tested the hypothesis that uncontrolled expansion of diabetogenic T-cells in patients occurs, resulting from failure to activate apoptosis. We compared function, transcriptome and epigenetic regulation thereof in relation with fate upon repeated exposure to islet-autoantigen of islet autoreactive T-cells from healthy and type 1 diabetic donors with identical islet epitope specificity and HLA-A2 restriction. Patient's T-cells proliferated exponentially, whereas those of non-diabetic origin succumbed to cell death. Transcriptome analysis revealed reduced expression of TRAIL, TRAIL-R2, FAS and FASLG (members of the extrinsic apoptosis pathway) in patient-derived compared to healthy-donor-derived T cells. This was mirrored by increased expression of microRNAs predicted to regulate these particular genes, namely miR-98, miR-23b and miR-590-5p. Gene specific targeting by these microRNAs was confirmed using dual-luciferase reporter assays. Finally, transfection of these microRNAs into primary T-cells reduced FAS and TRAIL mRNA underscoring their functional relevance. We propose that repression of pro-apoptotic pathways by microRNAs contributes to unrestricted expansion of diabetogenic cytotoxic T-cells, implicating microRNA-mediated gene silencing in islet autoimmunity in T1D.

overall_design: Human HLA-A2 restricted IGRP 268-273 reactive CD8 T cell clones derived from T1D patients (IGRP7 & IGRP32) were compared at mRNA and miRNA level with healthy individual derived HLA-A2 restricted IGRP 268-273 T cell clones. Total RNA was isolated after in the resting phase after antigen-specific stimualtion. Clones were generated as previously described in :PMID:  17376840; PMID:23155466

first: Vincent

last: de Jong

first: Arno

last: van der Slik

first: Sandra

last: Laban

first: Ruben

last: van 't Slot

first: Arnaud

last: Zaldumbide

first: Bart

last: Roep


title: Expression data from postnatal Plk3 WT and KO animals

summary: These data investigate the transcriptomic differences in the whole retinas of mice resulting from loss of Polo-like Kinase 3 (Plk3) over various stages of development, including adulthood, postnatal day (P)7, and P0.

overall_design: To determine transcriptomic differences resulting from Plk3 deficiency, microarrays were performed on retinas isolated from Plk3-KO mice and their WT littermates over various developmental timepoints


title: Time series trancriptional profiling of mouse liver after up to 13 weeks administration of Phenobarbital [mRNA]

status: Public on Apr 08 2016

city: Basel

first: Jonathan

last: Moggs

address: Fabrikstrasse 2

country: Switzerland

institute: Novartis

summary: The molecular events during nongenotoxic carcinogenesis and their temporal order are poorly understood but thought to include long-lasting perturbations of gene expression. Here, we have investigated the temporal sequence of molecular and pathological perturbations at early stages of phenobarbital (PB) mediated liver tumor promotion in vivo. Molecular profiling (mRNA, microRNA [miRNA], DNA methylation, and proteins) of mouse liver during 13 weeks of PB treatment revealed progressive increases in hepatic expression of long noncoding RNAs and miRNAs originating from the Dlk1-Dio3 imprinted gene cluster, a locus that has recently been associated with stem cell pluripotency in mice and various neoplasms in humans. PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, sug- gesting a role for β-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs. The carcinogenic relevance of Dlk1-Dio3 locus ncRNA induction was further supported by in vivo genetic dependence on constitutive androstane receptor and β-catenin pathways. Our data identify Dlk1-Dio3 ncRNAs as novel candidate early biomarkers for mouse liver tumor promotion and provide new opportunities for assessing the carcinogenic potential of novel compounds.

overall_design: To male B6C3F1/Crl mice were administered Phenobarbital (PB, 0.05% [wt/vol] in drinking water) was administered through ad libitum access to drinking water. The control group received drinking water ad libitum without PB. Mice were sacrificed after 1, 3, 7, 14, 28, 57, and 91 days of PB adminstration, and liver was removed, split into several sections, either frozen in liquid nitrogen and stored at −80°C for subsequent analyses.

first: Michael

last: Römer

first: Lempiäinen

last: Harri


title: Transcriptomics of murine ex vivo isolated alveolar type 2 epithelial cells from Influenza A respiratory infection

status: Public on Apr 11 2016

city: Braunschweig

first: Andreas

last: Jeron

state: Nierdersachsen

address: Inhoffenstraße 7

department: Viral Immunology

institute: Helmholtz Center for Infection Research

summary: Background: Influenza A virus (IAV) infections periodically cause substantial morbidity and mortality in the human population. In the lung, the primary targets for IAV replication are type II alveolar epithelial cells (AECII), which are increasingly recognized for their immunological potential. However, our knowledge of the role of AECII in anti-IAV immunity is incomplete and their in vivo response to infection has not been evaluated. To increase our understanding of their role in host-response to IAV-infection, we analyzed transcriptional regulation in primary AECII isolated from infected mice.     Results: Microarray analyses of AECII isolated on the first three days following IAV-infection revealed extensive transcriptional regulation. A multitude of differentially expressed transcripts was identified and in comparison to whole-lung tissue revealed a strong contribution of AECII to respiratory anti-IAV responses. Type I interferon played a major role in the detected gene expression profile and functional pathway analyses showed AECII to be highly active in pathogen recognition, cell recruitment and antigen-presentation. Analysis of Toll-like receptor 7 (TLR7) deficient mice indicated AECII to rely on the host’s expression of this innate IAV-sensor to elicit their full response. Importantly, the AECII transcriptional profiles correlated to cell recruitment and type I interferon levels detected in the lungs of infected animals.     Conclusions: Ex vivo analysis of primary murine AECII proved as a powerful tool to increase our understanding of AECII biology in infection. Our analysis revealed an exceptionally strong contribution of AECII to local host defenses by integrating signals provided by surrounding cells and direct pathogen recognition.

overall_design: The dataset contains microarray data from whole lungs as well as from FACS sorted AECII both derived either from WT or Tlr7ko mice which have been infected with IAV or mock treated. In case of AECII analysis (both WT and Tlr7ko mice) three time points have been analyzed after IAV infection (d1, d2, d3) with the mock treatment (d0) as the reference. Two independent replicates with pooled cells from five mice per group and experimental condition were generated for this analysis. In case of whole lung tissue (from WT and Tlr7ko mice) only d3 after IAV infection as well as an according mock treatment (d0) was analyzed. Three independent replicates were generated for the letter conditions.

first: Sabine

last: Stegemann-Koniszewski

first: Marcus

last: Gereke

first: Andrea

last: Kröger

first: Matthias

last: Gunzer

first: Dunja

last: Bruder


title: Gene Expression in Transformed Lymphocytes Reveals Phenotype-Modifying Pathways in Cystic Fibrosis

city: Chapel Hill

last: Knowles

state: NC

address: 7019 Thurston-Bowles Bldg; CB7248

institute: UNC-Chapel Hill

summary: Heritable genetic variants modify cystic fibrosis (CF) clinical phenotypes, e.g., lung disease, age-of-onset of persistent Pseudomonas aeruginosa (P. aeruginosa), and meconium ileus (MI).  Previous genome wide association studies (GWAS) have begun to inform the genetic architecture of CF phenotypes.  Analyses of gene expression will complement GWAS, as demonstrated by analyses of gene expression in lymphoblastoid cell lines (LCLs) to identify disease-related pathophysiological processes for non-CF complex traits.  In this study, global gene expression was measured in RNA from LCLs from 754 CF patients and analyzed for association with lung disease severity, age-of-onset of persistent P. aeruginosa pulmonary infection, and MI at birth.  Each phenotype displayed distinct expression associations.  Most pathways significantly associated with lung disease were related to membranes, vesicle traffic, and Golgi/endoplasmic reticulum (ER).  Pathways containing HLA genes (Class I and II) were significantly associated with both lung and P. aeruginosa phenotypes, but they displayed qualitative differences between phenotypes.  MI associated with pathways involving oxidative phosphorylation.  The results support the concept that gene expression associated with heritable variation acts to modify phenotypes in CF.

overall_design: 754 samples were analyzed; 2 control samples were plated by Expression Analysis per plate and 1 pooled sample from the patient set was added to one well on each plate.

first: Wanda

last: O’Neal


title: Late stages of T-cell maturation in the thymus involve NF-κB and tonic type I interferon signaling

status: Public on Apr 03 2016

city: Minneapolis

first: Kristin

middle: A.

last: Hogquist

state: MN

address: 2101 6th Street SE

department: Department of Laboratory Medicine and Pathology

institute: University of Minnesota

summary: Positive selection occurs in the thymic cortex, but critical maturation events occur later in the medulla.  We defined the precise stage at which T cells acquire competence to proliferate and emigrate. Transcriptome analysis of late gene changes suggested roles for NF-κB and interferon signaling. Mice lacking the IKK kinase TAK1, showed normal positive selection, but a specific block in functional maturation. NF-κB signaling provided protection from TNF, and was required for proliferation and emigration.  Alternatively, the interferon signature was independent of NF-κB, and IFNαR deficient thymocytes showed reduced STAT1 levels and phenotypic abnormality, but were competent to proliferate. Thus, both NF-κB and tonic IFN signals are involved in the final maturation of thymocytes into naïve T cells.

overall_design: Gene expression profile was performed on cells isolated from mouse thymus, including Pre-DP, Post-DP, SM&M1, M2 and Tak1-deficient SM&M1 cells.

first: Yan

last: Xing

first: Xiaodan

last: Wang

first: Stephen

last: Jameson

middle: A


title: Gene expression profiling of SF1 in mouse uterus tissues

status: Public on Apr 14 2016

city: Houston

first: Chad

last: Creighton

state: TX

address: One Baylor Plaza, Mail Stop: BCM305

department: Biostatistics, Ducan Cancer Center

institute: Baylor College of Medicine

summary: Epigenetic silencing of Steroidogenic Factor 1 (SF1) is lost in endometrial tissue in endometriosis and this is hypothesized to result in de novo local steroidogenesis favoring growth and inflammation. The goal of this study was to evaluate the endometrial specific transcriptional and functional role of SF1 in vivo by utilizing a mouse model in which SF1 was conditionally expressed in the uterus. SF1 expression resulted in the development of cystic endometrial glands and infertility. Endometriosis induction by auto-transplantation of a biopsy of uterine tissue sutured to the mesenteric membrane resulted in 4-fold increase in size ectopic lesions from SF1 expressing mice. Microarray analysis demonstrated SF1-regulated genes are involved in several pathways including epithelial and tube development, migration of lymphocytes and leukocytes, cellular movement and vascular development.

overall_design: experimental group (SF-1 transgenic) and control group

first: Yasmin

last: Vasquez

first: San-Pin

last: Wu

first: Yiqun

last: Zhang

first: Francesco

last: DeMayo


title: BRAF expression in a mouse melanoma model

status: Public on Apr 07 2016

first: Lawrence

last: Kwong

address: 1901 East Rd

institute: UT MD Anderson Cancer Center

summary: Expression was generated on tumors from 41 iBIP mice, which were previously described (Kwong, JCI, 2015).

overall_design: The BRAF-driven iBIP mouse model of melanoma was taken off dox and expression analyzed at various timepoints.


title: Expression data of ILC2 cells from Ets1-deleted and littermate control mice

status: Public on Apr 01 2016

city: Chicago

first: Barbara

last: Kee

state: Illinois

address: 924 E57th st

institute: The University of Chicago

summary: The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2

overall_design: ILC2 cells isolated from ETS1-deleted or litter mate control mice were cultured on OP9-DL1 with IL-7 and IL-33. Subsequently, RNA from ICOS+ cells was extracted, labelled and hybridized to Affymetrix microarrays. The goal of this study is to investigate ETS1-dependent genes in developing ILC2 cells.

first: Erin

last: Zook

first: Kevin

last: Ramirez

first: Xiaohuan

last: Guo

first: Grant

last: van der Voort

first: Mikael

last: Sigvardsson

first: Eric

last: Svensson

first: Yang-Xin

last: Fu


title: Progastrin dependent cancer cell proliferation

city: New York

first: Timothy

middle: Cragin

state: NY

address: 1130 St. Nicholas Avenue

department: Medicine- Division of Digestive and Liver Diseases

institute: Columbia University

summary:
Overexpression of human progastrin (hGAS) in mice has been observed  to increase colonic mucosa proliferation significantly,
but the mechanism and receptors of progastrin have not been defined.
We investigated this mechanism by observing the microarray gene expression in mGAS-/- mice,
WT mice, and hGAS transgenic mice.

overall_design: Gene expression of colonic mucosa of WT C57BL/6 mice,Gas-/- C57BL/6 mice, and hGAS transgenic mice, all 6 weeks old were compared.

first: Guangchun

last: Jin

first: Daniel

last: Worthley

first: Richard

last: Friedman

first: Xiangdong

last: Yang


title: Expression data from mouse intestinal organoids I

status: Public on Mar 31 2016

first: Ryoji

last: Yao

summary:
APC inactivation is the early process in the tumorigenesis of colorectal cancer. We established organoid cultures from intestines of genetically modifeid mice harboring Apcfl/fl and R26CreERT2 allele
We used microarrays to determine the alterations in intestinal stem cells in response to APC inactivation.

overall_design: Organoids were treated with 4OHT to induce recombination of APC or left untreated, and collected at 4 or 6 days after treatment. RNA were extracted and hybridization on Affymetrix microarrays.


title: Max as a biological blockade that restricts meiotic process in ESCs

city: Hidaka

first: Akihiko

last: Okuda

state: Saitama

address: 1397-1 Yamane

department: Research Center for Genomic Medicine

institute: Saitama Medical University

summary: We explored Max ablation-mediated up-regulation of germ-related genes, especially meiosis-related genes in mouse embryonic stem cells which were cultured either under conventional mouse ES medium or 2i condition using inhibitors against MEK and GSK3b.

overall_design: Effect of culture conditions (conventional mouse ES medium or 2i condition) on the expression profile of germ-related genes in Max expression ablated ES cells were examined using inducible Max-null ES cells in which Max gene had been homozygously disrupted, but carries Max cDNA in ROSA26 locus with tetracycline-off system.

first: Ayumu

last: Suzuki

first: Yutaka

last: Nakachi

first: Yosuke

last: Mizuno

first: Yasushi

last: Okazaki


title: Cell cycle-independent temporal identity transitions in cortical progenitor cells as revealed by single cell transcriptome analysis

city: Yokohama, Kanagawa

first: Takeya

last: Kasukawa

address: 1-7-22, Suehiro-cho, Tsurumi-ku

department: Center for Integrative Medical Sciences

institute: RIKEN

summary: During cerebral development, a variety of neurons are sequentially generated by self-renewing progenitor cells, apical progenitors (APs). A temporal change in AP identity is thought to produce a diversity of progeny neurons, while underlying mechanisms are largely unknown. Here we performed single cell genome-wide transcriptome profiling of APs at different neurogenic stages, and identified a set of genes that are temporally expressed in APs in a manner independent of differentiation state. Surprisingly, the temporal pattern of such AP gene expression was not affected by arresting cell cycling. Consistently, a transient cell cycle arrest of APs in vivo did not prevent descendant neurons to acquire their correct laminar fates. in vitro cell culture of APs revealed that transitions in AP gene expression involved in both cell-autonomous and non-autonomous mechanisms. These results suggest that timers controlling AP temporal identity run independently of cell cycle progression and Notch activation mode.

overall_design: We randomly picked up single cells from dorso-lateral portion of cerebral wall of a CD1 mouse at E11, E12 or small VZ/SVZ fragments of the same portion at E14 (3 days after in vivo electroporation of pCAG-NICD and pEF-p18) and E16. In 3 cases, cells are picked up from 3-days-in-vitro neurospheres derived from E11 dorso-lateral portion of cerebral wall. Single-cell cDNA samples were generated and amplified as descibed (Kurimoto et al.Nucreic Acid Res.34:e42, 2006).  After checking the quality of the samples, we then chose 30 (E11), 3 (APs from E12), 28 (E16), 4 (E14, NICD+p18 overexpressed APs), and 3 (APs from 3 days-in-vitro neurosphere) samples and applied them to GeneChip analysis.  We then performed analysis with these samples in addition to previously obtained data with E14 samples, which were deposited to GEO as GSE10881.

first: Mayumi

last: Okamoto

first: Takaki

last: Miyata

first: Daijiro

last: Konno

first: Hiroki

last: Ueda

first: Fumio

last: Matsuzaki

first: Ayano

last: Kawaguchi


title: Expression profiles of contsh- and Eva1sh-expressing NSCL61

city: Sapporo

first: Toru

last: Kondo

address: Kita-15, Nishi-7, Kita-ku,

department: Institute for Genetic Medicine

institute: Hokkaido University

summary: To find factors and pathways that Eva1 regulates in NSCL61

overall_design: We identified Eva1 as a new factor expressed in glioma-initiating cells (GICs). Eva1 regulates the proliferation of GICs.


title: Differential expression data for clonal EL4 mouse lymphoma cell lines

city: Spokane

first: Kathryn

middle: E

last: Meier

state: WA

address: PO Box 1495

department: Pharmaceutical Sciences

institute: Washington State University

summary:
Our group originally developed clonal cell lines by limiting dilution of the parental cell line, and also stably transfected one of these cell lines with human phospholipase D2.
The expression analysis was done to examine differences between a non-metastatic cell line (WT2), a metastatic cell line (V&), and a highly metastatic cell line (C5) that had been transfected with hPLD2.

overall_design: The cell lines, which had been serum-starved overnight, were analyzed without further treatment.

first: Manpreet

last: Chahal


title: Gene expression analysis in the aorta from non-diabetic or STZ-induced diabetic apolipoprotein E deficient (ApoE-/-) mice fed with high fat diet in the presence or absence of PKC β inhibitor, ruboxistaurin (RBX, or  LY333531)

status: Public on Mar 26 2016

city: Boston

first: George

last: King

state: Massachusetts

address: 1 Joslin Place Room 440

institute: Joslin Diabetes Center

summary:
We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C-β isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling.
To further investigate the effect of high fat diet and specific PKC β inactivation on STZ-induced atherosclerosis using the PKC β inhibitor, ruboxistaurin (RBX, or  LY333531), ApoE-/- mice were used and fed with high fat diet (42% of fat Kcal) with or without RBX after onset of diabetes. Isolated total RNA from whole aortas of each group was used and analyzed for gene expression.
The gene expression profiles were processed by using the Microarray Suite version 5.0 (MAS 5.0) with Affymetrix default analysis settings.

overall_design: ApoE-/- mice were used as a rodent atherosclerosis model. Isolated total RNA from aortas of each ApoE-/- mouse fed with high fat diet for 10 weeks after STZ-induced diabetes or control groups were used for preparation and hybridization on Affymetrix microarrays. There were total 4 different mice groups, which were fed with high fat diet with or without RBX. Each group had four individual mouse (N=4).

first: Kyoungmin

last: Park

first: Pedro

last: Geraldes

first: I-Hsien

last: Wu


title: The role of Clec4e (Mincle) in microglia response to transient ischemic injury

status: Public on Mar 24 2016

city: St. Lucia

first: Othmar

last: Korn

state: Queensland

address: University of Queensland

country: Australia

institute: Australian Institute for Bioengineering and Nanotechnology

summary: This data set shows dramatic changes in gene expression in microglia isolated from C57Bl6/J mice subjected to transient middle cerebral artery occlusion, as compared to those subjected to sham surgery. Mice deficient in Mincle (Clec4e-/-) showed significantly improved injury outcomes 3 and 7 days after transient middle cerebral artery occlusion. However, when comparing changes in gene expression in microglia 24 hours after blood reperfusion, there were no differences between wild-type and Clec4e-/- mice, indicating that Mincle does not participate in early microglial activation.

overall_design: Wild type and Mincle knock-out (Clec4e-/-) mice. After 1 h of transient middle cerebral artery occlusion (tMCAO) and 24 h of reperfusion, mice were perfused with PBS, their brains dissected, and 2 ipsilesional hemispheres (with cerebellum and brainstem removed) pooled for microglia isolation. For sham-operated animals, the whole forebrain was used and brains were not pooled. After myelin separation by Percoll gradient centrifugation, around 80,000 CD45intermediate, CD11b+ microglial cells were sorted from each sample. Sham samples n=3, tMCAO samples n=5.

first: Christine

last: Wells

first: Silvia

last: Manzanero

first: Thiruma

middle: V

last: Arumugam


title: Transcriptome Analysis of the Impact of Dexamethasone on the Immune Response in Mice with Pneumocystis Infection

city: Beijing

first: Yang

last: Hu

address: No. 8 GongTi Southern Road, Chao Yang District

department: Department of Respiratory Medicine and Critical Care Medicine

institute: Beijing Chao-Yang Hospital Affiliated to Capital Medical University

summary:
Pneumocystis pneumonia (PCP) is an opportunistic infectious disease prevalent in immunosuppressive host. Corticosteroids treatment is the most significant risk factor for HIV-negative patients with PCP, though little is known about how corticosteroids alters the host defense against Pneumocystis infection.
In the present study, we used transcriptomic analysis to examine the immune response in the lung of dexamethasone-treated PCP mice and compare the immune reaction of them with those without dexamethasone treatment.

overall_design: Healthy 4-5 week old male C57BL/6 mice were randomly assigned to 3 groups: wild-type PCP mice, dexamethasone-treated PCP mice and wild-type mice without infection (control). Then dexamethasone-treated PCP mice were given 4mg/l dexamethasone and 1 mg/ml tetracycline in drinking water consecutively from 14 days prior to Pneumocystis infection to euthanasia. Both dexamethasone-treated and wild-type PCP mice were inoculated intratracheally with 1 × 10^6 Pneumocystis nuclei and control mice were given lung homogenate from uninfected scid mice.Fourteen days after infection, mice were sacrificed and the left lung was excised. Affymetrix microarrays were performed in the lung of 5 dexamethasone-treated PCP mice, 5 wild-type PCP mice and 4 control mice.

first: Dong

last: Wang


title: Gene expression profiling of PBMC from coinfected or non-coinfected mice at d0, d3, d7, and d21 post YFV-17D challenge

status: Public on Mar 22 2016

first: Kevin

last: Bi

state: MA

address: 450 Brookline Ave.

department: Pediatric Oncology

institute: Dana-Farber Cancer Institute

summary: We tested the effects of co-infection on vaccine response to YFV-17D.

overall_design: Groups of mice were divided into either Mock infected or Co-infected groups.  Mock infected were housed in a biohazard facility and inoculated with PBS.  Co-infected were infected sequentially with murine gammaherpesvirus-68, murine cytomegalovirus, influenza WSN, and Heligmosimoides polygyrus.  Both mock and co-infected groups were challenged with Yellow Fever virus (YFV-17D).  Day 0 is prior to YFV.  Days 3, 7, and 21 were timepoints after YFV.

first: Tiffany

last: Reese


title: Heterogeneity in global gene expression profiles between biopsy specimens taken peri-surgically from primary ER-positive breast carcinomas (excision/x-ray samples)

status: Public on Mar 29 2016

city: London

first: Alice

last: Gao

state: London

address: 237 Fulham Road

department: Breast Cancer Now

institute: The Institute of Cancer Research

summary: Gene expression is widely used for the characterization of breast cancers. Variability due to tissue heterogeneity or measurement error or systematic change due to peri-surgical procedures can affect measurements but is poorly documented. We studied the variability of global gene expression between core-cuts of primary ER+ breast cancers and the impact of delays to tissue stabilization due to sample x-ray and of diagnostic core-cutting. Twenty-three and 56 sample pairs, respectively, were suitable for analysis. In general, there is a good correlation in gene expression between pairs of core-cuts except where genes have a narrow dynamic range. Increases in the expression of several stress/early-response genes (e.g., FOS, FOSB, JUN) were found in both studies. Substantial changes in expression of early response genes occur within an hour after surgery and in IL6, IGFB2 and MYC as a result of diagnostic core-cut biopsy. Similar correlation coefficients to the average gene expression profiles of intrinsic subtype, particularly LumA and LumB, can lead to discordances between assigned subtypes.

overall_design: Twenty-three paired core-cuts were taken immediately after tumour excision and up to 60 minutes delay due to sample x-ray. Whole genome expression analysis was conducted on extracted RNA. Correlations and differences were assessed between the expression of individual genes, gene-sets/signatures and intrinsic subtypes.

first: Qiong


title: High levels of canonical Wnt signaling lead to loss of stemness and increased differentiation in hematopoietic stem cells

status: Public on Mar 23 2016

city: Amsterdam

first: Erdogan

last: Taskesen

state: North Holland

address: Boelelaan 1085

department: Center for Neurogenomics and Cognitive Research (CNCR)

institute: VU University Amsterdam

summary: Canonical Wnt signalling regulates the self-renewal of most if not all stem cell systems. In the blood system, the role of Wnt signalling has been subject of much debate, with positive and negative roles of Wnt signalling proposed for hematopoietic stem cells (HSC). As we have shown previously, this controversy can be largely explained by the effects of different dosages of Wnt signalling. What remained unclear however, was why high Wnt signals would lead to loss of reconstituting capacity. To better understand this phenomenon, we have taken advantage of a series of hypomorphic mutant Apc alleles resulting in a broad range of Wnt dosages in HSCs, purified those HSCs and performed whole genome gene expression analyses. Gene expression profiling and functional studies show that HSCs with APC mutations lead to high Wnt levels , enhanced differentiation and diminished proliferation, but have no effect on apoptosis, collectively leading to loss of stemness.  Thus, we provide mechanistic insight into the role of APC mutations and Wnt signalling in HSC biology. As Wnt signals are explored in various in vivo and ex vivo expansion protocols for HSCs, our findings also have clinical ramifications.

overall_design: To investigate the effects of Wnt signals in hematopoietic cells, mice carrying floxed Apc or hypomorphic Apc mutants were crossed, LSK cells were isolated and treated with Cre IRES GFP gamma-retrovirus ex vivo, GFP+ cells were sorted and RNA expression was determined.

first: Farbod

last: Famili

first: Martijn

last: Brugman

first: Brigitta

last: Naber

first: Riccardo

last: Fodde

first: Frank

middle: J

last: Staal


title: To integrated functional genomics and craniofacial morphogenesis with in FaceBase Consortium

city: Los Angeles

first: Vasu

last: Punj

state: CA

address: Biggy Street

institute: USC

summary: Congenital malformations in facial bones significantly impact the overall representation of face. Establishing a correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investiation we will generate gene expression profile of different facial bones at different time intrevals over a period of 5 years to establish their roles in regulating craniofacial development

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla.

last: Chai

first: Carolina

last: Parada

first: Alexandre

last: Grimaldi

first: Thach

last: Ho

first: Jill

last: Harunaga

first: Bridget

last: Samuels


title: Gene expression microarray analysis on the dentate gyrus of alpha-CaMKII HKO mice

city: Toyoake

first: Hideo

last: Hagihara

address: 1-98 Dengakugakubo, Kutsukake-cho

department: Institute for Comprehensive Medical Science

institute: Fujita Health University

summary: We previously found that mice with heterozygous knockout of the alpha-isoform of calcium/calmodulin-dependent protein kinase II (alpha-CaMKII HKO mice) show various dysregulated behaviors, including cyclic variations in locomotor activity (LA), suggesting that alpha-CaMKII HKO mice may serve as an animal model showing infradian oscillation of mood. We performed gene expression microarray analysis of dentate gyrus from alpha-CaMKII HKO mice. Mice were selected for the sampling such that their LA levels varied among the mice.

overall_design: Dentate gyrus RNA isolated from alpha-CaMKII HKO mice.

last: HAGIHARA


title: Heterogeneity in global gene expression profiles between biopsy specimens taken peri-surgically from primary ER-positive breast carcinomas

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

overall_design: Refer to individual Series


title: Expression data from Suv420h1 knockout and mutant PREX2 expressing MEFs (mouse embryonic fibroblasts)

status: Public on Apr 06 2016

first: Lynda

last: Chin

address: 1515 Holcombe Blvd

department: Genomic Medicine

institute: MD Anderson Cancer Center

summary: PREX2 truncating mutations occur in melanoma. We used microarray based gene expression profiling to compare expression patterns between cells harboring Suv420h1 knockout and PREX2 mutant expressing

overall_design: Spontaneously immortalized MEFs from either wt or Suv420h1 knockout mice were used. Wt MEFs were transduced with lentivirus to express indicated PREX2 mutants. Suv420h1 ko MEFs were reconstituted either with control GFP or Suv420h1-GFP fusion. Total RNA was isolated and subjected to analysis

first: Yonathan

last: Deribe

first: Chia

last: Wu


title: Pretreatment microRNA expression impacting on epithelial to mesenchymal transition predicts intrinsic radiosensitivity in head and neck cancer cell lines and patients [FaDu]

status: Public on Mar 19 2016

first: Monique

middle: C.

last: de Jong

address: Plesmanlaan 121

department: Dept of Biological Stress Response and Dept. of Radiation Oncology

institute: Netherlands Cancer Institute

summary:
Purpose: Predominant causes of head and neck cancer recurrence after radiotherapy are rapid repopulation, hypoxia, fraction of cancer stem cells and intrinsic radioresistance. Currently, intrinsic radioresistance can only be assessed by ex-vivo colony assays. Besides being time-consuming, colony assays do not identify causes of intrinsic resistance. We aimed to identify a biomarker for intrinsic radioresistance to be used before start of treatment and to reveal biological processes that could be targeted to overcome intrinsic resistance.
Experimental design: We analyzed both micro- and messenger RNA expression in a large panel of HNSCC cell lines. Expression was measured on both irradiated and unirradiated samples. Results were validated using modified cell lines and a series of laryngeal cancer patients.
Results: MiRs, mRNAs and gene sets that correlated with resistance could be identified from expression data of unirradiated cells. The presence of epithelial to mesenchymal transition (EMT) and low expression of miRs involved in the inhibition of EMT were important radioresistance determinants. This finding was validated in two independent cell line pairs, in which the induction of EMT reduced radiosensitivity. Moreover, low expression of the most important miR (miR-203) was shown to correlate with local disease recurrence after radiotherapy in a series of laryngeal cancer patients.
Conclusions: These findings indicate that EMT and low expression of EMT-inhibiting miRs, especially miR-203, measured in pre-treatment material, causes intrinsic radioresistance of HNSCC, which could enable identification and treatment modification of radioresistant tumors.

overall_design: To test if the induction of epithelial to mesenchymal transition increases radioresistance, these cell lines were obtained from prof. Kou-Juey Wu (National Yang-Ming University, Taiwan) and tested. Detailed information about development of the cell lines can be read from the original publication (PMID:18297062).

first: Jelle

last: tenHoeve

first: Reidar

last: Grénman

first: Lodewyk

last: Wessels

first: Ron

last: Kerkhoven

first: Hein

last: te Riele

first: Michiel

middle: W

last: van den Brekel

first: Marcel

last: Verheij

first: Adrian

last: Begg


title: The cohesin offloading factor Wapal is required for proper polycomb-mediated gene silencing [array]

status: Public on Mar 21 2016

city: Milwaukee

first: Sridhar

last: Rao

state: WI

address: 8727 Watertown Plank Road

department: Blood Research Institute

institute: BloodCenter of Wisconsin

summary: The cohesin offloading protein Wapal also acts as a polycomb factor in flies.  We examined its role in transcriptional role in murine embryonic stem cells (ESCs)

overall_design: Two biological replicate for each condition, hybridized to single arrays, are included.  As a negative control we used the Empty Vector.  As experimental, we used two, independent shRNAs to Wapal

first: Kirthi

last: Pulakanti


title: Candesartan neuroprotection on Rat Primary cerebellar granule cells (CGCs)

status: Public on Mar 17 2016

city: BETHESDA

first: abdel

middle: G

last: Elkahloun

address: 50, SOUTH DRIVE

institute: NHGRI-NIH

summary: Neuronal cultures were treated with candesartan at neuroprotective concentrations followed by excitotoxic glutamate amounts. Candesartan significantly reduced glutamate-induced inflammation. To provide mechanistic insight into the potential targets and pathways that may underlie these benefits, we performed genome wide expression profile analysis and evaluated the data by Ingenuity Pathway Analysis (IPA) and Gene Set Enrichment Analysis (GSEA). We found that the inflammation signal transduction pathways were major components of the neuronal response to glutamate excitotoxicity, and that candesartan significantly ameliorated glutamate-induced alterations in gene expression. Further analysis showed significant associations of these genes with two  independent published networks identified by microarray analysis of hippocampal samples obtained post-mortem from brains of patients diagnosed with AD .

overall_design: 8 days old rat  Primary cerebellar granule cells (CGCs) were treated with DMSO, Glutamate, Candesartan or Glutamate +candesartan. Four replicates of each treatment were done.

first: Abdel

first: J

last: Saavedra


title: Expression data from murine GVH-SSc skin

status: Public on Mar 16 2016

city: Gaithersburg

first: Tracy

middle: Anne

last: Delaney

state: MD

address: One Medimmune Way

department: Research

institute: MedImmune LLC

summary: Murine GVH-SSc dorsal scapular skin samples were analyzed to determine the effect of IFNAR-1 inhibition on gene expression at day 14 and day 28.   Gene expression in GVH-SSc skin from mice treated with a neutralizing IFNAR-1 antibody was compared to that in  GVH-SSc skin from mice treated with isotype IgG, with skin from syngeneic graft controls as reference.

overall_design: For each timepoint, the following samples were analyzed: syngeneic control (n=4); GVH-SSc isotype (n=4); GVH-SSc anti-IFNAR-1 (n=4)


title: Pretreatment microRNA Expression Impacting on Epithelial-to-Mesenchymal Transition Predicts Intrinsic Radiosensitivity in Head and Neck Cancer Cell Lines and Patients [mRNA expression]

overall_design:
32 HNSCC cell lines from different subsites, 3 timepoints (mock irradiated, 2 hours after 4 Gy and 6 hours after 4 Gy)
All cell lines were obtained from Professor R. Grénman (University of Turku, Finland), who has a panel of well characterized HNSCC cell lines with known radiosensitivity.


title: Expression data of mesenchymal cells from mouse liver

status: Public on Mar 11 2016

first: Kinji

last: Asahina

address: 1333 San Pablo Street

department: Pathology

institute: University of Southern California

summary:
There are a few markers available to distinguish hepatic stellate cells (HSCs), portal fibroblasts (PFs), and mesothelial cells (MCs) in the adult mouse liver.
To identify genes uniquely expressed in these cells, we isolated HSCs having Vitamin A lipids by FACS based on their autofluorescence. We isolated a mixed population containing PFs and MCs as Vitamin A lipid-negative and GFP-positive cells by FACS from Collagen1a1 promoter-driven GFP transgenic mice. MCs were isolated by FACS using anti-GPM6A antibodies from adult mouse livers. PFs were isolated by FACS as Vitamin A lipid-negative, GFP-positive, and GPM6A-negative cells. We also isolated HSCs, MCs, and PFs from Collagen1a1 promoter-driven GFP transgenic mouse livers having biliary fibrosis by FACS. Biliary fibrosis was induced by bile duct ligation for 3 weeks. Sham operation was performed as a control. After separation of these cells, we isolated total RNAs and analyzed mRNA expression by microarray analysis.

overall_design: Total RNA was extracted with RNAqueous Micro (Ambion) and the probes for the microarray were synthesized using the Ovation RNA amplification system V2 and FL-Ovation cDNA Biotin module V2 (Nugen). The labeled probes were hybridized with GeneChip Mouse Genome 430 2.0 arrays (Affymetrix) and signals were analyzed with Genomic Suite software (Partek).


title: Expression data from bone marrow-derived macrophages

city: Gothenburg

first: Adil

last: Mardinoglu

state: Gothenburg

address: Kemivägen 10

department: Department of Biology and Biological Engineering

country: Sweden

institute: Chalmers University of Technology

summary: To identify factors that could explain why mice transplanted with Vim deficient  bone marrow display decreased atherosclerosis despite increased inflammation, we performed global gene expression profiling of bone-marrow derived macrophages from vimentin-deficient or wild-type littermates on C57BL/6 background.

overall_design: We elucidated the role of vimentin in atherogenic low-density receptor– deficient mice after bone marrow transplantation from vimentin-deficient mice.

first: Jan

last: Boren


title: A549 Gene Expression Following Treatment with a No-Observed-Effect Level of Cisplatin

status: Public on Mar 03 2016

city: Vancouver

first: Ada

last: Leung

state: British Columbia

address: 675 West 10th Avenue

department: Experimental Therapeutics

institute: BC Cancer Research Centre

summary: We compared the gene expression of A549 cells following 24 and 48 hours of treatment with a no-observed-effect level dose of cisplatin. The objective of the study is to identify genes that are differentially expressed in response to sub-lethal doses of cisplatin. This study helps identify not only treatment responses but also changes in gene expression that may confer cytoprotective mechanisms that allow these cells to survive treatment and to develop treatment resistance.

overall_design: A total of 12 samples were analyzed with two time points (24 and 48h treatments) and three replicates per condition (treated vs. untreated).

first: Stacy

last: Hung

first: Mohammed

last: Qadir

first: Christian

last: Steidl

middle: B

last: Bally


title: Expression data from the mouse ES cell-derived differentiated cells treated with or without MPA

status: Public on Mar 02 2016

city: Yokohama

first: nobuaki

last: shiraki

address: 4259-B-25 Nagatsuta-cho, Midori-ku

department: School of Life Science and Technology

institute: Tokyo Institute of Technology

summary:
Mycophenolic acid (MPA), effectively promoted ES cell pancreatic differentiation with a concomitant reduction of neuronal cells.
The targets of MPA were investigated by microarray analysis of cells treated on day 5 with MPA and harvested on day 6 and 8.

overall_design: Cells were harvested for RNA extraction and hybridization on Affymetrix microarrays. We performed gene expression profiles of differentiated mouse ES cells treated with or without 2 microM MPA at day5, 6, and 8

first: Nobuaki

last: Shiraki

first: Ryutaro

last: Nakashima


title: Expression of peripheral T lymphoma cells from p53 deficient

status: Public on Mar 04 2016

city: Oullins

first: GENESTIER

last: Laurent

address: Faculté de Medecine Lyon Sud. 165 Chemin du petit Revoyet

country: France

institute: INSERM

summary: Some infectious agents are associated with non-Hodgkin lymphoma development. Here we have used p53-deficient mice chronically injected with Streptococcus pneumoniae (Spn) with the aim to develop an animal model of infection-associated lymphomagenesis. We show that repeated stimulations with heat-killed Spn significantly enhanced the incidence of peripheral T-cell lymphoma (PTCL) in these mice. Phenotypic studies and gene expression profile analyses indicate that these PTCL arose from chronically stimulated natural killer T (NKT) cells, a T cell lineage that exhibits unique properties. Furthermore, lymphoma development was blocked when these PTCL were transferred to recipients lacking CD1d expression or treated with blocking CD1d mAbs, thus demonstrating that in vivo TCR/CD1d interactions are required for these PTCL survival. In conclusion, we have identified a new entity of peripheral T-cell lymphoma that originates from CD1d-restricted natural killer T (NKT) cells. Our results could refine the classification of PTCL and pave the way for the development of new immunotherapeutic approaches.

overall_design: 23 samples: 5 PTCL from PBS-injected mice; 4 PTCL from Spn-injected mice; 3 Thymic lymphoma (TL); 6 control T cells (3 repetitions of resting T cells and 3 repetitions of in vitro activated T cells); 5 control NKT cells (3 repetitions of resting NKT cells and 2 repetitions of in vitro activated NKT cells)

first: Anthony

last: BESSE

first: Séverine

last: CROZE

first: Joel

last: LACHUER

first: Laurent

last: GENESTIER


title: Expression data for 52 microsatellite stable (MSS) primary tumors from patients with proximal colon cancer.

city: Parkville

first: Oliver

last: Sieber

state: VIC

address: 1G Royal Parade

institute: Walter and Eliza Hall Insitute of Medical Reseach

summary: Samples were taken from surgically resected tumor specimens from patients with proximal colon cancer. The expression profiles were determined using the Affymetrix GeneChip Human Exon 1.0 ST Array version 2. APC gene mutation status was determined using Sanger sequencing. A classifier for APC mutation status was trained using these expression data.

overall_design: 52 microsatellite stable (MSS) proximal colon cancers samples were analyzed. 17 samples were APC wild-type and 35 had APC protein-truncating mutations.


title: Application of a clinical assay for staging and prognosis of prostate cancer diagnosed in needle core biopsy specimens

status: Public on Mar 09 2016

city: San Diego

first: Elai

last: Davicioni

address: 10355 Science Center Dr

institute: GenomeDx Biosciences

summary:
Molecular and genomic analysis of microscopic quantities of tumor from formalin-fixed and paraffin-embedded (FFPE) biopsies has many unique challenges. Here we evaluated the feasibility of obtaining transcriptome-wide RNA expression to measure prognostic classifiers from diagnostic prostate needle core biopsies.
158 samples from diagnostic needle core biopsies (Bx) and radical prostatectomies (RP) were collected from 33 patients at three hospitals, each patient provided up to 6 tumor and benign samples.  Genome-wide transcriptomic profiles were generated using Affymetrix Human Exon arrays for comparison of gene expression alterations and prognostic signatures between the Bx and RP samples.

overall_design: For 23 patients from UCSF and CSMC, six prostate tissue samples were obtained from each patient: tumor biopsy, tumor RP, benign adjacent biopsy, benign adjacent RP, and benign contralateral biopsy, and benign contralateral RP. For the 10 UHN patients only tumor biopsy and tumor RP samples were obtained. A total of 147 samples passed RNA, cDNA, and microarray quality control.

first: Beatrice

middle: S

last: Knudsen

first: Hyung

middle: L

last: Kim

first: Nicholas

last: Erho

first: Heesun

last: Shin

last: Alshalalfa

first: Lucia

last: Lam

first: Imelda

last: Tenggara

first: Karen

last: Chadwich

first: Theo

last: Van Der Kwast

first: Neil

last: Fleshner

first: Peter

last: Carroll

first: Matthew

last: Cooperberg

first: June

last: Chan

first: Jeffry

middle: P

last: Simko


title: Gene expression profiling of M0, M1 and M2a macrophages after 7 days of culture

first: Martin

last: Hessner

address: 8701 Watertown Plank Road

department: Pediatrics

institute: Medical College of Wisconsin

summary:
The relative contribution of polarized macrophages to the maintenance of tolerance is unknown. We examined their roles by in vivo adoptive transfer immunotherapy of M0, M1 and M2a macrophages as pre-treatment of colitis. In other experiments, M2a macrophages were used as pre-treatment or treatment of established colitis followed by immunotherapy with nTreg cells. Survival, weight gain, tissue infiltration, iTreg and Th17 cell development, T cell activation, and the frequency of proinflammatory cytokines were used as outcome measurements. Pre-treatment with M2a but not M1 macrophages increased the development of iTreg and Th17 cells. M2a macrophages used as pre-treatment or in treatment of established colitis allowed for successful therapy with nTreg cells.
M1 and M2a macrophages have distinct gene expression profiles.

overall_design: M0, M1 and M2a macrophages were cell sorted and were used to generate total RNA for each array set, which was labeled and hybridized to Affymetrix Mouse Genome 430 2.0 GeneChips in accordance to the manufacturer’s protocol. Three sets of arrays were performed, and the results were averaged. The subset of probe sets whose expression increased or decreased by two-fold or more relative to M0 cells as a common standard was identified and used for further analysis.

first: Dipica

last: Haribhai

first: Jennifer

last: Ziegelbauer

first: Shuang

last: Jia

first: Kyle

last: Upchurch

first: Ke

last: Yan

first: Erica

last: Schmitt

first: Nita

middle: H

last: Salzman

first: Pippa

middle: M

last: Simpson

first: Talal

last: Chatila

first: Calvin

last: Williams


title: Comparison of wild-type and Mfsd2a KO eye cups

city: Singapore

first: Bernice

last: Wong

address: 8 College Road, Level 8

department: Cardiovascular and Metabolic Disorders

country: Singapore

institute: Duke-NUS Medical School, Singapore

summary:
Eye photoreceptor membrane discs in outer rod segments are highly enriched in the visual pigment rhodopsin and the omega-3 fatty acid docosahexaenote (DHA). The eye acquires DHA from blood, but transporters for DHA uptake across the blood-retinal barrier (BRB) or retinal pigment epithelium have not been identified. Mfsd2a is a newly described sodium-dependent lysophosphatidylcholine symporter expressed at the BRB.
Microarrays were used to determine difference in gene expression between wild-type and Mfsd2a KO eye cups.

overall_design: RNA was extracted from eye cups from postnatal day 13 wild-type and Mfsd2a KO mice. Equal amounts of RNA from 6 wild-type eye cups were pooled for the wild-type sample, or 6 Mfsd2a KO eye cups were pooled for the Mfsd2a KO sample. Microarray profiling was done on pooled samples with a RIN cut-off of 7.0 using Mouse 430 2.0 arrays (Affymetrix).

first: David

last: Silver


title: Transcriptional consequences of DISC1 knockdown in human neural progenitor cells

status: Public on Mar 01 2016

city: Cardiff

middle: James

last: Hill

address: Maindy Road

institute: Cardiff University

summary: Background: One of the strongest identified risk factors for major psychiatric illness is a chromosomal translocation directly disrupting the DISC1 gene, which is observed in members of a large Scottish family. Although DISC1 is known to function through a variety of molecular pathways, no global assessment of the molecular consequences of cellular DISC1 perturbation has been carried out to date. Methods: Predicted effects of the t(1;11)(q42;q14) translocation on DISC1 expression were modelled in neural progenitor cells derived from human fetal cortex using RNA interference (RNAi). Downstream effects on the cellular transcriptome were assessed by microarray. The reproducibility of individual gene expression changes was tested in repeat experiments by quantitative PCR.Results: A total of 54 genes were differentially expressed between the DISC1 and control siRNA conditions at a false discovery rate (FDR) ≤ 0.05 in the primary experiment. Differentially expressed genes were significantly over-represented in Gene Ontology terms relating to the cell cycle, but included genes involved in a variety of other functions. Several genes showing reproducible differences in gene expression have been previously implicated in psychiatric disorders. Most consistent gene expression differences were seen for CCND2, MEG3, SPOCK2 and GABRA5.

overall_design: Total RNA extracted from human neural progenitor cells manipulated with either of two siRNAs: control siRNA or siRNA targeting DISC1 . 3 replicates per group. Genome wide transcript levels were then measured using gene expression microarrays.

first: Nick

last: Bray

first: Aaron

last: Jeffries

first: Richard

last: Killick

first: Federica

last: Buonocore

first: Dobril

last: Ivanov

first: Dafe

last: Uwanogho

first: Graham

last: Cocks

first: Oisin

last: Butler

first: Doris

last: Stangl

first: Michael

middle: C

last: O’Donovan

first: Brenda

first: Jack

last: Price


title: ECT2 and AURKB Modulate Formation of Stress Granules Containing Transcripts from Diverse Cellular Pathways in Astrocytoma Cells

status: Public on Feb 29 2016

city: Toronto

first: James

last: Rutka

state: Ontario

address: 686 Bay Street

department: Cell Biology

institute: Hospital for Sick Children

summary: Stress granules are small RNA-protein granules that modify the translational landscape during cellular stress to promote survival. The RhoGTPase RhoA is implicated in the formation of RNA stress granules.  Our data demonstrate that the cytokinetic proteins ECT2 and AurkB are localized to stress granules in human astrocytoma cells.  AurkB and its downstream target histone-3 are phosphorylated during arsenite-induced stress. Chemical (AZD1152-HQPA) and siRNA inhibition of AurkB results in fewer and smaller stress granules when analyzed utilizing high throughput fluorescent based cellomics assays. RNA immunoprecipitation with the known stress granule aggregates TIAR and G3BP1 was performed on astrocytoma cells and subsequent analysis revealed that astrocytoma stress granules harbour unique mRNAs for various cellular pathways including cellular migration, metabolism, translation and transcriptional regulation.  Human astrocytoma cell stress granules contain mRNA that are known to be involved in glioma signaling and the mTOR pathway. These data provide evidence that RNA stress granules are a novel form of epigenetic regulation in astrocytoma cells, which may be targetable by chemical inhibitors and enhance astrocytoma susceptiblity to conventional therapy such as radiation and chemotherapy.

overall_design: Astrocytoma cells were either untreated or treated with arsenite to induce stress granule formation and RNA immunoprecipitates were analyzed by exon array analysis. RNA species that were enriched in TIAR RIPs and G3BP1 RIPS, respectively were compared to compared to TIAR and G3BP1 RIPs from untreated cells and input controls. Ingenuity pathway analysis was performed on the stress granule enriched mRNAs from the TIAR and G3BP1 RIPs to identify significant functional biology networks.

middle: T


title: L. lactis MG1363 transcriptome analysis of 4 evolved strains

city: Delft

first: Claire

address: Alexander Fleminglaan

department: DFS

institute: DSM

summary:
L. lactis MG1363 was evolved in 4 fermentors in glucose-containing chemically defined medium (CDMPC) for 309 generations at a dilution rate of 0.5h-1
Glycerol stocks made during the evolution experiment were revived in CDMPC and further characterized.

platform_organism: Lactococcus cremoris subsp. cremoris MG1363

overall_design: Glycerol stocks from generation 309 were revived in CDMPC and grown to mid-exponential phase.  Strains from each of the 4 fermentors were compared to the original strain (Generation 0).