title: Protein microarray analysis of expression of murine cytokines in spleen interfered with IFN-α and (or) LPS

status: Public on Nov 10 2012

city: harbin

first: Huayang

last: Pan

state: heilongjiang

address: youzheng street

department: general  surgery

institute: The First Affiliated Hospital of Harbin Medical University

summary: 12 wild-type C57BL/6 (B6) mice were divided into 4 groups: control group, IFN-α group, LPS group, and IFN-α+ LPS group, every group contained 3 mice (n=3). IFN-α was administrated i.p. to IFN-α group and IFN-α+ LPS group once daily (QD) for 7 days at a medium dose of 105units/kg weight, PBS was administrated i.p. to control group and LPS group QD for 7 days at the same volume. LPS group and IFN-α+ LPS group were injected i.v. with 10 μg LPS for one mouse on the 8th day. Control group and IFN-α group were injected i.v. with PBS at the same volume. 6 h later, mice were sacrificed to harvest spleens for protein microarray experiment. Mouse Cytokine Antibody Array 3(62) was purchased from Ray Biotech, Norcross GA, US.

overall_design: Protein microarray of murine cytokines expression. Spleens from 12 mice (4 group) were treated as indicated in the summary.  Equal amount total protein from each spleen was pooled prior to gene expression analysis.

first: Pan

last: Huayang

first: Jiang

last: Hongchi


title: Genomic (in)stability of the breast tumor microenvironment

status: Public on Dec 21 2012

city: Windber

first: Rachel

last: Ellsworth

state: PA

address: 620 Seventh Street

department: Clinical Breast Care Project

country: USA

institute: Windber Research Institute

type:
Genome variation profiling by SNP array
SNP genotyping by SNP array

summary:
The breast tumor microenvironment plays an active role in tumorigenesis. Molecular alterations, including epigenetic modifications to DNA, and changes in RNA and protein expression have been identified in tumor-associated stroma; however, there is considerable debate as to whether the stroma is characterized by genomic instability or whether detection of chromosomal alterations in the breast stroma is a reflection of technological artifact rather than the true genomic content of the tumor microenvironment.
Methods: Surgically-removed breast stroma specimens from 112 women undergoing reductive mammoplasty (n=15), prophylactic mastectomy (N=6) or mastectomy for a diagnosis of breast disease (n=92) were frozen in optimal cutting temperature medium. Allelic imbalance (AI) analysis was performed in 484 stromal specimens from 98 women using a panel of 52 microsatellite markers; SNP data was generated from a subset of 86 stromal specimens using 250K SNP arrays (Affymetrix). Copy number alterations were identified using Partek Genomics Suite.
Results: AI was not detected in 92% (444/484) of stroma specimens.  When compared to previously generated AI data from 77 formalin-fixed, paraffin-embedded stroma specimens (Ellsworth et al., Ann Surg Oncol 2004), 32 (42%) of which harbored at least one detectable AI event, the frequency of AI in the FFPE specimens (4.62%) was significantly higher (P<0.0001) than that found in frozen specimens (0.45%).  Of the stroma specimens assayed using SNP arrays 95% (82/86) had no detectable alterations and the 11 copy number changes were small and not shared between specimens.
Conclusions: The data presented here support a model in which the tumor microenvironment is genetically stable.  The direct comparison of copy number alterations between FFPE and frozen research-grade specimens using identical methodologies suggests that past reports of significant AI in breast stroma, both adjacent to and distant from the tumor, reflects artifact in the archival specimens caused by formalin-fixation, paraffin-embedding and tissue storage.

overall_design: 250K STY data was generated for 86 breast stromal specimens.  The tissue specimens were analyzed by paired analysis to the SNP data from matched genomic (blood) DNAs

first: Seth

last: Rummel

middle: E


title: Genome-wide characterization of PhoB binding profile in Escherichia coli (ChIP-chip data)

status: Public on Oct 21 2012

city: Taipei

first: Chi

last: Yang

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

department: Institute of BioMedical Informatics

country: Taiwan

institute: National Yang-Ming University

type: Genome binding/occupancy profiling by genome tiling array

summary: Chromatin immunoprecipitation was combined with high-density tiling array (ChIP-chip) and gene expression microarray to reveal the adaptive responses of Escherichia coli to phosphate starvation. The first sketch of the genome-wide distribution of PhoB binding profile was unveiled and 43 regions were identified as the PhoB binding regions. The presence of a significant common motif in these binding regions allowed us to reconstruct the PhoB binding pattern. By comparing the ChIP-chip and microarray datasets, we were also able to identify genes directly or indirectly affected through PhoB regulation. Nineteen out of the 287 differentially expressed genes in the presence and absence of PhoB activity were considered as the genes directly regulated by PhoB. The adaptive responses affected through PhoB regulation are discussed and these responses involve in several important biological functions including transcriptional regulation, transportation, membrane component arrangement, sigma factor modulation and DNA replication inhibition.

platform_organism: Escherichia coli str. K-12 substr. MG1655

overall_design: Comparison of the E. coli K12 MG1655 wild type and a PhoB-FLAG fusion expressing strain (MG1655_PhoB_FLAG). The anti-FLAG antibody was used to recognize PhoB-FLAG fusion protein. Therefore, ChIPed DNA from the wild type strain was used as the control group. Three biological replicates were performed.

first: Shiau-Yi

last: Wen

first: Tzu-Wen

last: Huang

first: Chun-Yang

last: Chang

first: Shih-Feng

last: Tsai

first: Whei-Fen

last: Wu

first: Chuan-Hsiung


title: D. shibae luxI1

status: Public on Nov 03 2012

city: Třeboň

first: Jürgen

last: Tomasch

address: Novohradská 237

country: Czech Republic

institute: Center Algatech, Institute of Microbiology of the Czech Academy of Science

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

sample_organism: Dinoroseobacter shibae DFL 12 = DSM 16493

overall_design: Refer to individual Series


title: Comparison of the expression profiles of 630E JIR8094 strain and a ccpA mutant after 10h of growth in TY with 0.5% glucose.

status: Public on Oct 02 2012

city: Paris

first: Monot

last: Marc

address: 25, rue du docteur roux

department: Genomes and Genetics

country: France

institute: Institut Pasteur

summary: Transcriptionnal profiling of C. difficile 630E JIR8094 strain vs a ccpA mutant after 10h of growth in TY with 0.5% glucose

overall_design: two-conditions experiments, WT strain vs ccpA mutant strain, 4 biological replicates for each condition, in an indirect design using a 8h TY RNA preparation as Reference

first: Frederic

last: Barbut

first: Ana

last: Antunes

first: Marc

last: Monot


title: Overexpression of NUCKS1 in colorectal cancer correlates with recurrence after curative surgery (copy number analysis)

status: Public on Oct 16 2012

city: Bunkyo-ku

first: Kaoru

last: Mogushi

state: Tokyo

address: 2-1-1 Hongo

department: Intractable Disease Research Center

country: Japan

institute: Juntendo University

summary:
Purpose: The purpose of this study is to identify a novel biomarker related with distant metastases of colorectal cancer (CRC).
Experimental Design: We investigated mRNA expression profiles in 115 patients with CRC using an Affymetrix Gene Chip, and copy number profiles in 122 patients with CRC using an Affymetrix DNA Sty array. Genes in common between copy number and expression data were extracted as candidate genes. We analyzed the mRNA expression of candidate gene by quantitative reverse transcription polymerase chain reaction (RT-PCR) in 86 patients as a validation study. Furthermore, we analyzed the protein expression of candidate gene by immunohistochemical study in 269 patients, and investigated the relationship between protein expression and clinicopathologic features.
Results: By the combination of copy number analysis and gene expression analysis, We extracted 2 candidate genes related with distant metastases of CRC. Several reports show that NUCKS1, one of candidate genes, is overexpressed in several cancer tissues. But a study about the relationship between NUCKS1 and CRC is none. The mRNA expression of NUCKS1 in cancer tissues was significantly higher than those in normal tissues. Overexpression of NUCKS1 protein was associated with significantly worse　relapse-free survival of CRC. Overexpression of NUCKS1 protein was an independent risk factor for recurrence of CRC.
Conclusion: The overexpression of NUCKS1 would be a new biomarker predicting recurrence after colorectal surgery.

overall_design: Copy number analysis was performed using LCM samples of 122 colorectal cancer patients by GeneChip Human Mapping 250k Sty arrays. Non-tumor tissues obtained from 74 patients were used as unpaired reference samples.

first: Akifumi

last: Kikuchi

first: Toshiaki

last: Ishikawa

first: Satoru

last: Iida

first: Megumi

last: Ishiguro

first: Hiroshi

last: Mizushima

first: Hiroyuki

last: Uetake

last: Tanaka

first: Kenichi

last: Sugihara


title: Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors (SNP array)

status: Public on Oct 01 2012

city: Boston

first: Pasi

last: Janne

state: MA

address: 44 Binney Street Dana 820

department: Medical Oncology

institute: Dana-Farber Cancer Institute

summary: The clinical efficacy of EGFR kinase inhibitors is limited by the development of drug resistance. The irreversible EGFR kinase inhibitor WZ4002 is effective against the most common mechanism of drug resistance mediated by the EGFR T790M mutation. Here we show that in multiple complementary models harboring EGFR T790M, resistance to WZ4002 develops through aberrant activation of ERK signaling caused by either an amplification of MAPK1 or by downregulation of negative regulators of ERK signaling. Inhibition of MEK or ERK restores sensitivity to WZ4002, and the combination of WZ4002 and a MEK inhibitor prevents the emergence of drug resistance. The WZ4002 resistant MAPK1 amplified cells also demonstrate an increase both in EGFR internalization and a decrease in sensitivity to cytotoxic chemotherapy compared to the parental counterparts. Our findings provide insights into mechanisms of drug resistance to EGFR kinase inhibitors and highlight rational combination therapies that should be evaluated in clinical trials.

overall_design:
The EGFR mutant non-small cell lung cancer (NSCLC) cell line PC9 GR4 (delE746_A750/T790M) was exposed to increasing concentrations of WZ4002 similar to previously described methods. Individual clones from WZ4002-resistant (WZR) cells were isolated and confirmed to be drug resistant.
Number of samples: 5. PC9GR4 as a control. 4 clones of WZ4002-resistant PC9GR4.

middle: A

last: Jänne


title: Analysis of molecular signatures in mammalian hibernation

status: Public on Sep 01 2012

city: New York

first: Yichi

last: Xu

state: NY

address: 1275 York Avenue

institute: MSKCC

summary: Mammalian hibernators display phenotypes similar to physiological conditions in non-hibernating species under conditions of calorie restriction and fasting, hypoxia, hypothermia, ischemia-reperfusion, and sleep. However, whether or how similarities are also reflected on molecular and genetic levels is unclear. We identified molecular signatures of torpor and arousal in hibernation using a new custom-designed cDNA microarray for the arctic ground squirrel (Urocitellus parryii,) and compared them to molecular signatures of selected phenotypes in mouse. Our results show that differential gene expression related to metabolism during torpor is closely related to that during calorie restriction and hypoxia. PPARα is crucial for metabolic remodeling in hibernation. Genes related to the sleep-wake cycle and temperature response genes induced by hypothermia follow the same expression changes as in torpor-arousal cycle. Increased fatty acid metabolism might contribute to the protection against ischemia-reperfusion injury during hibernation. Further, by comparing with thousands of pharmacological signatures, we identified drugs that may induce similar expression patterns in human cell lines as during hibernation.

overall_design: Arctic ground squirrels sampled during winter hibernation were compared with the animals sampled during summer. Liver was hybridized on a custom 9,600 probes nylon membrane microarray platform.  Four squirrels in early torpor, five in late torpor, four in early arousal, four in late arousal, and seven in summer active were studied in experiments.

first: Chunxuan

last: Shao

first: Vadim

middle: B

last: Fedorov

first: Anna

middle: V

last: Goropashnaya

first: Brian

middle: M

last: Barnes

first: Jun

last: Yan


title: Affymetrix 250K StyI SNP array data for gastric and esophageal adenocarcinoma cancer types

status: Public on Sep 04 2012

first: Steven

last: Schumacher

address: 450 Brookline Ave

department: Cancer Biology

summary: Using data from high-density genomic profiling arrays, we describe the profiles of somatic copy-number aberrations (SCNAs) in 486 adenocarcinomas across all three major digestive organs, including 296 gastric and esophageal cancers. This analysis revealed that although patterns of broad, chromosome arm-level alterations are similar across the three types of adenocarcinoma, focal genomic amplifications are substantially more prevalent in gastric/esophageal adenocarcinoma. A statistical analysis identified 64 regions of significantly recurrent amplification and deletion, including those shared across these tumors and those uniquely significant in adenocarcinomas from a single organ.  Among significantly amplified genes are those encoding therapeutically targetable kinases such as ERBB2, FGFR1, FGFR2, EGFR, and MET, events noted in 14% of colorectal adenocarcinomas and 37% of gastric/esophageal tumors suggesting that analysis of genomic amplification will be a critical source of biomarkers to guide therapies in upper gastrointestinal adenocarcinomas.  While many of the other significant loci of amplifications implicate genes recognized to play roles in gastrointestinal and other cancers, other loci point to regions that may harbor novel genes contributing to these cancers.  One such event is a recurrent focal deletion present in 15% of esophageal adenocarcinomas, which we narrow to a single likely target, the Runt transcription factor subunit RUNX1. Indeed, reintroduction of RUNX1 into a cell model with this deletion inhibited anchorage-independent growth. Overall, these results demonstrate genomic features common to these tumors and identify key differences that reflect distinctive biology and potential opportunities for therapeutic intervention.

overall_design:
Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from 87 cancer DNAs derived from primary tumor tissues, as well as from DNA obtained from 1,480 normal DNA samples.
Signal intensities were normalized to raw copy number estimates using the tangent normalization method, as described in Beroukhim et al., In Press and Mermel et al., In preparation. The 250K Sty data from this submission were combined with data for 128 colon adenocarcinomas (Firestein et al, Nature 2008) and segmented using GLAD. These segmented data were then combined with segmented SNP 6.0 data for 62 colon, 97 gastric and 112 esophageal adenocarcinomas using common markers to anchor the segments.  Data analysis across samples was performed using this GISTIC 2.0 algorithm (Mermel C et al, Genome Biology 2011).

first: Austin

last: Dulak

first: Rameen

last: Beroukhim

first: Adam

middle: J

last: Bass


title: Genome-wide copy number analysis for occult lymph node metastasis in oral squamous cell carcinoma

city: Tokyo

first: Ken

last: Miyaguchi

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

institute: Tokyo Medical and Dental University

type:
SNP genotyping by SNP array
Genome variation profiling by SNP array

summary: Using Affymetrix Mapping 250K array, we studied copy number aberrations in oral squamous cell carcinoma (OSCC) to identified biomarkers associated with occult lymph node metastasis. We used frozen specimens from 60 OSCC patients.

overall_design: Copy number analysis was performed using homogenized samples of 60 oral squamous cell carcinoma patients by GeneChip Human Mapping 250k Sty arrays. As a reference, SNP array data set of 50 normal Asians (Japanese & Chinese) from HapMap database was used.

first: Narikazu

last: Uzawa

first: Kaoru

last: Mogushi

first: Ken-Ichiro

last: Takahashi

first: Chieko

last: Michikawa

first: Yoshimi

last: Nakata

last: Sumino

first: Norihiko

last: Okada

first: Yutaka

last: Fukuoka


title: Comparison of the expression profiles of 630E JIR8094 strain and a ccpA mutant

first: Monot

last: Marc


title: Transcriptome analysis of Streptococcus mutans biofilms in response to cranberry proanthocyanidins

status: Public on Aug 22 2012

city: Ithaca

first: Guoping

last: Feng

address: 262 Stocking Hall

department: Food Science

institute: Cornell University

summary: The influence of cranberry proanthocyanidins on the transcriptomic responses of Streptococcus mutans during biofilm formation was investigated.

overall_design: Treatment regimens simulating topical exposures experienced clinically (twice-daily, 60 s each) were used over saliva-coated hydroxyapatite biofilm model. Cranberry proanthocyanidins (1.5 mg/ml) in 15% ethanol was used to treat the biofilms. Four biological replicates each for the treatment and vehicle control were used for RNA extraction and microarray.

first: Hyun

last: Koo


title: MicroRNA expression in subcutaneous and visceral fat of beef steers fed different high or low fat diets

status: Public on Jul 01 2012

city: Edmonton

first: Josue

middle: Moura

last: Romao

state: Alberta

address: 116 St. and 85 Ave.

department: AFNS

country: Canada

institute: University of Alberta

summary: MicroRNAs are a class of molecular regulators found to participate in numerous biological processes, including adipogenesis. However, whether dietary changes impact on microRNA (miRNA) in ruminants has not been reported. Therefore, this study aimed to evaluate the dietary effect on miRNA expression in subcutaneous (backfat) and visceral fat depots (perirenal fat) from beef steers fed with different diets containing high or low fat levels. Fat tissues were collected from 16 Hereford x Aberdeen Angus cross bred steers (15.5 month old) fed high fat diet (5.85% fat, n=8) or control diet (1.95% fat, n=8). Total RNA from each animal was subjected to miRNA microarray analysis using a customized Agilent miRNA microarray containing 672 bovine miRNA probes. Expression of miRNAs was not equally detected under two diets; 169 miRNAs were commonly expressed while 75 were diet specific. The number of miRNAs detected per animal under high fat diet was higher than those fed control diet (p= 0.037 in subcutaneous fat and p= 0.002 in visceral fat).. Further qRT-PCR analysis confirmed that the expression of some miRNAs was highly influenced by diet (miR-19a, -92a, -92b, -101, -103, -106, -142-5p, and 296) or fat depot (miR-196a and -2454). Our results revealed that the miRNA expression can be influenced by types of fat tissues or diet, suggesting that miRNAs may regulate bovine adipogenesis when diet alters.

overall_design: In this study, a total of 32 adipose tissue samples were analyzed by microRNA microarrays, being 16 subcutaneus (backfat) and 16 visceral (perirenal fat) fat depots were collected from 16 animals (Control diet = 8) (High fat diet = 8).

first: Weiwu

last: Jin

first: Maolong

last: He

first: Tim

last: McAllister

first: Le

middle: L

last: Guan


title: Human and mouse lupus nephritis cross-species transcriptional analysis

status: Public on Aug 02 2012

city: Ann Arbor

first: Celine

middle: C

last: Berthier

state: MI

address: 1150 W. Medical Center Dr, MSRB2

institute: University of Michigan

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Identification of type A spermatogonia specific transcriptome in rainbow trout immature testis

status: Public on Jun 12 2012

city: Minato-ku

first: Makoto

last: Hayashi

address: Konan 4-5-7

department: Department of Marine Biosciences

institute: Tokyo University of Marine Science and Technology

summary: To identify the transcripts preferentially expressed in type A spermatogonia in rainbow trout immature testis, we compared the transcriptome between type A spermatogonia and testicular somatic cells by microarry analysis. We used fluorescence-activated cell sorting (FACS) to isolate type A spermatogonia or testicular somatic cells from the fishes carrying the transgene, pvasa-GFP, which expresses GFP in spermatogonia.

overall_design: RNA from type A spermatogonia and from testicular somatic cells were hybridized to a microarray after Cy3 labeling.

first: Goro

last: Yoshizaki


title: Expression data from lupus NZB/W, NZM2410, NZW/BXSB mouse kidneys prenephritic and nephritic.

summary:
Nephritis (LN) is a serious manifestation of SLE. Therapeutic studies in mouse LN models do not always predict outcomes of human therapeutic trials, raising concerns about the human relevance of these models. In this study we used an unbiased transcriptional network approach to define similarities and differences between three lupus models and human LN. Affymetrix-based expression profiles were analyzed using Genomatix Bibliosphere software and transcriptional networks were compared using the Tool for Approximate LargE graph matching (TALE).  The 20 network hubs (nodes) shared between all three models and human LN reflect key pathologic processes, namely immune cell infiltration/activation, macrophage/dendritic cell activation, endothelial cell activation/injury and tissue remodeling/fibrosis. Each model also shares unique features with human LN. Pathway analysis of the TALE nodes highlighted macrophage/DC activation as a cross-species shared feature. To distinguish which genes and activation pathways might derive from mononuclear phagocytes in the human kidneys the gene expression profile of isolated NZB/W renal mononuclear cells was compared with human LN kidney profiles. Network analysis of the shared signature highlighted NFkappaB1 and PPARgamma as major hubs in the tubulointerstitial and glomerular networks respectively. Key nodes in the renal macrophage inflammatory response form the basis for further mechanistic and therapeutic studies.
We used microarrays to analyze the renal transcriptome of three different lupus mouse models, at early stage of lupus and during lupus nephritis.

overall_design: RNA from whole kidneys was extracted and processed for hybridization on Affymetrix microarrays.

first: Tania

last: Gonzalez-Rivera

first: Ramalingam

last: Bethunaickan

first: Viji

last: Nair

first: Meera

last: Ramanujam

first: Weija

last: Zhang

first: Erwin

middle: P

last: Bottinger

first: Stephan

last: Segerer

first: Anne

last: Davidson

first: Matthias

last: Kretzler


title: Characterization of transcriptional and fitness effects of a loss of function mutation in rho

status: Public on Jun 01 2012

first: Lydia

last: Freddolino

address: 1150 W. Medical Center Dr., MSRB 3 room 3315

department: Biological Chemistry

type: Expression profiling by genome tiling array

type: Genome variation profiling by genome tiling array

summary: In order to study the effects of a mutation to the transcriptional termination regulator Rho (referred to as rho*), we made use of expression microarrays to observe the direct and indirect effects of rho* on gene expression. In addition, we used arrays to map the fitness of strains from transposon mutagenized libraries under four conditions, showing that in each case the majority of genes with significant fitness effects were dependent on the genotype at rho.

sample_organism: Escherichia coli str. K-12 substr. MG1655

overall_design: For expression arrays, we performed two-color microarrays comparing transcript levels in rho* and wild type cells during exponential growth in glucose minimal media. For selection experiments, transposon insertions were mapped through selective amplification of genomic regions adjacent to them. We then measured the fitness effects of insertions throughout the genome using two-color microarrays, comparing amplified DNA from a population grown under a selective condition of interest to an isogenic control population grown under a reference condition (glucose minimal media). All arrays were performed in duplicate, and the source material for the duplicates came from separate biological replicates.

first: Peter

first: Hani

last: Goodarzi


title: Human lung adenocarcinoma DNA methylation profiling by MSNP

status: Public on May 17 2012

city: Chapel Hill

first: Matthew

middle: D

last: Wilkerson

state: NC

address: 450 West Drive

department: Lineberger Comprehensive Cancer Center

institute: University of North Carolina at Chapel Hill

summary: Lung adenocarcinoma’s genomic alterations exhibit vast variation. Lung adenocarcinoma also has previously described intrinsic gene expression subtypes (Hayes et al. 2006, PMID: 17075127). This study detect global methylation differences among gene expression subtypes. These specimens were also assayed for genomewide transcription in GSE26939 and copy number in GSE36363.

overall_design: 33 tumor samples and 10 normal samples were quantified for DNA methylation by MSNP (Yuan et al, PMID: 16585166) using Affymetrix SNP 250K_StyI microarrays.

first: D

middle: N

last: Hayes


title: Investigating gene expression differences in two chicken lines with variable propensity to feather pecking

status: Public on Mar 17 2012

city: Freising-Weihenstephan

first: Michal

last: Wysocki

address: Liesel-Beckmann-Straße (Hochfeldweg) 1

department: Chair of Animal Breeding

country: Germany

institute: Technical University Munich

summary: Feather pecking is a major welfare problem in egg production. It may be caused by genetic, physiological and environmental factors. The main aim of this study was to uncover variability in gene expression between individuals from high (HFP) and for low feather pecking (LFP) line using Chicken Gene Expression Microarrays (Agilent Technologies).

overall_design: Samples were assorted to two groups, each containing 9 biological replicates from high feather pecking (HFP) and low feather pecking (LFP) line.

first: Jörn

last: Bennewitz


title: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (SNP)

status: Public on Apr 18 2012

city: Pamplona

first: Xabier

last: Agirre

state: Navarra

address: Pio XII, 55

department: Oncology

country: Spain

institute: CIMA

type:
Expression profiling by SNP array
SNP genotyping by SNP array

summary: Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia.  In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. In vivo administration of LBH589 in BALB/c-RAG2-/-γc-/- mice in which T and B-cell leukemic cell lines were injected induced a significant reduction in tumor growth (TOM-1, p<0.01 and MOLT-4 p<0.05). Leukemic cells from patients were employed to establish a xenograft model of human leukemia in BALB/c-RAG2-/-γc-/- mice and further transplanted in consecutive generations of mice. Treatment of these xenografts with LBH589 induced an increase in the acetylation of H3 and H4 and prolonged the survival of mice in comparison with the animals treated with Vincristine and Dexametasone (p<0.05) and this effect was significantly higher when LBH589 was combined with Vincristine and Dexametasone (p<0.001). Our results that the use of LBH589 in combination with standard chemotherapy represents an attractive option for treatment of patients with ALL.

overall_design: Two primary samples of ALL (one ALL-B and one ALL-T) and two samples of each leukemia after passages in immunodeficient mice.

first: Amaia

last: Vilas-Zornoza

first: Gloria

last: Abizanda

first: Cristina

last: Moreno

first: Victor

last: Segura

first: Alba

last: Rodriguez

first: Edurne

last: San José-Eneriz

first: María

last: Blanco-Prieto

first: Jose

last: García de Jalón

first: José

last: Rifón

first: Juan

last: Cigudosa

last: Martinez-Climent

last: Román-Gómez

last: Calasanz

first: Felipe

last: Prósper


title: miRNA Profiling in mucosal biopsies of Eosinophilic Esophagitis patients pre and post glucocorticoid steroid treatment

status: Public on Mar 23 2012

city: Providence

first: Shaolei

last: Lu

state: Rhode Island

address: 593 Eddy Steet

department: Pathology

institute: Rhode Island Hospital

summary: Eosinophlic esophagitis (EoE) is increasely recognized as an antigen-drived disorder. The goal of this study is to reveal the miRNA expression changes in EoE before and after a successful glucocorticoid steroid treatment.

overall_design: Total RNA was extracted from the esophageal epithelial layers of 5 paired paraffin-embedded biopsies before and after treatment with glucocorticosteroids using RecoverAll Total Nucleic Acid Extraction Kit for FFPE tissues (Ambion, Austin, TX). Five nanograms of total RNA was reverse-transcribed using the Taqman MicroRNA Reverse Transcription Kit and the Megaplex RT primer Human Pool A (Applied Biosystems).  The reverse-transcribed cDNA was then pre-amplified in 12 cycles of PCR using Taqman PreAmp Master Mix and the Megaplex PreAmp primers, Human Pool A (Applied Biosystems).  The cDNA’s were then diluted and loaded on to a Taqman Human miRNA Array card A (Platform GPL9731 ; Applied Biosystems), which contains probes for 377 distinct miRNAs.  The Array cards were run on an ABI HT7900 qPCR instrument.  Ct values were obtained for all miRNAs represented on the cards and fold changes in expression were calculated using the delta delta Ct (ddCt) method.

first: Kelly

last: Cleveland

first: Alexander

middle: S

last: Brodsky

first: Vincent

last: Mukkada

first: Murray

last: Resnick


title: DNA unmethylome profiling via covalent capture of CpG sites

status: Public on Mar 08 2012

city: chungli

first: sun-chong

last: wang

state: taoyuan

address: chungda road

department: systems biology

institute: national central university

summary: Cytosine 5-modification is a widespread epigenetic mark in eukaryote genomes including humans, but its large scale populational studies are hampered by substantial limitations of the existing analytical techniques. We have developed a new approach for mapping of the unmodified fraction of the genome, i.e. DNA unmethylome, which is based on covalent tagging of unmodified CpG sites with biotin. Sequence-specific tagging of DNA was achieved by using an engineered version of the SssI cytosine-5 methyltransferase and a synthetic analog of the S-adenosylmethionine cofactor carrying a transferable 6-aminohex-2-ynyl group. Analysis of the streptavidin-enriched human unmethylome on tiling DNA microarrays showed that the new approach (named mTAG-chip) offers nanogram sensitivity, a substantially higher precision in the low and medium CpG density regions and added versatility as compared with the existing epigenome profiling techniques.

overall_design:
AC103, AC13 and AC31 are DNA samples from three postmortem brains. Nr1 and Nr2 are two replicates of each sample. 5%, 20% and 70% are labeling efficiency. K means 0% labeling efficiency. We were testing which labeling efficiency was best by comparing to published seq data using correlation.

**All of the data described in PMID 23877302 is included in Series GSE48994 and GSE49044.

first: Saulius

last: Klimašauskas

first: Art

last: Petronis


title: Differentially expressed microRNAs revealed by molecular signatures of Preeclampsia and IUGR in human placenta

status: Public on Feb 07 2012

city: Raleigh

first: Ling

last: Guo

address: 1060 William Moore Drive

institute: North Carolina State University

summary: The placenta plays an important role as a regulator of fetal nutrition and growth throughout development and placental factors contribute to gestational abnormalities such as preeclampsia. This study describes the genome-wide gene expression profiles of a large (n=94) set of human placentas in order to uncover gene expression patterns (or molecular signatures) associated with preeclampsia and IUGR. Besides modulated modularity clustering and pathway analysis, a set of candidate miRNAs were predicted by Gene Set Enrichment Analysis (GSEA) based on differentially expressed genes. A case-control study was conducted to examine the expression patterns of these candidate miRNAs in human placentas

overall_design: 35 IUGR (including 8 technical repeats for batch effect), 19 preeclamptic and 40 control placentas included in this study were collected during the years of 2004-2008 and hybridized in two batches to microarrays.  Samples were randomized across arrays to control for array and batch variability.

first: Shengdar

last: Tsai

first: Nicholas

last: Hardison

first: Andra

middle: H

last: James

first: Alison

last: Motsinger-Reif

first: Betty

last: Thames

first: Jorge

last: Piedrahita


title: Affymetrix SNP array data for oral squamous cell carcinoma samples

status: Public on Dec 30 2011

city: miyazaki city

first: kentarou

last: nagai

state: miyazaki

department: Miyazaki university

institute: biochemistry

summary: The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. To identify genes responsible for OSCC development, we performed high-density single-nucleotide polymorphism array analysis and genome-wide gene expression profiling on OSCC tumors. These analyses identified "absent in melanoma (AIM2)" and "interferon-inducible gene 16 (IFI16)," mapped to the hematopoietic IFN-inducible nuclear proteins with 200-amino acid repeat (HIN-200) gene cluster in the amplified region of chromosome 1q23, with overexpression in OSCCs. AIM2 and IFI16 are cytoplasmic double-stranded DNA sensors for innate immunity and act as tumor suppressors in several human cancers. Knockdown of AIM2 or IFI16 in OSCC cells resulted in the suppression of cell growth and the induction of apoptosis, accompanied by the downregulation of NF-κB activation. Because all of the OSCC cell lines had impairment of p53 activity, wild-type p53 was introduced in p53-deficient OSCC cells, and as a result, the expression of wild-type p53 suppressed cell growth and induced apoptosis via suppression of NF-κB activity. Finally, the coexpression of AIM2 and IFI16 significantly enhanced cell growth in p53-deficient cells; in contrast, the expression of AIM2 and/or IFI16 in cells bearing wild-type p53 suppressed cell growth. Moreover, AIM2 and IFI16 synergistically enhanced NF-κB signaling in p53-deficient cells.  Thus, expression of AIM2 and IFI16 may have oncogenic functions in OSCC cells inactivating p53 system.

overall_design: Copy number analysis of Affymetrix 250K SNP arrays was performed for 5 oral leukoplakia samples, 20 oral squamous cell carcinoma samples, and 8 oral squamous cell carcinoma cell lines.

first: Yuudai

last: Kondo

first: Kazuhiro

last: Morishita


title: Expression data from macrophages isolated from lupus NZB/W mouse kidneys prenephritic, nephritic or after complete remission.

status: Public on Dec 31 2011

first: Celine

last: Berthier

summary:
Renal infiltration with mononuclear cells is associated with poor prognosis in SLE. A renal macrophage/dendritic cell signature is associated with onset of nephritis in NZB/W mice and immune modulating therapies can reverse this signature and the associated renal damage despite ongoing immune complex deposition. Our findings suggest that mononuclear phagocytes with an aberrant activation profile contribute to tissue damage in lupus nephritis by mediating both local inflammation and excessive tissue remodeling.
We used microarrays to analyze the gene expression of renal isolated macrophages at early stage of lupus (young) during lupus nephritis (sick) and after induction of remission (Rem)

overall_design: NZB/W F4/80hi mouse cells were isolated using flow cytometry; RNA from cells (young, sick and after complete remission) was extracted and processed for hybridization on Affymetrix microarrays.

first: Ramalingam

last: Bethunaickan

first: Meera

last: Ramanujam

first: Weijia

last: Zhang

first: Erwin

last: Bottinger

first: Lionel

last: Ivashkiv

first: Matthias

last: Kretzler

first: Anne

last: Davidson


title: IRF-8 extinguishes neutrophil production and promotes dendritic cell lineage commitment in both myeloid and lymphoid progenitors (Illumina).

status: Public on Jan 07 2012

city: St. Louis

first: Amy

middle: M.

last: Becker

state: MO

address: 660 S. Euclide Ave.

department: Pathology and Immunology

institute: Washington University School of Medicine

summary: While most blood lineages are assumed to mature through a single cellular and developmental route downstream of hematopoietic stem cells (HSCs), dendritic cells (DCs) can be derived from both myeloid and lymphoid progenitors in vivo.  To determine how distinct progenitors can generate similar downstream lineages, we examined the transcriptional changes that accompany loss of in vivo myeloid potential as common myeloid progenitors (CMPs) differentiate into common dendritic cell progenitors (CDPs), and as lymphoid-primed multipotent progenitors (LMPPs) differentiate into all lymphoid progenitors (ALPs).  Microarray studies revealed that Interferon regulatory factor 8 (IRF-8) expression increased during each of these transitions.  Competitive reconstitutions using Irf8-/- bone marrow demonstrated cell-intrinsic defects in the formation of CDPs and all splenic dendritic cell subsets.  Irf8-/- CMPs and, unexpectedly, Irf8-/- ALPs produced more neutrophils in vivo than their wild type counterparts at the expense of DCs.  Retroviral expression of IRF-8 in multiple progenitors led to reduced neutrophil production and increased numbers of DCs, even in the granulocyte-macrophage progenitor (GMP), which does not normally possess conventional DC potential.  These data suggest that IRF-8 represses a neutrophil module of development and promotes convergent DC development from multiple lymphoid and myeloid progenitors autonomously of cellular context.

overall_design: CMP (Lineage-c-kithiSca-1-CD11c- CD34+Flk2+CD16/32-CD115- ) or ALP (Lin-Ly6D-B220-c-kit+Flk2+IL7R alpha+) were double sorted from the bone marrow of wild type C57BL/6 mice.  RNA was extracted from 2,000-15,000 sorted cells using Qiagen RNeasy Mini kit, amplified using Nugen pico-amplification kit , and 750 ng of aRNA was hybridized to Illumina MouseRef-8 v 2.0 bead chips

first: Drew

middle: G

last: Michael

first: Ansuman

middle: T

last: Satpathy

first: Roger

last: Sciammas

first: Harinder

last: Singh

first: Deepta

last: Bhattacharya


title: Preoperative Administration of Donor-derived Human M regs to Kidney Transplant Recipients (Agilent RISET 2.0)

status: Public on Nov 28 2011

city: Bergisch-Gladbach

first: Stefan

last: Tomiuk

address: Friedrich-Ebert-Str. 68

department: Bioinformatics

institute: Miltenyi Biotec GmbH

summary:
Experiments in preclinical transplant models have indicated that preoperative administration of donor-derived M regs to transplant recipients may promote beneficial regulatory responses to a subsequent allograft. This contention is supported by results from the TAIC-I and –II clinical studies, which demonstrated that infusion of a crude cell preparation containing regulatory macrophages was both safe and could promote a state of donor-specific hyporesponsiveness. In an extension of this work, two patients were treated with donor-derived M regs prior to receiving a living-donor kidney transplant.

Keywords: Classification of clinical samples

overall_design: Whole blood samples of two patients collected at various time points before and after kidney transplantation before and after the administration of M regs were analyzed on a custom Agilent 8x15K 60mer oligonucleotide microarray encomprising 5069 probes in triplicates (GPL8136). The microarray is dedicated to transplantation research and was designed based on current literature and published and unpublished data provided by the RISET consortium. For the probe selection procedure we specially focused on the detection of multiple transcript variants of a gene, on optimized hybridization properties of the probes, and on the avoidance of crosshybridization.

first: James

last: Hutchinson

first: Edward

last: Geissler

first: Paloma

last: Riquelme

first: Uwe

last: Janssen

first: Fred

last: Fändrich


title: Activation of ERBB2 signaling causes resistance to the EGFR-directed therapeutic antibody cetuximab

status: Public on Nov 23 2011

first: Pasi

middle: Antero

last: Jänne

address: 450 Brookline Ave.; M422A

summary: HCC827 cells were grown in gradually increasing concentrations of cetuximab beginning at 0.1 ug/ml. Drug concentrations were slowly increased until the resistant cells were able to proliferate in 100 ug/ml of cetuximab. Individual clones of cetuximab resistant (CR; CR1 to CR4) cells were isolated and confirmed to be drug resistant.

overall_design: Number of samples: 5.  Parental HCC827 as a control. 4 Cetuximab resistant clones

last: Janne


title: DamID data for SUUR binding in 12-14h Embryo, larval salivary glands and larval brain

city: Novosibirsk

first: Daniil

last: Maksimov

address: Lavrentjeva ave., 8/2

country: Russia

institute: MCB NSC RAS

type: Genome binding/occupancy profiling by array

summary:
SUUR protein was found to be a major component of three repressive chromatin states named BLACK, BLUE and GREEN chromatins. Here we addressed a question of developmental dynamics of these chromatin states using SUUR as a marker.
SUUR binding in larval salivary glands, brains and 12-14 hours embryos was determined using DamID technique.

overall_design: Comparison of Dam-SUUR binding to Dam-alone signal in duplicate for each sample type.

first: Stepan

last: Belyakin

first: Dmitry

last: Korjakov


title: Secretoneurin: A new hormone? Auratus: The goldfish environmental genomics project

status: Public on Oct 06 2011

city: Gainesville

first: Christopher

middle: Joseph

last: Martyniuk

state: FL

address: CEHT Mowry Road

department: Physiological Sciences

institute: UF

summary: The objectives of this study were to examine the effect of secretoneurin (SN) on pituitary gene expression. A mixture of goldfish pituitaries from both males and females were dispersed using Typsin type II and DNase II enzymes. The cells were plated in 24-well culture plates at a density of ~2.5 x 105 cells/well. After at least 12-hr plating period, cells were washed with testing medium and pre-incubated for 1 hr to stabilize basal LH secretion. Dispersed pituitary cells were treated with 10 nM gfSN for 12 hours in static incubation after which the cells were carefully washed by 1X PBS. Total RNA was isolated by utilizing RNeasy Micro Kit (QIAGEN GmbH, Hilden, Germany) following the company’s standard protocol. RNA concentrations were determined using the NanoDrop ND-100 spectrophotometer (Thermo Scientific, Wilmington, DE). cDNA synthesis, cDNA purification and microarray slide hybridization followed our validated and established microarray protocol (Martyniuk et al., 2006; Zhang et al., 2009; Popesku et al., 2010).

platform_organism:
Carassius auratus
Cyprinus carpio

overall_design: 4 control and 4 treatment samples were hybridized using dual channel micrarray with cy3 and cy5

first: Ajoy

last: Basak

first: Wayne

last: Decatur

first: Hongxia

last: Hu

first: Hélène

last: Volkoff

first: E

last: Zhao

first: Vance

last: Trudeau


title: A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers

status: Public on Nov 03 2011

city: Charlestown

first: Stephen

middle: Michael

last: Rothenberg

address: 13th Street, Bldg. 149, 7th Floor

department: Cancer Center

institute: Massachusetts General Hospital

summary: In a genome-wide screen of human cancer cell lines, we identified homozygous intragenic microdeletions involving genes encoding components of the apical-basal cell polarity complexes.  Among these,  PARD3 is disrupted in cell lines and primary tumors from squamous carcinomas and glioblastomas.  Reconstituting PARD3 expression in both cell types restores tight junctions and retards contact-dependent proliferation. Searching specifically for small intragenic microdeletions using high-resolution genomic arrays may be complementary to other genomic deletion screens and resequencing efforts in identifying new tumor suppressor genes.

overall_design: 444 human cancer cell lines of diverse tissue origin and 6 EBV-transformed B-lymphocyte cell lines (Coriell Institute for Medical Research, Camden, NJ) as controls.

first: S

first: Jeffrey

last: Settleman

first: Daniel

middle: A

last: Haber


title: MYC drives resistance to PI3K/mTOR targeted inhibition (Sty SNP array)

status: Public on Aug 31 2011

city: Boston

first: Nina

last: Ilic

address: 44 Binney Street

institute: Dana-Farber Cancer Institute

summary: Genomic copy-number changes were measured using 250K StyI SNP arrays after selection of cells to enrich for resistance to BEZ235. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted using Qiagen DNeasy from engineered human cell-lines.

overall_design: Resulting alterations in copy numbers were calculated based on SNP intensities.

first: Thomas

last: Roberts


title: Evaluation of the testicular toxicity of prenatal exposure to bisphenol A and phthalate based on microarray analysis

status: Public on Jul 25 2011

city: Noda

first: Masakazu

last: Umezawa

state: Chiba

address: 2641 Yamazaki

department: Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences

institute: Tokyo University of Science

summary: In the present study, the effects of prenatal exposure to bisphenol A (BPA) and diethyl hexyl phthalate (DEHP) on male reproductive system of offspring were examined by a tissue-specific microarray and gene annotation with Medical Subject Headings (MeSH) indicative of testicular components. The aim of this study was to investigate the validity of microarray analysis with MeSH as a method for obtaining and evaluating an overview of testicular toxicity mechanisms in maternally exposed specimens. Pregnant mice were treated with BPA or DEHP by subcutaneous administration on days 7 and 14 of pregnancy. Tissue and blood samples were collected from 6-week-old male offspring. Testes were subjected to gene expression analysis using quantitative RT-PCR and cDNA microarray (testis2). To interpret the microarray data, genes were classified using MeSH related to the functions of testis and sperm. As a result, MeSH categories related to androgen of dysregulated genes and Sertoli cells of downregulated genes were only enriched in BPA-treated groups. These results were consistent with the observations in the sperm properties and histological examination of testes. This article concludes that 1) microarray analysis of expression changes of genes associated with testicular function and spermatogenetic process, and 2) a method using MeSH to extract common terms among dysregulated genes, are useful for predicting an overview of the testicular and reproductive toxicity of prenatal exposure to chemical substances.

overall_design: RNA sample was taken from testis of 6 weeks old mouse prenatally received BPA (5 and 50 mg/kg/time) or DEHP (2 and 20 mg/kg/time), while control RNA was taken from control counterpart prenatally received corn oil alone. Direct dye-swap comparisons of sample/control were made on a pair of arrays with normalized data from Cy3/Cy5 channels for data analysis and comparison to the control data.

first: Hitoshi

last: Tainaka

first: Hikari

last: Takahashi

first: Hiromitsu

last: Tanaka

first: Yoshitake

last: Nishimune

first: Shigeru

last: Oshio

first: Ken

last: Takeda


title: L2_PolII_8wg16 set2 ChIP-chip

status: Public on Mar 30 2011

city: Toronto

first: DCC

last: modENCODE

state: Ontario

address: MaRS Centre, South Tower, 101 College Street, Suite 800

institute: Ontario Institute for Cancer Research

summary:
modENCODE_submission_904
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of all the Transcription Factors (TF) and DNA associated proteins on the genome of Drosophila melanogaster. The main technique that will be used for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested TF. ChIP-seq, meaning direct sequencing of the ChIP sample on the Solexa platform, has also been used to validate some datasets and will become- as the project advances- the main production platform. To support ChIP-chip and ChIP-seq datasets, and in order to link association of factors to the DNA with regulation of transcription, several RNA-seq (direct sequencing of the transcriptome on the Solexa platform) datasets will be genrated for the time-points under scrutiny.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: L2; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage L2; Antibody PolII (target is RNA Polymerase II); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )

first: Kevin

last: White

first: Nicolas

last: Negre

first: Nick

last: Bild


title: R13_1-6_eve-GFP

summary:
modENCODE_submission_2603
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of all the Transcription Factors (TF) and DNA associated proteins on the genome of Drosophila melanogaster. The main technique that will be used for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested TF.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: R13-YFP; Developmental Stage: Embryo 1-6h; Genotype: eveR13; [BACRO1LO1 eve YFP]attP2; Transgene: PhiC31;  NUMBER OF REPLICATES: 2;  EXPERIMENTAL FACTORS: Developmental Stage Embryo 1-6h; Antibody odg-GFP (target is eGFP); Strain R13-YFP


title: ISO1_8-16_Ez

summary:
modENCODE_submission_2585
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of all the Transcription Factors (TF) and DNA associated proteins on the genome of Drosophila melanogaster. The main technique that will be used for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested TF.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp; Developmental Stage: Embryo 8-16h; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1];  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage Embryo 8-16h; Antibody KW4-E(z)-D2 (target is Enhancer of zeste); Strain Y cn bw sp


title: MozAtlas: A comprehensive gene expression atlas of sex- and tissue-specificity in the malaria vector, Anopheles gambiae.

status: Public on May 16 2011

city: Cambridge

first: Dean

last: Baker

address: Department of Genetics, Downing Street

country: United Kingdom

institute: University of Cambridge

summary:
Background.
The mosquito, Anopheles gambiae, is the primary vector of human malaria, a disease responsible for millions of deaths each year.  To improve strategies for controlling transmission of the causative parasite, Plasmodium falciparum, we require a thorough understanding of the developmental mechanisms, physiological processes and evolutionary pressures affecting life-history traits in the mosquito.  Identifying genes expressed in particular tissues or involved in specific biological processes is an essential part of this process.
Results.
In this study, we present transcription profiles for ~82% of annotated Anopheles genes in dissected adult male and female tissues.  The sensitivity afforded by examining dissected tissues found gene activity in an additional 20% of the genome that is undetected when using whole-animal samples.  The somatic and reproductive tissues we examined each displayed patterns of sexually dimorphic and tissue-specific expression.  By comparing expression profiles with Drosophila melanogaster we also assessed which genes are well conserved within the Diptera versus those that are more recently evolved.
Conclusions.
Our expression atlas and associated publicly available database, the MozAtlas (www.tissue-atlas.org), provides information on the relative strength and specificity of gene expression in several somatic and reproductive tissues, isolated from a single strain grown under uniform conditions.  The data will serve as a reference for other mosquito researchers by providing a simple method for identifying where genes are expressed in the adult, however, in addition our resource will also provide insights into the evolutionary diversity associated with gene expression levels among species.

platform_organism:
Plasmodium falciparum
Anopheles gambiae

overall_design: MozAtlas is composed of data covering 15 distinct adult tissues with 4 replicates using Affymetrix chips. To provide other researchers with the ability to compare their own experiments with our analyses, we have constructed a database and web-browser for querying tissue expression in Anopheles.  This framework will in the future be expanded to include additional tissues and developmental stages, as well as additional species when available.

first: Tony

last: Nolan

first: Bettina

last: Fisher

first: Alex

last: Pinder

first: Andrea

last: Crisanti

first: Steven

last: Russell


title: E0-4_H3K4Me3

summary:
modENCODE_submission_771
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of all the Transcription Factors (TF) and DNA associated proteins on the genome of Drosophila melanogaster. The main technique that will be used for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested TF.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp; Developmental Stage: E0-4; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 9;  EXPERIMENTAL FACTORS: Developmental Stage E0-4; Antibody H3K4me3 (target is H3K4me3); Strain Y cn bw sp


title: Genomic Profiling of NHL Entities

status: Public on Jan 01 2011

city: Southport

first: Michael

middle: Richard

last: Green

state: Queensland

address: 58 Parklands Drive

department: Griffith Insitute for Health & Medical Research

country: Australia

institute: Griffith University

summary: Genomic analysis of DLBCL, FL and CLL.

overall_design: Genomic DNA from tumor samples analysed using Affymetrix 250K Sty Single Nucleotide Polymorphism microarrays.

middle: R

first: Lyn

last: Griffiths


title: E12-16_CBP ChIP-chip

status: Public on Dec 10 2010

summary:
modENCODE_submission_905
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of many of the non-histone chromosomal proteins on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested chromatin-binding protein.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: E12-16; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage E12-16; Antibody No Antibody Control (target is Not Applicable); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )


title: E0-4_H3K27Ac set2 ChIP-chip

summary:
modENCODE_submission_970
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of the main post-translationally modified histones on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested histone modification.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: E0-4; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage E0-4; Antibody H3K27Ac (target is H3K27Ac); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )


title: E12-16_PolII ChIP-chip

summary:
modENCODE_submission_906
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of many of the non-histone chromosomal proteins on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested chromatin-binding protein.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip


title: microRNA profile of human liver tissues: hepatocellular carcinoma vs. matched noncancerous liver tissue

status: Public on Aug 16 2011

city: Guangzhou

first: Rongrong

last: Wei

address: 651 Dongfeng East Road

country: China

institute: Sun Yat-sen University

summary: microRNA profiling of  hepatocellular carcinoma vs. matched noncancerous liver tissue

overall_design: 166 pairs of  hepatocellular carcinoma and matched noncancerous liver tissues

first: Guoliang

last: Huang

first: Huiyun

last: Wang


title: E0-4_H3K9Me3-Set2 ChIP-chip

summary:
modENCODE_submission_971
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of the main post-translationally modified histones on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested histone modification.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: E0-4; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage E0-4; Antibody H3K9me3 (target is H3K9me3); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )


title: ISO1_8-16_mod_mdg4

summary:
modENCODE_submission_2602
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of all the Transcription Factors (TF) and DNA associated proteins on the genome of Drosophila melanogaster. The main technique that will be used for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested TF.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp; Developmental Stage: Embryo 8-16h; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1];  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage Embryo 8-16h; Antibody KW4-mod(mdg4)-D2 (target is mod(mdg4)); Strain Y cn bw sp


title: AdultMale-H3K27me3

summary:
modENCODE_submission_372
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of the main post-translationally modified histones on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested histone modification.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: Adult Male; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Male;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage Adult Male; Antibody H3K27me3 (target is H3K27me3); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )

first: Parantu

last: Shah


title: AdultFemale_H3K9Ac

summary:
modENCODE_submission_581
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of the main post-translationally modified histones on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested histone modification.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: Adult Female; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Female;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage Adult Female; Antibody No Antibody Control (target is Not Applicable); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )


title: E8-12_CBP_Set2

summary:
modENCODE_submission_903
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of many of the non-histone chromosomal proteins on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested chromatin-binding protein.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: E8-12; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage E8-12; Antibody No Antibody Control (target is Not Applicable); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )


title: AdultFemale_H3K9Me3

summary:
modENCODE_submission_429
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of the main post-translationally modified histones on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested histone modification.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip


title: E16-20_H3K9Ac

summary:
modENCODE_submission_411
This submission comes from a modENCODE project of Kevin White. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The White Lab is aiming to map the association of the main post-translationally modified histones on the genome of Drosophila melanogaster. One technique that we use for this purpose is chromatin immunoprecipitation-on-chip (ChIP-on-chip) utilizing whole-genome tiling arrays. The data generated by ChIP-chip experiments consist basically of a plot of signal intensity across the genome. The highest signals correspond to positions in the genome occupied by the tested histone modification.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
CHIP-chip

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] ); Developmental Stage: E16-20; Genotype: y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1]; Sex: Unknown;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Developmental Stage E16-20; Antibody H3K9Ac (target is H3K9Ac); Strain Y cn bw sp(genotype : y[1] oc[R3.2]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] lab[R4.2] MstProx[1] GstD5[1] Rh6[1] official name : y[1]; Gr22b[1] Gr22d[1] cn[1] CG33964[R4.2] bw[1] sp[1]; LysC[1] MstProx[1] GstD5[1] Rh6[1] )


title: Global gene expression of chemical carcinogen (N-methyl-N-nitrosourea), Helicobacter pylori infection, and high-salt diet-treated mouse gastric mucosa

status: Public on May 25 2011

city: Tokyo

first: Takeshi

last: Toyoda

address: 1-18-1 Kamiyoga, Setagaya-ku

department: Division of Pathology

institute: National Institute of Health Sciences

summary: Helicobacter pylori (H. pylori) infection and excessive salt intake are known as important risk factors for stomach cancer in humans. However, interactions of these two factors with gene expression profiles during gastric carcinogenesis remain unclear. In this study, we established a mouse gastric tumor model combining a chemical carcinogen, H. pylori infection and a high-salt diet. The tumor incidence and multiplicity in N-methyl-N-nitrosourea-treated mice were significantly increased by combination of H. pylori with a high-salt diet. In addition, detailed examination indicated that excessive salt could regulate progression of gastric tumor. Global gene expression profiles in glandular stomach of the mouse model were investigated by cDNA microarray analysis, and 36 and 31 more than twofold up-regulated and down-regulated genes, respectively, were detected in the H. pylori-infection and high-salt diet combined group compared with the other groups. Quantitative RT-PCR confirmed significant over-expression of several candidate genes including Cd177, Reg3g, and Muc13. These results suggest that our mouse model combined with H. pylori infection and high-salt diet is useful for gene expression profiling in gastric carcinogenesis.

overall_design: Five- to six-week-old male C57BL/6J mice (CLEA Japan, Tokyo, Japan) were inoculated with Helicobacter pylori (Sydney strain 1) (Sample No. 2 and 4) or Brucella broth (Sample No. 1 and 3). The animals were administered 120 ppm N-methyl-N-nitrosourea (MNU) in their drinking water on alternate weeks (total exposure, 5 weeks). Mice were given basal diet (CE-2, CLEA Japan) (Sample No. 1 and 2) or high-salt diet containing 10% NaCl (Sample No. 3 and 4). At 40 weeks, the animals were subjected to deep anesthesia and laparotomy with excision of the stomach.

first: Takashi


title: Hoxd genes and fiber type-specific markers specify adult mouse muscle type in a diet-independent way

status: Public on Sep 03 2010

city: Maastricht

first: Janneke

last: de Wilde

address: Universiteitssingel 50

department: Human Biology

country: Netherlands

institute: Maastricht University

summary:
Introduction: The mouse skeletal muscle is composed of four distinct fiber types that differ in contractile function, number of mitochondria and metabolism. Every muscle group has a specific
composition and distribution of the four fiber types. Until now, three genes (CnA, PGC1α and PPARδ) are identified that are involved in the generation of more oxidative muscle types. In the present
study we searched for novel genes that are involved in specifying different muscle types. Methods: Gastrocnemius and quadriceps muscles were dissected from 20-week old C57BL/6J mice. Gene
expression profiles were compared at the level of the whole-transcriptome. The diet-sensitivity of genes differentially expressed between muscle types was explored by comparing mice fed a low fat
diet with mice fed a high fat diet. Results: We identified 162 differentially expressed genes in the gastrocnemius as compared with the quadriceps. Genes with the strongest regulations were markers for
oxidative fiber types, Hoxd8, Hoxd9 and Hoxd10 and others involved in embryogenesis. Additionally, diet did not influence the expression levels of genes specifying muscle types. Finally, when
extrapolating our data to the soleus we could not find a corresponding gene expression pattern between Hoxd8, Hoxd9 and any of the fiber-type specific markers. However, based on these gene
expression patterns we could distinguish the gastrocnemius, quadriceps and soleus from each other. Conclusion: Hoxd genes and genes that are markers for the different fiber types specify muscle
type in a diet-independent way

overall_design:
The  aim of the present study was to find novel genes that may play a role in specifying muscle types. Therefore we compared gene expression profiles of the
gastrocnemius with the quadriceps at the level of the whole-transcriptome. Functional implications were assessed by the analyses of predefined gene sets based on
Gene Ontology, biochemical, metabolic and signaling pathways.
muscle-type comparison

first: J

first: E

last: Smit

first: M

last: Boekschoten

first: P

last: de Groot

last: Hulshof

last: Mariman


title: Genomic Acquisition of Virulence Factors in Natural Isolates of Burkholderia

status: Public on Aug 15 2010

city: SINGAPORE

first: BERNICE

middle: MENGQI

last: SIM

state: SINGAPORE

address: 60 Biopolis Street, Genome; #02-01

department: INFECTIOUS DISEASES 2

country: Singapore

institute: GENOME INSTITUTE OF SINGAPORE

summary:
An important, but rarely performed, test of Koch’s molecular postulates involves evaluating the capacity of candidate virulence genes to confer pathogenicity in otherwise non-virulent species. Unbiased genomic surveys of avirulent natural isolates might reveal rare variants possessing specific virulence features, which might prove useful in testing their functional sufficiency. Using a custom pan-genome array, we analyzed a panel of avirulent Burkholderia thailandensis (Bt) isolates related to Burkholderia pseudomallei (Bp), the causative agent of the often fatal human and animal disease melioidosis. We report the discovery of variant Bt isolates exhibiting isolated acquisition of a capsular polysaccharide biosynthesis gene cluster (BpCPS), long regarded as an critical species-specific virulence factor essential for Bp mammalian virulence.
BpCPS-expressing Bt strains exhibited certain pathogen-related phenotypes including resistance to human complement binding, but did not exhibit enhanced virulence when assessed in two different in vivo animal infection models. Phylogenetic analysis revealed that the BpCPS-expressing Bt strains likely reside within an evolutionary subgroup distinct from the majority of previously-described Bt strains. Our findings suggest that BpCPS acquisition alone is unlikely to fully explain the ability of Bp to colonize humans and animals, highlighting the importance of other collaborating factors in the pathogenesis of mammalian melioidosis.

overall_design: Genomic DNA of several Bt strains were hybridized against a common reference strain (Bt E264), to see gain/loss

first: Bernice

middle: M

last: Sim

first: Chi

last: Lin

first: W

middle: F

last: Ooi


title: Integration of transcript expression, copy number and LOH analysis of infiltrating ductal carcinoma of the breast: copy number analysis

status: Public on Jul 17 2010

city: Augusta

first: Lesleyann

last: Hawthorn

state: GA

department: Molecular Oncology

institute: Medical College of Georgia Cancer Center

summary:
Introduction: A major challenge in the interpretation of genomic profiling data generated from breast cancer samples is the identification of driver genes as distinct from bystander genes which do not impact tumorigenesis. One way to assess the relative importance of alterations in the transcriptome profile is to combine complementary analyses that assess changes in the copy number alterations (CNAs). This integrated  analysis  permits the identification of genes with altered expression that map within specific chromosomal regions that demonstrate copy number alterations, providing a mechanistic approach to  identify the 'driver genes’.

Methods:  We have performed whole genome analysis of CNAs using the Affymetrix 250K Mapping array on 22 infiltrating ductal carcinoma samples (IDCs). Analysis of transcript expression alterations was performed using the Affymetrix U133 Plus2.0 array on 16 IDC samples. Twelve IDC samples were analyzed using both platforms and the data integrated. We also incorporated data from LOH analysis to identify genes showing loss of expression in LOH regions.

Results:  Copy number analysis results demarcated smaller boundaries for many previously reported CNAs, and in some cases, the CNAs were defined as more than a single contiguous event. Additionally, we were able to assign driver genes to these commonly reported regions using a rigorous methodology. For example, RAB25 showed a large increased expression in the tumors and mapped to the commonly reported amplification at 1q22. We also identified 5 genes in the 8q24 amplicon and TSEN4 in the 17q25 amplified region. LOH analysis confirmed some previously reported regions, and integration with copy number data determined that the detected LOH were copy neutral events. Finally, we have identified several RXR pathways that demonstrated down-regulation in IDC whose members may represent further targets of therapeutic intervention.

Conclusion: We have demonstrated the utility of the application of integrated analysis using high-resolution CGH and whole genome transcript analysis for detecting driver genes in IDC. The high resolution platform allowed a refined demarcation of CNAs, and gene expression profiling provided a mechanism to detect genes directly impacted by the CNA. This is the first report of LOH in IDC using a high resolution platform.

overall_design: 22 IDC samples were analyzed for CNA and an overlapping 16 samples were analyzed for gene expression


title: Affymetrix SNP array data for soft tissue sarcoma samples

status: Public on Jul 06 2010

city: New York

first: Barry

middle: Stephen

last: Taylor

address: 1275 York Avenue, Box #460

institute: Memorial Sloan-Kettering Cancer Center

summary: Soft tissue sarcomas are aggressive mesenchymal cancers that affect more than 10,600 new patients per year in the US, about 40% of whom will die of their disease. Soft tissue sarcomas exhibit remarkable histologic diversity, with more than 50 recognized subtypes, but our knowledge of their genomic alterations is limited. Here we describe the results of an integrative analysis of DNA sequence, copy number, and mRNA expression in 207 samples encompassing seven major subtypes. Genes mutated in more than 5% of samples within a subtype were KIT (in gastrointestinal stromal cell tumors, or GISTs), TP53 (pleomorphic liposarcomas), PIK3CA (myxoid/round-cell liposarcoma), and NF1 (both myxofibrosarcoma and pleomorphic liposarcoma). We show evidence that PIK3CA mutations, found in 18% of myxoid/round-cell liposarcomas, activate AKT in vivo and are associated with poor outcomes. Point mutations in the tumor suppressor gene NF1 were discovered in both myxofibrosarcomas and pleomorphic liposarcomas, while genomic deletions were observed in all subtypes at varying frequencies. Finally, we found that short hairpin RNA-based knockdown of a subset of genes that are amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell proliferation. Our study yields the most detailed map of molecular alterations across diverse sarcoma subtypes to date and provides potential subtype-specific targets for therapy.

overall_design: Human soft tissue sarcoma samples and their matched normal DNA were profiled on Affymetrix 250K SNP (Sty) arrays per manufacturer's instructions

first: Jordi

last: Barretina

first: Matthew

last: Meyerson

first: Samuel

last: Singer


title: Indices of Tolerance (IOT): Cross-platform biomarkers that identify kidney transplant tolerance

status: Public on May 25 2010

first: Stefan

last: Tomiuk

summary:
Being able to identify patients in whom immunological tolerance has been established or is developing would allow an individually tailored approach to post-transplant management of kidney allograft recipients. Ex vivo immunological monitoring was performed on samples from five groups of European renal transplant recipients (“IOT samples”): ten drug-free tolerant recipients who were functionally stable despite remaining immunosuppression-free for more than one year (Tol-DF); also functionally stable patients on minimal immunosuppression (<10 mg/day prednisone, s-LP); stable patients maintained with calcineurin inhibitors (s-CNI); stable patients maintained on CNI-free immunosuppression regimen (s-nCNI); patients showing signs of chronic rejection (CR) and healthy controls (HC). Among the investigation of other biomarkers and bioassays, gene expression profiles were generated on custom Agilent 8x15K 60mer oligonucleotide microarrays (“RISET 2.0”) on the IOT cohort (training set) and on an independent cohort of patients from the ITN (USA) that contained similar groups of patients and included 23 tolerant recipients (“ITN samples”, test set). Set of genes were identified, whose expression on whole blood allowed the identification of 100% of the tolerant recipients in the training set and 84% in the test set.

Keywords: classification of clinical samples, tolerance prediction

overall_design: IOT samples: 13 samples from 10 Tol-DF patients, 16 samples from 11 s-LP patients, 8 samples from 8 s-nCNI patients, 40 samples from 28 s-CNI patients, 10 samples from 9 CR patients, and 8 samples from 8 HC donors were analysed on a custom Agilent 8x15K 60mer oligonucleotide microarray encomprising 5069 probes in triplicates. The microarray is dedicated to transplantation research and was designed based on current literature and published and unpublished data provided by the RISET consortium. For the probe selection procedure we specially focused on the detection of multiple transcript variants of a gene, on optimized hybridization properties of the probes, and on the avoidance of crosshybridization. The sampling dates of replicate samples from the same patient range from one day to 1.5 years. ITN samples: 31 samples from 23 Tol-DF patients, 14 samples from 11 s-LP patients, 52 samples from 34 s-CNI patients, 25 samples from 18 CR patients, and 20 samples from 20 HC donors were analysed on the same microarray platform and served as test set. The samples of the two cohorts differ in the protocol of RNA preparation.

first: Uwe

last: Janssen

first: Maria

middle: P

last: Hernandez-Fuentes

first: Birgit

last: Sawitzki

first: Pervinder

last: Sagoo

first: Esperanza

last: Perucha

first: David

last: Stephens

first: Patrick

last: Miqueu

first: Stephanie

last: Chapman

first: Ligia

last: Craciun

first: Ruhena

last: Sergeant

first: Sophie

last: Brouard

first: Flavia

last: Rovis

first: Elvira

last: Jimenez

first: Amany

last: Ballow

first: Magali

last: Giral

first: Alain

last: Le Moine

first: Cecile

last: Braudeau

first: Rachel

last: Hilton

first: Bettina

last: Peters

first: Kasia

last: Bourcier

first: Adnan

last: Sharif

first: Magdalena

last: Krajewska

first: Graham

last: Lord

first: Ian

last: Roberts

first: Michel

last: Goldman

first: Kathryn

middle: J

last: Wood

first: Kenneth

last: Newel

first: Vicki

last: Seyfert-Margolis

first: Lawrence

last: Turka

first: Anthony

last: Warrens

first: Hans-Dieter

last: Volk

first: Jean-Paul

last: Soulillou

first: Robert

middle: I

last: Lechler


title: A high fat diet causes obesity and insulin resistance in mice, but induces small changes in the muscle transcriptome

status: Public on Aug 10 2010

first: Janneke

last: de Wilde

summary:
An 8-week high fat palm oil diet causes obesity and insulin resistance in C57BL/6J mice, but induces only small changes in the muscle transcriptome.
Introduction: The metabolic syndrome (MS) is a cluster of metabolic abnormalities linked to an increased risk of type 2 diabetes and cardiovascular diseases. Two major characteristics of the MS are obesity and insulin resistance. In the present study we investigated the effect of obesity and insulin resistance on the mouse muscle transcriptome.
Methods: C57BL/6J mice were fed a palm oil-based low fat diet (LFD) or high fat diet (HFD) for eight weeks. Microarray analysis was performed by using two complementary strategies: (1) 8-week HFD transcriptome versus 8-week LFD transcriptome and (2) transcriptome of mice sacrificed at the start of the intervention versus 8-week LFD transcriptome and 8-week HFD transcriptome, respectively.
Results: HFD mice develop obesity and whole-body insulin resistance. Despite these metabolic disturbances we found that HFD induces relatively small changes in gene expression (< 1.3 fold). Only the up-regulation of FA oxidation and the down-regulation of the MAPK cascade were specific for the HFD intervention. Eight-weeks of aging induced more changed gene expression levels than the HFD, including genes involved in cell-cell interaction and development.
Conclusion: Eight weeks of aging induce more pronounced changes in the muscle transcriptome than an HFD.  Since only one strategy revealed the transcriptional down-regulation of the MAPK cascade, whereas both strategies showed the up-regulation of FA oxidation we suggest the use of complementary analysis strategies by the genome-wide search of gene expression changes induced by mild interventions, such as an HFD.

Keywords: diet intervention and time course

overall_design:
In this study, C57BL/6J mice were fed a high fat (HF) diet for 8 weeks to induce obesity and insulin resistance. Plasma levels of the adipokines leptin and adiponectin were measured.
To investigate how these metabolic disturbances will influence the skeletal muscle transcriptome we performed whole-genome microarray analysis. Functional implications were assessed by analyses of predefined gene sets based on Gene Ontology, biochemical, metabolic and signaling pathways.

first: J

first: E

last: Smit

first: R

last: Mohren

first: M

last: Boekschoten

first: P

last: de Groot

first: S

last: van den Berg

last: Bijland

last: Voshol

first: K

last: Willems - Van Dijk

first: N

last: de Wit

first: A

last: Bunschoten

first: G

last: Schaart

last: Hulshof

last: C Mariman


title: Affymetrix 250K StyI SNP array data from PBMCs and cell lines of metastatic melanoma patients

status: Public on Apr 13 2010

city: Heidelberg

first: Andreas

last: Gast

state: BW

address: INF 580

department: Division of Molecular Genetic Epidemiology

institute: Gernman Cancer Research Center

summary: Allele call files from on 250K StyI SNP array using DNA from 60 human cell lines from metastasized melanoma and from 44 corresponding peripheral blood mononuclear cells (CEL and CHP files provided).

overall_design: Analysis of the 250K StyI arrays was performed for 60 malignant melanoma cell lines derived from metastatic tumors of melanoma patients with GCOS and GTYPE (Affymetrix). In addition, DNA from peripheral blood mononuclear cells (PBMC) was available for 44 of the 60 samples.

first: Dominique

last: Scherer

first: Bowang

last: Chen

first: Sandra

last: Bloethner

first: Stephanie

last: Melchert

first: Antje

last: Sucker

first: Kari

last: Hemminki

first: Dirk

last: Schadendorf

first: Rajiv

last: Kumar


title: Affymetrix 250K StyI SNP array data across multiple human cancer types

status: Public on Feb 18 2010

first: Craig

last: Mermel

state: MA

address: 7 Cambridge Center

department: Cancer Program

institute: Broad Institute

summary: A powerful way to discover key genes playing causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. We have reported high-resolution analyses of somatic copy-number alterations (SCNAs) from 3131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across multiple cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several candidate genes and families are enriched among these regions of focal SCNA, including members of the BCL2 family of apoptosis regulators and the NF-κΒ pathway. We show that cancer cells harboring amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend upon expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in multiple cancer types.

overall_design:
Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from 3,131 cancer DNAs derived from primary tissues or cell line material, as well as from DNA obtained from 1,480 normal DNA samples.

Signal intensities were normalized to raw copy number estimates using the tangent normalization method, as described in Beroukhim et al., In Press and Mermel et al., In preparation. Data analysis across samples was performed using this GISTIC algorithm (Beroukhim R et al, PNAS 2007).

The 250K SNP array data used in this study were obtained from several sources, including 2,327 previously or concurrently published data from our laboratory and other groups and 804 previously unpublished data from cancer and normal specimens (included in this submission).  The 2,327 published cancer copy-number profiles not included in our submission consist of data from the following publications (see below for full references):
- 510 non-small cell lung cancers (Ramos et al 2009; GlaxoSmithKline; Bass et al; Weir et al; and Sos et al)
- 388 acute lymphoblastic leukemias (GlaxoSmithKline; Mullighan et al 2007; Mullighan et al 2008)
- 215 myeloproliferative disorders (Kilpivaara et al)
- 130 breast cancers (GlaxoSmithKline; Haverty et al; Nikolsky et al)
- 151 colorectal cancers (GlaxoSmithKline; Firestein et al)
- 115 miscellaneous other types of cancer (GlaxoSmithKline)
- 111 renal cancers (GlaxoSmithKline; Beroukhim et al)
- 106 hepatocellular cancers (GlaxoSmithKline; Chiang et al)
- 77 melanomas (GlaxoSmithKline; Lin et al)
- 54 prostate cancers (GlaxoSmithKline; Demichelis et al)
- 40 esophageal squamous cell carcinomas (GlaxoSmithKline; Bass et al)
- 31 neuroblastomas (GlaxoSmithKline; George et al)
- 21 non-Hodkgin's lymphomas (GlaxoSmithKline)
- 21 small cell lung cancers (GlaxoSmithKline)
- 10 gliomas (GlaxoSmithKline)
- 4 thyroid cancers (GlaxoSmithKline)
- 2 medulloblastomas (GlaxoSmithKline)
- 7 ovarian cancers (GlaxoSmithKline)
- 212 sarcoma samples of various subtypes (Barretina et al, in review)
- 73 esophageal adenocarcinoma samples (Ramos et al, in Preparation)
- 26 mesotheliomas (Barchmann et al, in preparation)
- 23 gastric cancer samples (GlaxoSmithKline; Ramos et al, in preparation).

Full references:
Bass, A., Watanabe, H., Mermel, C. & al, e. SOX2 is an amplified lineage-survival oncogene in lung and esophageal squamous cell carcinoma. Nat Genet 41, 1238-42 (2009).
Beroukhim, R. et al. Patterns of gene expression and copy-number alterations in VHL disease-associated and sporadic clear cell carcinoma of the kidney. Cancer Res 69, 4674-4681 (2009).
Chiang, D. Y. et al. Focal gains of VEGFA and molecular classification of hepatocellular carcinoma. Cancer Res 68, 6779-6788 (2008).
Demichelis, F. et al. Distinct genomic aberrations associated with ERG rearranged prostate cancer. Genes Chromosomes Cancer 48, 366-380 (2009).
Firestein, R. et al. CDK8 is a colorectal cancer oncogene that regulates [bgr]-catenin activity. Nature 455, 547-551 (2008).
George, R. E. et al. Genome-wide analysis of neuroblastomas using high-density single nucleotide polymorphism arrays. PLoS ONE 2, e255 (2007).
GlaxoSmithKline. GSK Cancer Cell Line Genomic Profiling Data, https://cabig.nci.nih.gov/tools/caArray_GSKdata  (2008).
Haverty, P. M. et al. High-resolution genomic and expression analyses of copy number alterations in breast tumors. Genes Chromosomes Cancer 47, 530-542 (2008).
Kilpivaara, O. et al. A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasms. Nat Genet 41, 455-459 (2009).
Lin, W. M. et al. Modeling genomic diversity and tumor dependency in malignant melanoma. Cancer Res 68, 664-673 (2008).
Mullighan, C. G. et al. Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia. Nature 446, 758-764 (2007).
Mullighan, C. G. et al. BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature 453, 110-114 (2008).
Nikolsky, Y. et al. Genome-wide functional synergy between amplified and mutated genes in human breast cancer. Cancer Res 68, 9532-9540 (2008).
Ramos, A. et al. Amplification of PDGFRA and KIT in Non-small Cell Lung Cancer. Cancer Biology and Therapy 8, 2051-3 (2009).
Sos, M. L. et al. Predicting drug activity in non-small cell lung cancer based on genetic lesions. JCI 119, 1727-1740 (2009).
Weir, B. A. et al. Characterizing the cancer genome in lung adenocarcinoma. Nature 450, 893-898 (2007).

first: Rameen

last: Beroukhim

middle: H

first: Matthew

middle: L

last: Meyerson