title: Gene expression data ARID1A knockdown OE33 cells versus mock OE33 cells

city: Baltimore

first: Mirte

middle: Mayke

last: Streppel

state: Maryland

address: 1550 Orleans street, CRBII rm341

department: Pathology

institute: Johns Hopkins Hospital

summary:
A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells.
ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen)

overall_design: Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.

first: Anirban

last: Maitra

middle: M


title: Transcriptomic analysis of Etoposide-treated 293 cells expressing p65 wt or p65 S547A

status: Public on May 31 2012

city: Liege

first: Helene

last: Sabatel

address: avenue de l'hopital

country: Belgium

institute: Universite de Liege

summary: We reported a direct phosphorylation of the Ser547 of the RelA/p65 subunit of NF-kB by ATM kinase. A comparative transcriptomic analyse with HEK293 cells expressing exclusively HA-p65wt or a non-phosphorylable mutant HA-p65S547A was conducted to identify the genes regulated by this phosphorylation after an Etoposide treatment.

overall_design: HEK293 cells expressing exclusively HA-p65wt or HA-p65S547A were treated during four or eight hours with Etoposide or left untreated. This was performed three times to obtain independent triplicates for the microarray expermiment.

first: Emmanuel

last: Divalentin

first: Geoffrey

last: Gloire

first: Frank

last: Dequiedt

first: Jacques

last: Piette

first: Yvette

last: Habraken


title: Bisquinolinium Compounds Induce Quadruplex-Specific Transcriptome Changes in HeLa S3 Cell Line

status: Public on May 30 2012

city: Konstanz

first: Joerg

last: Hartig

address: Universitätsstr. 10

department: Dept. of Chemistry

country: Germany

institute: University of Konstanz

summary: The effect of bisquinolinium compounds PhenDC3 and 360A genome wide gene expression changes modulated via promoter based G-quadruplex (G4) motifs.

overall_design: The total RNA was extracted after treating HeLa S3 cells with 10 µM of no molecule (DMSO), 8979A (control molecule), PhenDC3 (G4 specific molecule) or 360A (G4 specific molecule) for 48 hrs in triplicate.

first: Rashi

last: Halder

middle: S


title: Microarray study to understand acquired resistance to EGFR-targeted therapy in lung cancer

city: NEW YORK

first: Zhenfeng

last: Zhang

state: NY

address: 1130 ST.NICHOLAS AVENUE R1001

department: Cancer center

country: USA

institute: Columbia University Medical Center

summary: Activating mutations of EGFR have been characterized as important mechanisms for carcinogenesis in a subset of EGFR-dependent non-small cell lung cancers (NSCLC). EGFR tyrosine kinase inhibitors (TKI), such as erlotinib and gefitinib, have dramatic clinical effects on EGFR-addicted lung cancers and are used as first-line therapy for EGFR-mutant tumors. However, eventually all tumors acquire secondary resistance to the drugs and progress. We established a model to better understand mechanisms of acquired resistance. NCI- HCC827 cells are EGFR-mutant and highly erlotinib-sensitive. In this study we exposed HCC827 cells to increasing concentrations of erlotinib and two highly erlotinib-resistant subclones were developed (ER3 and T15-2). In these subclones no acquired alterations of EGFR or MET were found. We hereby performed a gene expression microarray studies to understand changes that might explain mechanisms of resistance. Through these studies we demonstrated in one resistant clone (ER3) overexpression of AXL, a tyrosine kinase implicated in imatinib and lapatinib resistance.

overall_design: Gene expression profilings were measured in NSCLC cell line HCC827 and two erlotinib-resistant HCC827-originated sublines ER3 and T15-2.

first: Thomas

last: LaFramboise

first: Balazs

last: Halmos


title: Comparison of intestinal surface CD3- refractory celiac disease type II (RCDII) cell lines with intestinal surface CD3+ cell lines of non-RCDII patients

status: Public on Jun 12 2012

city: Leiden

first: Frederike

last: Schmitz

address: Albinusdreef 2

department: Immunohematology and Blood Transfusion

country: Netherlands

institute: LUMC

summary: Analysis of transcriptional differences between aberrant (surface CD3-) RCDII cell lines and regular (surface CD3+) intraepithelial cell lines in order to characterize aberrant RCDII cells. All cell lines were cultured from duodenal biopsies of RCDII or non-RCDII (either celiac or non-celiac) patients.

overall_design: We compared 3 RCDII cell lines from RCDII patients P1-P3 with the following control cell lines: CD3+CD4+ T cell line from P1 and P3,  CD3+CD8+ T cell line from P3 and mixed CD4/CD8+ T cell lines from non-RCDII patients. All control cells matched the phenotype of mature T cells (CD3+CD4+ and/or CD3+CD8+). Samples were randomly distributed among two BeadChips and measured in duplicates.

first: Yuching

last: Lai

first: Jennifer

last: Tjon

first: Allan

last: Thompson

first: Yvonne

last: Kooy-Winkelaar

first: Jeroen

last: Bergen

first: Frits

last: Koning


title: An induced pluripotent stem cell model for ataxia telangiectasia

status: Public on May 28 2012

city: St. Lucia

first: Othmar

last: Korn

state: Queensland

address: University of Queensland

country: Australia

institute: Australian Institute for Bioengineering and Nanotechnology

summary: The difficulty associated with generating induced pluripotent stem cells (iPSC) from patients with chromosomal instability syndromes suggests the cellular DNA damage response poses a barrier to reprogramming. Here we demonstrate that fibroblasts from patients with ataxia-telangiectasia (A-T) can be reprogrammed to bona-fide iPSC, albeit at a reduced efficiency. A-T iPSC display defective radiation-induced signaling, radiosensitivity and cell cycle checkpoint defects. Bioinformatic analysis of gene expression in the A-T iPSC identifies abnormalities in DNA damage signaling pathways  as well as changes in mitochondrial and pentose phosphate pathways. A-T iPSC can be differentiated into functional neurons and thus represent a suitable model system to investigate A-T associated neurodegeneration.  Collectively our data show that iPSC can be generated from a chromosomal instability syndrome and that these cells can be used to discover early developmental consequences of ATM deficiency, such as altered mitochondrial function, that may be relevant to A-T pathogenesis and amenable to therapeutic intervention.

overall_design: Three different cell types: fibroblasts, human embyronic stem cells, and induced pluripotent stem cells with heterozygote, homozygote A-T compared to normal samples.

first: Sam

last: Nayler


title: Peripheral Blood Monocyte Gene Expression in Recent-Onset Type 1 Diabetes

status: Public on Jun 01 2012

city: Brisbane

first: Katharine

last: Irvine

address: Translational Research Institute

institute: Mater Research Institute UQ

summary: OBJECTIVE: Novel biomarkers of disease progression after type 1 diabetes onset are needed. RESEARCH DESIGN AND METHODS: We profiled peripheral blood (PB) monocyte gene expression in 6 healthy subjects and 16 children with type 1 diabetes diagnosed ~3 months previously, and analyzed clinical features from diagnosis to 1 year. RESULTS: Monocyte expression profiles clustered into two distinct subgroups, representing mild and severe deviation from healthy controls, along the same continuum. Patients with strongly divergent monocyte gene expression had significantly higher insulin dose-adjusted HbA1c levels during the first year, compared to patients with mild deviation. The diabetes-associated expression signature identified multiple perturbations in pathways controlling cellular metabolism and survival, including endoplasmic reticulum and oxidative stress (e.g. induction of HIF1A, DDIT3, DDIT4 and GRP78). qPCR quantitation of a 9-gene panel correlated with glycaemic control in 12 additional recent-onset patients. The qPCR signature was also detected in PB from healthy first-degree relatives. CONCLUSIONS: A PB gene expression signature correlates with glycaemic control in the first year after diabetes diagnosis, and is present in at-risk subjects. These findings implicate monocyte phenotype as a candidate biomarker for disease progression pre- and post-onset, and systemic stresses as contributors to innate immune function in type 1 diabetes.

overall_design: CD14+ monocytes from a total of 16 children with recent-onset type 1 diabetes and 6 adult healthy controls were profiled in 2 independent microarrays.


title: The influence of retinoic acid on immortalized human meibomian gland epithelial cells

status: Public on May 19 2012

city: Boston

first: David

middle: A

last: Sullivan

state: MA

address: 20 Staniford Street

institute: Schepens Eye Research Institute

summary: HumanHT-12v4 microarray of cells in proliferation and differentiation conditions treated with or without 2 uM retinoic acid

overall_design: Cells were treated with or without 2 uM retinoic acid, in proliferation (KSFM + 5 ng/ml EGF + 50 ug/ml bovine pituitary extract) and differentiation (DMEM/F12 + 10 ng/ml EGF + 10% FBS) media

first: Juan

last: Ding


title: Expression profiling of attenuated mitochondrial function identifies retrograde signals in Drosophila

status: Public on May 20 2012

city: Los Angeles

first: William

middle: Alexander

last: Freije

state: CA

address: 650 Charles Young Drive, South CHS B8-127

department: Obstetrics and Gynecology

institute: UCLA

summary: Mitochondria are able to modulate cell state and fate during normal and pathophysiologic conditions through a nuclear mediated mechanism collectively termed as a retrograde response. Our previous studies in Drosophila have clearly established that progress through the cell cycle is precisely regulated by the intrinsic activity of the mitochondrion by specific signaling cascades mounted by the cell. As a means to further our understanding of how mitochondrial energy status affects nuclear control of basic cell decisions we have employed Affymetrix microarray-based transcriptional profiling of Drosophila S2 cells knocked down for the gene encoding subunit Va of the complex IV of the mitochondrial electron transport chain. The profiling data identifies up-regulation of glycolytic genes and metabolic studies confirm this increase in glycolysis. The transcriptional portrait which emerges implicates many signaling systems, including a p53 response, an insulin response, and up-regulation of conserved mitochondrial responses. This rich dataset provides many novel targets for further understanding the mechanism whereby the mitochondrion may direct cellular fate decisions. The data also provides a salient model of the shift of metabolism from a predominately oxidative state towards a predominately aerobic glycolytic state, and therefore provides a model of energy substrate management not unlike that found in cancer.

overall_design: Drosophila S2 cells were transfected with siRNA specific for either green flourescent protein (GFP) or cytochrome oxidase subunit va (COVA) thereby knocking down electron transport in the COVA transfectants

first: Utpal

last: Banerjee


title: Gene expression profile of FOXM1 with Doxorubicin in MDA-MB-231 breast cancer cells

status: Public on May 15 2012

city: Houston

first: Yun-Yong

last: Park

state: TX

address: 7435 Fannin St.

department: Systems Biology

institute: UT, MD Anderson Cancer Center

summary: Transcription factors (TFs) play a crucial role in diverse cellular physiology by controlling down-stream target genes. It has been well recognized that TFs are attractive target for treating human cancer since transcriptional activity or gene expression level of TFs can be directly modulated. To explore which TF functions as survival factor in human breast cancer, we applied gene expression data sets for survival analysis. We identified that FOXM1 is a potent oncogenic survival factor out of eleven TFs. Loss of FOXM1 function leads to breast cancer cells more sensitized to Doxorubicin (Dox). To investigate how FOXM1 sensitizes cancer cell in the presence of Dox, we carried out gene expression array experiment to monitor how down-stream target genes are changed by FOXM1. MDA-MB-231 cells were incubated with siLuc or siFOXM1. Thirty six hours later, cells were incubated with Dox (5micro mol) for 36 hrs.

overall_design: 3 siLuc., 3 siFOXM1, 3 siLuc and Dox treatment, 3 siFOXM1 and Dox treatment

first: Sang-Bae

last: Kim

first: Ju-seog

last: Lee


title: Relation between smoking history and gene expression profiles in lung adenocarcinomas

status: Public on May 17 2012

city: Lund

first: Johan

last: Staaf

address: Medicon Village

country: Sweden

institute: SCIBLU - Swegene Centre for Integrative Biology at Lund University

summary: Lung cancer is the worldwide leading cause of death from cancer. Tobacco usage is the major pathogenic factor, however, not all lung cancers can be attributable to smoking. The genetic aberrations that differ between smokers' and never-smokers’ lung carcinomas remain to a large extent unclear. We analyzed 72 early-stage primary lung carcinomas including small cell lung cancers LCNEC, adenocarcinomas and squamous cell carcinomas by Illumina HT12 gene expression microarrays.

overall_design: Gene expression profiling of 72 lung carcinomas using Illumina HT-12 V3.0 microarrays.

first: Göran

last: Jönsson

first: Mats

first: Anna

last: Karlsson

first: Sofi

last: Isaksson

first: Annette

last: Salomonsson

first: Helen

last: Pettersson

first: Maria

last: Soller

first: Sven-Börje

last: Ewers

first: Leif

last: Johansson

first: Per

last: Planck


title: PSORS2 is due to mutations in CARD14

status: Public on May 09 2012

city: St. Louis

first: Elisha

last: Roberson

state: MO

address: 660 South Euclid Ave., CB 8045

department: Internal Medicine & Genetics

institute: Washington University in St. Louis

summary: Psoriasis is a common, immune-mediated, genetic disorder of the skin associated with arthritis in approximately 30% of cases. Previously, we localized PSORS2 (psoriasis susceptibility locus 2) to chromosome 17q25.3-qter following a genome-wide linkage scan in a family of European origin with multiple cases of psoriasis and psoriatic arthritis. Linkage to PSORS2 was also observed in a multiply affected psoriasis family from Taiwan. With genomic capture and DNA sequencing, we identified unique gain-of-function mutations in caspase recruitment domain family, member 14 (CARD14) that segregated with psoriasis. The mutations, c.349G>A (p.Gly117Ser) and c.349+5G>A respectively, altered splicing between exons 3 and 4 of CARD14. A de novo mutation in CARD14, c.413A>C [p.Glu138Ala], was detected in a child with sporadic, early-onset, generalized pustular psoriasis. CARD14 activates nuclear factor kappa B (NF-kB), and the p.Gly117Ser and p.Glu138Ala substitutions were shown to lead to enhanced NF-kB activation and upregulation of a subset of psoriasis-associated genes in keratinocytes compared to wildtype CARD14. These included chemokine (C-C motif) ligand 20 (CCL20) and interleukin 8 (IL8). CARD14 is localized mainly in the basal and suprabasal layers of healthy skin epidermis, while in lesional psoriatic skin it is reduced in the basal layer and more diffusely upregulated in the suprabasal layers of the lesional epidermis. We propose that, following a triggering event that can include epidermal injury, rare gain-of-function mutations in CARD14 initiate a process that includes inflammatory cell recruitment by keratinocytes. This perpetuates a vicious cycle of epidermal inflammation and regeneration that is the hallmark of psoriasis.

overall_design: No replicates are included. Three sample sets. [1] Skin biopsies had RNA extracted for expression within target tissue. [2] HEK cells were transfected with different constructs (including wildtype) of CARD14 to determine the mutational effect in keratinocytes. [3] Keratinocytes derived from psoriasis patients with CARD14 mutations were cultured and compared with and without stimulation with TNFalpha.

first: Catherine

middle: T

last: Jordan

first: Li

last: Cao

middle: D

first: Katherine

middle: C

last: Pierson

first: Chi-Fan

last: Yang

first: Cailin

middle: E

last: Joyce

first: Caitriona

last: Ryan

first: Shenghui

last: Duan

first: Cynthia

last: Helms

first: Yin

last: Liu

first: Yongqing

last: Chen

first: Alison

last: McBride

first: Wuh-Liang

last: Hwu

first: Jer-Yuarn

last: Wu

first: Yuan-Tsong

first: Alan

last: Menter

first: Raphaela

last: Goldback-Mansky

first: Michelle

last: Lowes

first: Anne

last: Bowcock


title: Rare and common variants in CARD14, an epidermal regulator of NF-kappaB, in psoriasis

first: Elisha

last: Roberson

summary: Psoriasis is a common inflammatory disorder of the skin and other organs. We have determined that mutations in CARD14, encoding an NF-kB activator within skin epidermis, account for PSORS2. Here we describe fifteen additional rare, missense variants in CARD14, their distribution in seven psoriasis cohorts (>6,000 cases and >4,000 controls), and their effects on NF-kB activation and the transcriptome of keratinocytes. There was an excess of rare variants within CARD14 in cases versus controls (burden test p-value = 0.0015). Some variants were only seen in a single case and included putative pathogenic mutations (c.424G>A [p.Glu142Lys], c.425A>G [p.Glu142Gly]) and the generalized pustular psoriasis mutation, c.413A>C (p.Glu138Ala), that lie within the coiled-coil domain of CARD14. The c.349G>A (p.Gly117Ser) familial psoriasis mutation was present at a frequency of 0.0005 in cases of European ancestry. CARD14 variants led to a range of NF-kB activities, with putative pathogenic variants leading to levels >2.5-fold higher than wildtype CARD14. Two variants (c.511C>A [p.His171Asn] and c.536G>A [p.Arg179His]) required stimulation with TNF-a to achieve significant increases in NF-kB levels. Transcriptome profiling of wildtype and variant CARD14 transfectants in keratinocytes differentiated likely pathogenic mutations from neutral variants such as polymorphisms. Over 20 CARD14 polymorphisms were also genotyped and meta-analysis revealed association of psoriasis with rs11652075 (c.2458C>T/p.Arg820Trp; p-value = 2.1x10-6). In the two largest psoriasis cohorts, evidence for association increased when rs11652075 was conditioned on HLA-Cw*0602 (PSORS1). These studies contribute to our understanding of the genetic basis of psoriasis and illustrate the challenges faced in identifying pathogenic variants in common disease.

overall_design: Keratinocytes were transfected with wildtype Cardsh or one of 16 Card14 mutations (17 total samples). The cells were collected and RNA extracted to determine the effect of these mutations compared to wildtype Card14. No replicates are included.

first: Catherine

last: Jordan

first: Li

first: Rajan

middle: P

last: Nair

first: Kristina

last: Duffin

first: Philip

last: Stuart

first: David

last: Goldgar

first: Genki

last: Hayashi

first: Emily

middle: H

last: Olfson

first: Bing-Jian

last: Feng

first: Clive

middle: R

last: Pullinger

first: John

last: Kane

first: Carol

last: Wise

last: Goldbach-Mansky

first: Lynette

last: Peddle

first: Vinod

last: Chandran

first: Wilson

last: Liao

first: Proton

last: Rahman

first: Gerald

middle: G

last: Krueger

first: Dafna

last: Gladman

first: James

last: Elder


title: HER2-enriched tumor initiating cell (HTIC) genomic predictor of response following neoadjuvant trastuzumab-based chemotherapy in HER2+ breast cancer

status: Public on May 12 2012

first: Francisco

middle: J.

last: Esteva

address: 1515 Holcombe Blvd, Unit 1354

department: Department of Breast Medical Oncology

institute: MD Anderson Cancer Center

summary: We identified a 17-gene Her2-enriched tumor initiating cell (HTIC) signature in MMTV-Her2/Neu mouse mammary TICs. Here, we show that patients with HTICS+ HER2+:ERα− tumors are more likely to achieve a pathologic complete response to trastuzumab-based neoadjuvant chemotherapy compared with HER2+:ER+ tumors.

overall_design: Neoadjuvant study of 50 HER2-positive breast cancer cases treated with trastuzumab-based chemotherapy pre-operatively. Pre-treatment FNA from primary tumors were obtained and RNA extracted and hybridized to Affymetrix microarrays according to manufacturer protocol. Pathologic response was assessed at the end of neoadjuvant treatment.

middle: J

first: Lajos

last: Pusztai

first: William

middle: F

last: Symmans


title: Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and their Differentiated Derivatives [Illumina HT12v3 Gene Expression]

status: Public on May 14 2012

city: La Jolla

first: Kristopher

middle: L.

last: Nazor

address: 10550 North Torrey Pines Road

department: Regenerative Medicine

institute: The Scripps Research Institute

summary: Human pluripotent stem cells (hPSCs) are potential sources of cells for modeling disease and development, drug discovery, and regenerative medicine. However, it is important to identify factors that may impact the utility of hPSCs for these applications. In an unbiased analysis of 205 hPSC and 130 somatic samples, we identified hPSC-specific epigenetic and transcriptional aberrations in genes subject to X chromosome inactivation (XCI) and genomic imprinting, which were not corrected during directed differentiation. We also found that specific tissue types were distinguished by unique patterns of DNA hypomethylation, which were recapitulated by DNA demethylation during in vitro directed differentiation. Our results suggest that verification of baseline epigenetic status is critical for hPSC-based disease models in which the observed phenotype depends on proper XCI or imprinting, and that tissue-specific DNA methylation patterns can be accurately modeled during directed differentiation of hPSCs, even in the presence of variations in XCI or imprinting.

overall_design: To obtain a comprehensive view of hPSC-specific epigenomic patterns, we collected 136 hESC and 69 hiPSC samples representing more than 100 cell lines for analysis.  In order to establish expected variation in human tissues, we collected 80 high-quality and well-replicated samples representing 17 distinct tissue types from multiple individuals. Finally, we selected 50 additional samples from primary cell lines of diverse origin to control for any aberrations that may arise as a general, non-hPSC-specific, consequence of in vitro manipulation. With these samples, we performed genome-wide DNA methylation and mRNA expression profiling using the Illumina Infinium 27K and 450K DNA Methylation BeadChips as well as the Illumina HT12v3 Gene Expression BeadArray.

middle: L

first: Gulsah

last: Altun

first: Candace

last: Lynch

first: Ha

last: Tran

first: Julie

middle: V

last: Harness

first: Ileana

last: Slavin

first: Ibon

last: Garitaonandia

first: Franz-Josef

last: Müller

first: Yu-Chieh

last: Wang

first: Francesca

last: Boscolo

first: Eyitayo

last: Fakunle

first: Sunray

last: Lee

first: Hyun

last: Park

first: Marina

last: Martynova

first: Tsaiwei

last: Ole

first: Darryl

last: D'Lima

first: Ruslan

last: Semechkin

first: Mana

last: Parast

first: Vasiliy

last: Galat

first: Andrew

last: Laslett

first: Uli

last: Schmidt

first: Hans

last: Keirstead

first: Jeanne

last: Loring

first: Louise

last: Laurent


title: Overexpression of Snail is associated with lymph node metastasis and poor prognosis in patients with gastric cancer

status: Public on May 18 2012

city: Busan

first: Chae Hwa

last: Kwon

address: 1-10 Ami-Dong, Seo-Gu

country: South Korea

institute: Cancer Research Institue, Pusan National University

summary: Epithelial-mesenchymal transition (EMT) is in the highlights as a significant role in tumor progression and invasion. Snail was known as the one of regulators of EMT in various malignant tumors. The aim of this study was to investigate the effect of Snail on invasiveness/migratory ability of gastric cancer cell lines and clinicopathological and prognostic significance of Snail over-expression using immunohistochemistry in tissue microarray of 314 gastric adenocarcinomas (GC). Differential gene expression in Snail over-expressed GC was investigated using cDNA microarray analysis. Silencing of Snail by ShRNA induced decreased of invasion, migration of gastric cancer cell lines. In contrast, over-expression of Snail induced increased invasiveness and migratory ability of gastric cancer cell lines in accordance increase of VEGF and MMP11. Furthermore, the over-expression of Snail (≥75% nuclear staining of Snail) was significantly associated with tumor progression (p<0.0001), lymph node metastases (p=0.002), lymphovascular invasion (p=0.002), and perineural invasion (p=0.002) in 314 GC patient. Snail over-expression was also associated with poor prognosis (shorter survival) in GC patients (p=0.023). cDNA microarray revealed 213 differential expressed genes in Snail over-expressed GC tissues, including genes related to metastasis, invasion. Based on above results, it was suggested that Snail plays a significant role in invasiveness/migratory ability of GCs. In addition, Snail might be used to predictive biomarker for evaluation of prognosis or aggressiveness in GCs.

overall_design: 48 primary gastric adenocarcinoma fresh frozen tissues were used for microarray. All the tissues were obtained after curative resection after pathologic confirm at Pusan National University Hospital (PNUH, Busan, Korea) and Cheonnam University Hospital (CNUH, Cheonnam, Korea). Microarray experiment and data analysis were done at Cancer research institute, PNUH, Busan, Korea.

first: Do-Youn

first: Chang-In

last: Choi

first: Tae-Yong

last: Jeon

first: Dae-Hwan

last: Kim

first: Jae-Hyuk


title: Gene expression profiling of human Th17 cell differentiation

status: Public on May 04 2012

city: Turku

first: Soile

last: Tuomela

address: P.O. Box 123

department: Turku Centre for Biotechnology

country: Finland

institute: University of Turku

summary:
The study aims at identifying transcriptional changes induced by in vitro polarization of human cord blood CD4+ cells towards Th17 subtype with combination of IL6, IL1b and TGFb by using timeseries data.
In this study, we identified gene expression changes characterizing early stages of human Th17 cell differentiation program through genome-wide gene expression profiling. Primary T helper cells isolated from umbilical cord blood were used to construct detailed kinetic patterns of gene expression after initiation of Th17 differentiation with IL1b, IL6 and TGFb. The dataset described provides the starting point for defining the gene regulatory networks and identifying new candidates regulating the Th17 differentiation in human.

overall_design: Altogether 57 samples were analyzed representing 3 biological replicates of timeseries data (0, 0.5, 1, 2, 4, 6, 12, 24, 48 and 72 hours) of Th17 polarized cells and control Th0 cells

first: Verna

last: Salo

first: Subhash

last: Tripathi

first: Zhi

last: Chen

first: Kirsti

last: Laurila

first: Tarmo

last: Äijö

first: Bhawna

last: Gupta

first: Lotta

last: Oikari

first: Brigitta

last: Stockinger

first: Harri

last: Lähdesmäki

first: Riitta

last: Lahesmaa


title: Age-specific variation in immune response in Drosophila melanogaster has a genetic basis.

status: Public on May 03 2012

city: Urbana

first: Jenny

last: Drnevich

state: IL

address: 1206 W. Gregory Dr.

institute: University of Illinois

summary:
Immunosenescence, the age-related decline in immune system function, is a general hallmark of aging.  While much is known about the cellular and physiological changes that accompany immunosenescence, we know very little about the genetic influences on this phenomenon.
We used microarrays to determine genome-wide expression profiles in twelve inbred D. melanogaster lines that varied in their ability to to clear an E. coli infection at one and four weeks of age.

overall_design: Bacterially infected and sham-injected flies from each of the lines were frozen at -80°C six hours post-injection at one and four weeks of age for use in the microarray study.  Lines were chosen to represent the range of changes in age-specific clearance ability: four of the lines chosen exhibited the most dramatic decline in clearance ability with age, four of the lines exhibited the least amount of change in clearance, and the remaining four lines exhibited the most dramatic improvement in clearance ability with age (Please note that the clearance ability of each line was not considered in the microarray data analysis).  In this case all of the expression data came from pooling the RNA extracted from individuals from each line (8-15 individuals) at each age from each treatment (sham injected vs. infected).

first: Tashauna

middle: M

last: Felix

first: Kimberly

last: Hughes

first: Eric

last: Stone

first: Jeff

last: Leips


title: North American Brain Expression Consortium and UK Human Brain Expression Database: Gene Expression

city: Bethesda

first: J Raphael

last: Gibbs

state: MD

address: 35 Convent Drive, Bldg 35/1A1015, MSC3707

department: Computational Biology Core

institute: National Institutue on Aging, NIH

summary:
A fundamental challenge in the post-genome era is to understand and annotate the consequences of genetic variation, particularly within the context of human tissues. We describe a set of integrated experiments designed to investigate the effects of common genetic variability on mRNA expression distinct human brain regions. We show that brain tissues may be readily distinguished based on expression profile. We find an abundance of genetic cis regulation mRNA expression. We observe that the largest magnitude effects occur across distinct brain regions. We believe these data, which we have made publicly available, will be useful in understanding the biological effects of genetic variation.

Authorized Access data:
Mapping of GEO sample accessions to dbGaP subject/sample IDs is available through dbGaP Authorized Access, see http://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000249

overall_design: Because of our interest in genomic regulation of expression and neurological disorders we embarked upon a series of experiments to provide a brain region-specific contextual framework for genetic and epigenetic regulation of gene expression. We obtained frozen brain tissue from the cerebellum and frontal cortex from 396 subjects (total 911 tissue samples).

first: Jesse

first: Dena

last: Hernandez

first: Allisa

last: Dillman

first: Mina

last: Ryten

first: Daniah

last: Trabzuni

first: Bryan

last: Traynor

first: Michael

middle: A

last: Nalls

first: Sampath

last: Arepalli

first: Adaikalavan

last: Ramasamy

first: Marcel

last: van der Brug

first: Juan

last: Troncoso

first: Robert

last: Johnson

first: Richard

last: O'Brien

first: H

last: Zielke

first: Alan

last: Zonderman

first: Luigi

last: Ferrucci

first: Dan

last: Longo

first: Colin

last: Smith

last: Walker

first: Mike

last: Weale

first: John

last: Hardy

first: Mark

last: Cookson

first: Andrew

middle: B

last: Singleton


title: Rapid identification of prognostic imaging biomarkers for non-small cell lung cancer by leveraging public gene expression microarray data

city: Stanford

first: Olivier

last: Gevaert

address: 1265 Welch Road

department: Medicine

institute: Stanford University

summary: To rapidly identify new prognostic imaging biomarkers, we propose a bioinformatics approach that integrates gene expression and image data and leverages public gene expression data. We demonstrate our approach in non-small cell lung carcinoma patients for whom CT, PET/CT and gene expression data are available but without clinical follow-up. We extracted 180 image features and 56 high quality gene expression clusters, represented by metagenes. 115 image features were expressed in terms of metagenes, using sparse linear regression and cross-validation, with an accuracy of 65-86%. After mapping the signatures to a public gene expression dataset, 26 image features were significantly associated with recurrence-free survival and 22 with overall survival. A multivariate analysis identified multiple image features that were prognostic, independent of clinical covariates. Identifying prognostic imaging biomarkers by linking images and gene expression with outcomes in public gene expression datasets promises to accelerate the role of imaging in personalized medicine.

overall_design: We studied 26 cases of NSCLC with both PET/CT and microarray data under IRB approval from Stanford University and the Veterans Administration Palo Alto Health Care System. The collection of tissue samples consisted of a distribution of poorly- to well-differentiated adenocarcinomas and squamous cell cancers. The surgeon had removed necrotic debris during excision and sampled cavitary lesions to include as much solid component as practical. Then, from the excised tumor, he cut a 3 to 5 mm thick slice along its longest axis, and froze it within 30 minutes of excision. We retrieved the frozen tissue and extracted the RNA that was then processed by the Stanford Functional Genomics Facility using Illumina Whole Genome Bead Chips (Human HT-12 v3.0)

first: Sylvia

last: Plevritis


title: Expression data from Drosophila S2 cells

city: Hachioji-shi

first: Sato

middle: M.

last: Yukiko

state: Tokyo

address: 1-1 Minami-Osawa

country: Japan

institute: Tokyo Metropolitan University

summary: An Affimetrix GeneChip Drosophila genome 2.0 array was used to study the effect of protocatechuic aldehyde on gene expression. The addition of 0.1 mM protocatechuic aldehyde to Drosophila S2 cells significantly affected the expression of 52 genes, with 29 being up-regulated and 23 being down-regulated.

overall_design: Drosophila S2 cells were incubated with protocatechuic aldehyde (0.1 mM). After 2 hr, the gene expression in Drosophila S2 cells was analyzed using  Affymetrix microarrays.

first: Yuzo

last: Nakagawa-Yagi

first: Yukiko

last: Sato

first: Emi

last: Matsumoto

first: Shin-ichi

last: Nakatsuka

first: Tsuyoshi

last: Sakaki

last: Muramatsu

first: Takaaki

last: Hara

first: Toshiro

last: Aigaki


title: Expression analysis of genes responding to ARID1A knockdown

status: Public on May 02 2012

city: Baltimore

first: Tian-Li

last: Wang

address: 1550 Orleans St., CRB II, Rm 376

institute: Johns Hopkins University School of Medicine

summary: Illumina array was employed to analyze the genes whose expression are altered when ARID1A gene is downregulated by shRNA in normal ovarian surface epithelial cells OSE4 and IOSE80pc.  This leads to discovery of p53-regulated genes such as p21 and SMAD3.

overall_design: ARID1A knockdown in OSE4 and IOSE80pc

first: B

last: Guan

first: T

first: L

last: Shih


title: Phytochrome Interacting Factor 4 and 5 regulate different set of genes in high and low red/far-red light

city: Lausanne

first: Markus

middle: Volker

last: Kohnen

state: Vaud

address: Genopode Building

department: Center for Integrative Genomics (CIG)

country: Switzerland

institute: Université de Lausanne

summary: As sessile organisms plants developed a veriety of adaptive responses to the ever changing environment. One of these responses is the shade avoidance syndrome which is composed of different responses like elongation growth, hyponastic leafs or early flowering to shade (low R/FR). Phytochrcome Interacting Factor 4 and 5 are bHLH transcription factors reported to activate gene expression upon perception of low R/FR. Using this miroarray experiment we identified new genes regulated by PIF4 and PIF5 in response to shade and investigated their genome wide role.

overall_design: Here pif4pif5 double mutant, pif5 single mutant and PIF5 overexpressing line were compared to Col-0 wild type A. thaliana plants when grown under 12:12 DL circles for 14 days in high R/FR and either kept in high R/FR or transferred to low R/FR for additional 2 hours

first: Patricia

last: Hornitschek

first: Severrine

last: Lorrain

first: Sylvain

last: Pradervand

first: Ioannis

last: Xenarios

first: Christian

last: Fankhauser


title: Defining the molecular response to trastuzumab, pertuzumab and combination therapy in ovarian cancer

city: Carrington Crescent

first: Andrew

last: Sims

state: Edinburgh

address: Systems Medicine Building

department: Institute of Genetics and Molecular Medicine

country: United Kingdom

institute: University of Edinburgh

summary:
The purpose of this study was to characterise the effects of trastuzumab and pertuzumab, either as single agents or as combination therapy on gene and protein expression in human ovarian cancer in vivo. Illumina BeadChips were used to profile the transcriptome after four days treatment of SKOV3 tumor xenografts. Although genes involved with HER2, MAP-kinase and p53 signaling pathways were commonly induced by all treatments, a greater number and variety of genes were differentially expressed by the complementary combination therapies compared to either drug on its own. The protein level of the CDK-inhibitors p21 and p27 were increased in response to both agents alone and further by the combination; pERK signaling was inhibited by all treatments; but only pertuzumab alone inhibited pAkt signaling. The expression of proliferation, apoptosis, cell division and cell cycle markers was distinct in a panel of primary ovarian cancer xenografts, suggesting heterogeneity of response in ovarian cancer and the need to establish biomarkers of response.
This first comprehensive study of the molecular response to trastuzumab, pertuzumab and combination therapy in vivo highlights that there are both common and distinct downstream effects to different HER2 antibodies and that pathways may be invoked more strongly or in a different manner by a combination of agents. Some of the in vivo results for ovarian tumors differ from previous in vitro studies in breast cancer cells, emphasizing that the molecular response to anti-cancer agents involves variable and complex disease-specific interactions of signaling mechanisms.

overall_design: SCOV3 Ovarian cell line xenografts treated with Trastuzumab, pertuzumab or combination after 4 days


title: Ontogenetic study of gene expression in human cerebral cortex tissue using genome-wide microarray

city: Eugene

first: Kirstin

last: Sterner

state: OR

address: 1218 University of Oregon

department: Anthropology

institute: University of Oregon

summary: In this study we sought to examine gene expression in the cerebral cortex during development in the context of adaptive plasticity. In order to do this we introduced an approach designed to discriminate genes with variable as opposed to uniform patterns of gene expression and found that greater inter-individual variance is observed among children than among adults.

overall_design: RNA was extracted from surgically resected control (e.g., electrophysiologically inactive) tissues taken primarily from the temporal lobe. Individuals sampled ranged from age 10 months old to 53 years old. Gene expression data were collected using a genome-wide microarray [Illumina Human HT-12v3 chip].

middle: N

first: Amy

last: Weckle

first: Harry

middle: T

last: Chugani

first: Adi

last: Tarca

first: Chet

middle: C

last: Sherwood

first: Patrick

last: Hof

first: Christopher

middle: W

last: Kuzawa

last: Boddy

first: Asad

last: Abbas

first: Ryan

last: Raaum

first: Lucie

last: Gregoire

first: Leonard

last: Lipovich

first: Lawrence

middle: I

last: Grossman

first: Monica

last: Uddin

first: Morris

last: Goodman

first: Derek

last: Wildman


title: Expression data from low R:FR - JA crosstalk in Arabidopsis

status: Public on May 01 2012

city: Utrecht

first: Ronald

last: Pierik

address: Padualaan 8

department: Plant Ecophysiology

institute: Utrecht University

summary:
Low reduced red:far-red ratio [R:FR] signaling through phytochromes induces shade avoidance responses, including petiole elongation. Jasmonic acid-mediated defense against herbivores and pathogens is inhibited under these conditions.
Using microarrays we studied the crosstalk between low R:FR and JA at the global gene expression level in Arabidopsis thaliana.

overall_design: Plants were exposed for 2 h. to the following treatments: high R/FR with mock spray, low R/FR with mock spray, high R/FR with JA spray, low R/FR with JA spray. Gene expression was determined in petioles.

first: Mieke

last: de Wit


title: CEACAM6 is a PDEF induced gene in breast cancer

city: Buffalo

first: Ashwani

last: Sood

state: New York

address: Elm & Carlton Streets

department: Immunology

institute: Roswell Park Cancer Institute

summary:
Identifying PDEF regulated genes may shed light on the mechanism by which PDEF may induce breast cancer progression. To that purpose, we have used the MCF-7 human breast tumor cell line model to identify PDEF induced genes. Briefly, PDEF expression was down regulated by shRNA in MCF-7 cells and RNA probes from PDEF-down regulated and control MCF-7 cells were used to screen the Affymetrics HG-U133A Gene Chips. This analysis found 62 genes that were induced 2-fold or higher by PDEF. Further analysis of 3 of these genes namely S100A7, CEACAM6 and B7-H4 in primary breast tumors showed CEACAM6 as a frequently elevated and co-exressed gene with PDEF in these tumors.
We previously reported a role for PDEF (prostate derived Ets transcription factor) in breast tumor progression and its association with poor clinical outcome in ER+ breast cancer. To gain further insights into PDEF action in breast cancer, we down regulated PDEF expression by shRNA in MCF-7 human breast tumor cell line, and screened the HG-U133A human gene chips with probes from PDEF down-regulated and control MCF-7 cells. This analysis identified CEACAM6 as one of the genes induced by PDEF. Further analysis of CEACAM6 expression in relation to PDEF in 93 ER+ primary breast tumors showed largely concordant expression of these molecules. To our knowledge, our findings of CEACAM6 as a PDEF induced gene and their elevated co-expression in breast cancer have not been described before.

overall_design: Data from one replicate experiment is included as a representative example of the data obtained. HG-U133A gene chip pairs were screeened with biotinylated RNA probes from PDEF-down regulated MCF-7 cells (experimental) or from control MCF-7 cells.

middle: K

first: Alka

last: Mukhopadhyay

first: Leighton

last: Stein


title: Expression data from LCM-captured Arabidopsis root cells after challenge with Meloidogyne incognita

status: Public on Apr 27 2012

city: Gainesville

first: Lauren

last: McIntyre

state: FL

address: 2033 Mowry Rd

department: Department of Molecular Genetics and Microbiology

institute: University of Florida

summary: The differentiation of specialized feeding sites in Arabidopsis root cells in response to nematode infestation involves substantial cellular reprogramming of host cells that is not well characterized at the molecular level. Expression data was generated from Arabidopsis root cells undergoing giant cell formation due to nematode infestation and from non-infested control root cells. Cells were laser captured 14 and 21 days after infestation.

overall_design:
Samples, collected 14 days post infestation, consisted of three biological replicates per treatment (control root cells or giant cells). RNA samples were isolated from ~150 control cells or from ~80 giant cells using the PicoPure RNA Isolation Kit (Arcturus, Mountain View, USA). RNA amplifications were carried out with the NuGEN WT-Ovation Pico kit.
GSM546568-GSM546577: Control and giant cells collected 21 days post infestation.

first: Alison

last: Morse

first: Valentina

last: Carballo

middle: G

last: Taylor


title: TMPRSS2-ERG, HDACs and EZH2 are involved in an AR centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression after ERG KD)

city: Singapore

first: Kern Rei

last: Chng

address: 60 Biopolis Street #02-01 Genome

department: Cancer Biology and Pharmacology 3

country: Singapore

institute: GIS

summary: Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. However, the exact mechanics and the functional consequences associated with this crosstalk between ERG and AR still remains relatively unknown. Interestingly, through chromatin immunoprecipitation coupled with massively parallel sequencing, we discover that ERG and other commonly over-expressed transcriptional co-repressors (HDAC1, HDAC2, HDAC3 and EZH2) are wired into an AR centric transcriptional network via a spectrum of distal enhancers and/or proximal promoters. We show that ERG represses several AR target genes involved in epithelial differentiation. Furthermore, we demonstrated that suppression of the androgen induced gene, Vinculin, by ERG and histone deacetylases increases cancer cell invasiveness. From our results, we propose that ERG, histone deactelyases and the histone methyltransferase, EZH2, could impede epithelial differentiation and contribute to prostate cancer progression, in part through modulating the transcriptional output of AR.

overall_design: Gene expression profiling of human prostate cancer VCaP cells with time course DHT stimulation using microarray.

first: K

middle: R

first: C

last: Chang

first: S

last: Tan

last: Yang

middle: Z

last: Hong

first: N

middle: Y

last: Sng

first: E

last: Cheung


title: Impact of FOXA1 over-expression on progestin signalling in transformed normal breast cells

status: Public on Apr 26 2012

city: Westmead

first: J

middle: Dinny

last: Graham

state: NSW

address: 176 Hawkesbury Rd

department: Westmead Institute for Medical Research

institute: University of Sydney

summary:
Genome wide gene expression profiling of response to synthetic progestin ORG2058 in AB32 cells, a PR positive clone of the MCF-10A cell line, was determined after lentiviral transduction with an expression construct
encoding human FOXA1. Cells were treated for 6h or 24h with 10nM ORG2058 or vehicle, 48h after transduction with the FOXA1 construct or empty vector control. Gene expression was measured in total RNA my Illumina whole genome gene expression array.

overall_design: Duplicate monolayer cultures of AB32 cells transduced 48h with pCDH-CMV-FOXA1-EF1-copGFP virus or negative control empty vector pCDH-CMV-mcs-EF1-copGFP virus were treated 6h or 24h with 10nM ORG2058 or 0.1% ethanol vehicle control. Cells were harvested for total RNA isolation and each sample was labelled and hybridized to a single Illumina human whole genome microarray, resulting in three replicate datasets for each of four conditions. Data were analysed separately and combined to give a mean signal intensity for each array probe.

middle: D

first: Christine

middle: L

last: Clarke


title: Root nitrate response of Ws plants and afb3-1 mutant plants

city: Santiago

first: Elena

middle: A

last: Vidal

address: Avenida Libertador Bernardo O'Higgins 340

department: Genetica Molecular y Microbiologia

country: Chile

institute: Pontificia Universidad Catolica de Chile

summary: Auxin is a key phytohormone regulating central processes in plants that include embryo development, lateral root growth and flower maturation among others. Auxin is sensed by a set of F-Box proteins of the TIR1/AFB3 family triggering auxin dependent responses by a pathway that involves an interplay between the Aux/IAA transcription repressors and the ARF transcription factors. We have previously shown that the AFB3 auxin receptor has a specific role in coordinating primary and lateral root growth to external and internal nitrate availability (Vidal et al., 2010). In this work, we used an integrated genomics, bioinformatics and molecular genetics approach to dissect regulatory networks acting downstream AFB3 that are activated by a transient nitrate treatment in Arabidopsis roots.  Our systems approach unraveled key components of the AFB3 regulatory network leading to changes in lateral root growth in response to nitrate.

overall_design: Arabidopsis seedlings of the Ws and afb3-1 genotypes were grown on hydroponic medium containing 1X MS salts without Nitrogen, supplemented with 0.5 mM ammonium succinate as Nitrogen source and 3 mM sucrose on a Percival chamber under a photoperiod of 16 hours of light (100 μE/m2/sec) and 8 hours of dark at 22°C for 14 days. The plants were treated at the onset of the light cycle with 5 mM KNO3 or 5 mM KCl as control for 2 hours. Whole roots were cut from seedlings and frozen on liquid Nitrogen. Total RNA was extracted using the TriZol reagent. 3 independent biological replicates were performed.

first: Tomás

last: Moyano

first: Eleodoro

middle: J

last: Riveras

first: Orlando

last: Contreras-López

first: Rodrigo

last: Gutiérrez


title: Microcolony formation by the opportunistic pathogen Pseudomonas aeruginosa requires pyruvate and pyruvate fermentation.

city: Aurora

first: Michael

last: Schurr

state: CO

department: Microbiology

institute: University of Colorado School of Medicine

summary: A hallmark of the biofilm architecture is the presence of microcolonies. However, little is known about the underlying mechanisms governing microcolony formation. In the human pathogen Pseudomonas aeruginosa, microcolony formation is dependent on the two-component regulator MifR, with mifR mutant biofilms exhibiting an overall thin structure lacking microcolonies, and overexpression of mifR resulting in hyper-microcolony formation. Here, we made use of the distinct MifR-dependent phenotypes to elucidate mechanisms associated with microcolony formation. Using global transcriptomic and proteomic approaches, we demonstrate that cells located within microcolonies experience stressful, oxygen limited, and energy starving conditions, as indicated by the activation of stress response mechanisms and anaerobic and fermentative processes, in particular pyruvate fermentation. Inactivation of genes involved in pyruvate utilization including uspK, acnA and ldhA abrogated microcolony formation in a manner similar to mifR inactivation. Moreover, depletion of pyruvate from the growth medium impaired biofilm and microcolony formation, while addition of pyruvate significantly increased microcolony formation. Addition of pyruvate partly restored microcolony formation in ∆mifR biofilms. Moreover, addition of pyruvate to or expression of mifR in lactate dehydrogenase (ldhA) mutant biofilms did not restore microcolony formation. Consistent with the finding of denitrification genes not demonstrating distinct expression patterns in biofilms forming or lacking microcolonies, addition of nitrate did not alter microcolony formation. Our findings indicate the fermentative utilization of pyruvate to be a microcolony-specific adaptation to the oxygen limitation and energy starvation of the P. aeruginosa biofilm environment.

overall_design:
For biofilm growth experiments, three independent replicates of P. aeruginosa strains PAO1 and ΔmifR were grown as biofilms in a flow-through system using a once-through continuous flow tube reactor system for biofilm sample collection and in flow cells (BioSurface Technologies) for the analysis of biofilm architecture as previously described (Sauer et al., 2002, Sauer et al., 2004, Petrova & Sauer, 2009).  Cells were treated with RNAprotect (Qiagen) and total RNA was extracted using an RNeasy mini purification kit (Qiagen) per the manufacturer’s instructions.  RNA quality and the presence of residual DNA were checked on an Agilent Bioanalyzer 2100 electrophoretic system pre- and post-DNase treatment.  Ten micrograms of total RNA was used for cDNA synthesis, fragmentation, and labeling according to the Affymetrix GeneChip P. aeruginosa genome array expression analysis protocol.
Sauer, K., A. K. Camper, G. D. Ehrlich, J. W. Costerton & D. G. Davies, (2002) Pseudomonas aeruginosa displays multiple phenotypes during development as a biofilm. J. Bacteriol. 184: 1140-1154.
Sauer, K., M. C. Cullen, A. H. Rickard, L. A. H. Zeef, D. G. Davies & P. Gilbert, (2004) Characterization of nutrient-induced dispersion in Pseudomonas aeruginosa PAO1 biofilm. J. Bacteriol. 186: 7312-7326.
Petrova, O. E. & K. Sauer, (2009) A novel signaling network essential for regulating Pseudomonas aeruginosa biofilm development. PLoS Pathogens 5: e1000668.

first: Olga

middle: E

last: Petrova

first: Jill

first: Karin

last: Sauer


title: Expression profiles of Drosophila melanogaster males with DX mothers and X-chromosomes that were subjected to male-limited evolution

status: Public on Apr 17 2012

city: Lund

first: Jessica

middle: K.

last: Abbott

address: Sölvegatan 37

department: Dept. of Biology

institute: Lund University

summary: Intralocus sexual conflict, where males and females have different fitness optima for the same trait, has been suggested to potentially be resolved by genomic imprinting, whereby expression in offspring is altered according to parent-of-origin. However, this idea has not yet been empirically tested. Here, we designed an experimental evolution protocol in Drosophila melanogaster which enabled us to look for imprinting effects on the X-chromosome. We enforced father-to-son transmission of the X-chromosome for many generations, and compared fitness and gene expression levels between control males, males with a control X-chromosome that had undergone one generation of father-son transmission (CDX), and males with an X-chromosome that had undergone many generations of father-son transmission (MLX). Although fitness differences were consistent with lowered fitness of males with a paternally inherited X-chromosome, expression differences suggested that this was due to deleterious maternal effects rather than imprinting. We conclude that imprinting is unlikely to resolve intralocus sexual conflict in Drosophila melanogaster.

overall_design: 18 samples were analyzed. There were 3 replicate populations within each of 3 treatments (Control, CDX, and MLX), and two males were analyzed from each population, for a total of 18 males.

first: Paolo

last: Innocenti

first: Adam

last: Chippindale

first: Edward

middle: H

last: Morrow


title: Gene expression analysis in MZ twins discordant for IAR

status: Public on Apr 15 2012

city: Linköping

first: Fredrik

last: Barrenas

address: Sandbäcksgatan 7, level 2

department: Dept of Clinical and Experimental Medicine

institute: Linköping University Hospital

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

overall_design: Refer to individual Series


title: Ionizing Radiation-induced expression response in Drosophila Larvae

status: Public on Apr 18 2012

city: Boulder

first: Joseph

last: Heimiller

address: 347 UCB

department: MCDB

institute: Univ of Colorado Boulder

summary: Genome-wide expression analysis comparison with and without ionizing radiation in p53 mutant and wild type Drosophila larvae

overall_design: Genome-wide expression analysis comparison with and without ionizing radiation in p53 mutant (p53^5A-1-4) and wild type (y^1 w^1118)  Drosophila third instar larvae. 4000R of X-rays used in IR-treated Drosophila. Analyzed 2hr and 18hr after exposure with age-matched larvae in non-treated controls.

first: Petra

last: van Bergeijk

first: Lyle

last: Uyetake

first: Tin

middle: T

last: Su


title: Follicular Lymphoma expression array

status: Public on Apr 30 2012

city: New York

first: Elisa

last: Oricchio

address: 1275 York Avenue

institute: MSKCC

summary: We used microarrays to detail gene expression profile of several follicular lymphoma patient samples with different grades

overall_design: We analyzed 72 FL samples

first: Gouri

last: Nanjangud


title: Gene expression analysis in MZ twins discordant for IAR [in vivo]

summary: Gene expression analysis in CD4+ T cells extracted from PBMCs, isolated from discordant MZ twins with IAR during season

overall_design: MZ twins discordant for intermittent allergic rhinitis (IAR)

first: Mikael

last: Benson

first: Anna

last: Sjögren


title: Differential expression of Wnt signalling molecules between pre- and post-menopausal endometrial epithelial cells suggests that a population of putative epithelial stem/progenitor cells reside in the basalis layer

status: Public on Apr 11 2012

city: CLAYTON

first: HONG

last: NGUYEN

state: VIC

address: 27-31 Wright St

institute: Monash Institute of Medical Research

summary: The human endometrium is a highly regenerative tissue that undergoes cyclical proliferation, differentiation and shedding each month. The upper functionalis layer of the endometrium is shed in response to circulating levels of estrogen and progesterone, while the lower basalis layer remains. Clonogenic epithelial stem/progenitor cells likely responsible for regenerating endometrial epithelium have been identified in pre-menopausal (Pre-M) and post-menopausal (Post-M) endometrium and may reside in the basalis layer. We undertook a transcriptional profiling of purified epithelial cells from full-thickness Pre-M and Post-M endometrium to identify differentially expressed genes. The hypothesis tested in the present study was that Post-M endometrial epithelial gene profile would be similar to the quiescent basalis epithelium of Pre-M endometrium. We found striking differential gene expression of many Wnt family members between Pre-M and Post-M and other stem cell network genes. Comparative analysis of our endometrial epithelial gene expression profiles to that of endometrial epithelial cells in remodelling endometrium also provides new evidence showing that Post-M endometrial epithelium has a similar gene signature to that of basalis epithelium of menstrual endometrium.

overall_design: Human endometrial tissue was obtained from 8 pre-menopausal and 3 post-menopausal women undergoing hysterectomy for various benign gynaecologic conditions. Endometrial tissue was digested and isolated using combination of DNase and collagenase. Anti-human EpCAM antibody-coated magnetic Dynabeads was used to positively select total epithelial cells from the digested single cell suspensions. Total RNA was extracted from the purified endometrial epithelial cells and hybridised to Illumina Sentrix HT12 beadchip. Resulting data was compared between pre-menopausal and post-menopausal samples.

first: Hong

middle: P

last: Nguyen

first: Carl

middle: N

last: Sprung

first: Caroline

last: Gargett


title: miR-93/106b and their host gene, MCM7, are differentially expressed in leiomyomas and functionally target F3 and IL-8

status: Public on Apr 10 2012

city: Torrance

first: Tsai-Der

last: Chuang

state: California

address: 1124 WEST CARSON STREET

department: OB-GYN

institute: LA Biomed at UCLA medical center

summary: miR-93/106b and their host gene minichromosome maintenance complex component 7 (MCM7) reside at chr7q22, a region frequently rearranged in leiomyomas. We explored the expression of miR-93/106b in leiomyoma and paired myometrium (N=62) from untreated and patients exposed to hormonal therapies (GnRHa, Depo-Provera and oral contraceptives) from African Americans and Caucasians, and their regulatory functions in isolated paired (N=15) leiomyoma and myometrial smooth muscle cells (LSMC and MSMC) and leiomyosarcoma cell line (SKLM-S1). At tissue level leiomyomas expressed significantly lower levels of miR-93 and elevated MCM7 as compared to myometrium with limited racial influence or hormonal exposure on their expression. Assessing the regulatory function of miR-93/106b through doxycycline-inducible lentiviral transduction in microarray analysis, tissue factor (F3) and IL-8 were identified as their possible targets. At tissue level leiomyomas expressed a significantly lower level of F3 and an elevated IL-8 which exhibited an inverse relationship with miR-93, but with limited racial or hormonal influences. Gain-of-function of miR-93/106b in LSMC, MSMC and SKLM-S1 dose-dependently repressed F3 and IL-8 through direct interactions with their respective 3’UTRs and indirectly through F3 repression inhibited IL8, CTGF and PAI-1 expression, confirmed by using siRNA silencing or factor Vlla (FVIIa) activation of F3, as well as reducing the rate of proliferation, while increasing caspase 3/7 activity. We concluded that differential expression of miR-93/106b and their direct and/or indirect regulatory functions on F3, IL-8, CTGF and PAI-1 expression, with key roles in inflammation and tissue turnover may be of significance in the outcome of leiomyoma growth and associated symptoms.

overall_design: Total RNA isolated from TF324 cells transfected with DOX-inducible lentiviral construct carrying miR-106b~25 cluster with and without Dox treatments for 6 days was subjected to gene expression profiling using Sentirx Beadchip Array HumanHT-12_v4.

first: Xaioping

last: Luo

first: Harekrushna

last: Panda

first: Nasser

last: Chegini


title: Progestin regulation of gene expression in breast cancer and minimally transformed breast cell lines

first: J

last: Graham

summary:
Time course of response to synthetic progestin ORG2058 in T-47D and ZR-75-1 breast cancer cell lines and in two PR positive clones of the MCF-10A cell line: AB9 and AB32.
Transcriptional response to synthetic progestin, 10nM ORG2058, was compared between the four cell lines at three treatment times.

overall_design: T-47D breast cancer cells were treated in triplicate with 10nM ORG2058 or ethanol vehicle and harvested at 2, 6 and 24h after treatment for gene expression profiling

first: Christine

last: Clarke


title: Small molecules enable highly efficient neuronal conversion of human fibroblasts

status: Public on Apr 08 2012

city: Kiel

first: Franz-Josef

last: Müller

address: Niemannsweg 147

department: Klinik für Psychiatrie und Psychotherapie

institute: Zentrum für Integrative Psychiatrie Kiel

summary: Forced expression of pro-neural transcription factors was shown to mediate direct neuronal conversion of human fibroblasts. Since neurons are postmitotic, the conversion efficiency represents an important parameter. Here we present a minimalist approach combining two factor neuronal programming with small molecule-based inhibition of GSK3ß and SMAD signaling, which gives rise to functional neuron-like cells (iNs) of various neurotransmitter phenotypes with an overall yield of up to >200% and a final neuronal purity of up to >80%.

overall_design: Timcourse of reprogramming of fibroblasts towards an neuronal phenotype in two independent fibroblast lines

first: Philipp

last: Koch

first: Oliver

last: Brüstle


title: Epigenetically heritable alteration of fly development in response to toxic challenge

city: Rehovot

first: Shay

last: Stern

address: 234 Herzl Street

department: Biological Chemistry

country: Israel

institute: Weizmann Institute of Science

summary: Developing organisms have evolved a wide range of mechanisms for coping with recurrent environmental challenges. How they cope with rare or unforeseen challenges is, however, unclear as are the implications to their unchallenged offspring. Here we investigate these questions by confronting the development of the fly, D. melanogaster, with artificial tissue distributions of toxic stress that are not expected to occur during fly development. We show that under a wide range of toxic scenarios, this challenge can lead to modified development which may coincide with increased tolerance to an otherwise lethal condition. Part of this response was mediated by suppression of Polycomb group genes, which in turn leads to de-repression of developmental regulators and their expression in new domains. Importantly, some of the developmental alterations were epigenetically inherited by subsequent generations of unchallenged offspring. These results show that the environment can induce alternative patterns of development that are stable across multiple generations.

overall_design: Measuring differences in RNA levels between larvae that were exposed to a toxic challenge and unchallenged larvae. measuring differences in RNA levels between F3 larvae with or without past exposure to the challenge in F1 generation.


title: Expression of Human naïve B cell priming for plasma cell differentiation

status: Public on Apr 09 2012

city: Rennes

first: Delphine

last: Rossille

address: 2 avenue du Pr. Léon Bernard

country: France

institute: INSERM U1236-MOBIDIC

summary:
To explore events that govern the differentiation of human naïve B cells (NBCs) into memory B cells and plasma cells (PCs), we designed an in vitro 2-step culture model leading non-switched NBC precursors to differentiate into two cell compartments: CD20loCD38hi and CD20+CD38+.
Both populations are characterized by distinct cell fates, the former one corresponding to plasmablasts that undergo PC terminal differentiation, with intermingled relationship between cell division and bona fide differentiation two events that are usually viewed as mutually exclusive.
Postulating that extracellular cues mediated by distinct receptor-ligand interactions are likely involved in this phenomenon we explored one by one factors used in our model and found that T-cell-produced IL-2 was critical for the PC’s commitment.
Interestingly, this IL-2 effect operates independently of proliferation and survival functions and required an ERK signaling. Based on our study we proposed to complete previous scheme of PRDM1/Blimp-1 controlling PC differentiation by adding the T-cell-delivered IL-2 effect, which sustains indirectly the mitogenic-induced Blimp-1 expression by downregulating IRF8 and BACH2 via an ERK signal This study highlight early events that could take place when cognate B and T cells meet and interact before seeding follicle, where crucial inputs may condition final GC B destiny.

overall_design: GEP was performed on the RNA of purified B cells from 3 healthy blood donors, stimulated at Day 0 and with addition or not of IL-2. Four time points were assessed Day 0, Day 0+16h, Day 0+22h and Day 4.

first: Simon

last: Le Gallou

first: Thierrry

last: Fest


title: mRNA profiling during infection with H1N1 influenza A virus (A/Mexico/InDRE4487/H1N1/2009)

city: Vancouver

first: Victoria

last: Svinti

address: 2350 Health Sciences Mall

country: Canada

institute: University of British Columbia

summary: MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection.

overall_design: Control (mock-infected) samples: 12 (2 technical replicates, averaged), Infected samples: 6, for each time-point (0, 4, 8, 24, 48 and 72 hours post infection). The experiment was performed in six replicates.

first: Emma-Kate

last: Loveday

first: Sandra

last: Diederich

first: John

last: Pasick

first: François

last: Jean


title: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 4)

status: Public on Apr 06 2012

city: New haven

first: Natalia

last: Ivanova

state: ct

address: 10 Amistad

department: genetics

institute: Yale

summary: The transcription factors Nanog, Oct4 and Sox2 are the master regulators of pluripotency in mouse embryonic stem cells (mESCs), however, their functions in human ESCs (hESCs) have not been rigorously defined.  Here we show that the requirements for NANOG, OCT4 and SOX2 in hESCs differ from those in mESCs.  Both NANOG and OCT4 are required for self-renewal and repress differentiation. OCT4 controls both extraembryonic and epiblast-derived cell fates in a BMP4-dependent manner.  OCT4-depleted hESCs commit to trophectoderm and primitive endoderm in the presence of BMP4, but undergo neuroectoderm differentiation in the absence of BMP4. NANOG represses neuroectoderm and neural crest commitment, but has little or no effect on the other lineages. We find that SOX2 is not required for self-renewal because it is redundant with SOX3, which is induced in SOX2-depleted hESCs.  Simultaneous depletion of both SOX2 and SOX3 induces differentiation into the primitive streak. Unexpectedly, we identify significant variability in the usage of pluripotency factors by individual hESC lines, suggesting that the pluripotency network is remodelled to support a continuum of developmental states. Our study revises the general view of how NANOG, OCT4 and SOX2 orchestrate self-renewal in hESCs.

overall_design: Total RNA obtained from EF1a-control-, OE-NANOG-, OE-OCT4- or OE-SOX2-transduced hESCs.


title: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells


title: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 3)

overall_design: Total RNA obtained from SOX2-KD stable hESC clones and H1P control stable hESC clones.


title: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 2)

overall_design: Total RNA obtained from hESCs with or without BMP4 treatment for 8 days time course.


title: Host-influenza A virus(infA) interactions

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


title: Buffering and proteolysis are induced upon segmental haploidy in Drosophila melanogaster.

status: Public on Apr 05 2012

city: Umea

first: Jan

last: Larsson

address: Umea University

department: Molecular Biology

institute: Umea University

summary: Aneuploidy, i.e., variation in the number of individual chromosomes (chromosomal aneuploidy) or chromosome segment (segmental aneuploidy) is associated with developmental abnormalities and reduced fitness in all species examined, is the leading cause of miscarriages and mental retardations and a hallmark of cancer. Despite their documented importance in disease the effects of aneuploidies on the transcriptome remains largely unknown. Here we have examined the expression output in seven deficiency heterozygotes as single deficiencies and in all pairwise combinations. The results show that genes in one copy are buffered, i.e., are expressed above the expected 50% expression level compared to wild type and the buffering is general and not influenced by additional haploid regions. Long genes are significantly better buffered than short genes and our analysis suggests that gene length is the primary determinant for the degree of buffering. For short genes the degree of buffering depends on expression level and expression pattern. Furthermore, the results show that in deficiency heterozygotes the expression of genes involved in proteolysis is enhanced and negatively correlates with the degree of buffering. Our results suggest that proteolysis is a general response induced by aneuploidy.

overall_design: We prepared total RNA from flies heterozygous for seven different deletions, Df(3R)ED10953, Df(2L)ED4559, Df(2R)ED1770, Df(2R)ED1612, Df(2L)ED3, Df(3R)ED5071 or Df(3R)ED7665 in two or three single biological replicates or in pairwise combinations, as well as from six biological replicates of wild type control flies.

first: Lina

last: Lundberg

first: Margarida

last: Figueiredo

first: Per

last: Stenberg


title: Global gene expression divergence among mutation-accumulation Y-chromosome substitution lines of Drosophila melanogaster

city: Cambridge

first: Jun

last: Zhou

state: MA

address: 16 Divinity Ave. Rm2112

department: Organismic and Evolutionary Biology

institute: Harvard University

summary:
Gene expression profiling revealed that hundreds of genes were differentially expressed among these Y introgression lines, and that global gene expression pattern diverged between the low-PEV and high-PEV (defined in the accompanying publication) flies. The results further expand our understanding of the role of the Y chromosome in modulating global gene expression, and suggest a link with modifications of chromatin state.

Keywords: position-effect variegation (PEV)
The Y chromosomes of H15 and H23 have lower level of suppression on the expression of white gene, therefore show lower level of eye color variegation. In contrast, the Y chromosomes of H5 and H7 have higher level of suppression on the expression of white gene resulting higher level of eye variegation.

overall_design: A loop design was used with all the Y introgression lines. In addition to biological replicates, a Cy5-Cy3 dye swap was performed.


title: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 1)

overall_design: Total RNA obtained from H1P (control)-, shNANOG (Nanog shRNA knockdown)-, shOCT4 (Oct4 shRNA knockdown)- or shSOX2 (Sox2 shRNA knockdown)-transduced hESCs for 8 days time course.


title: Genome-wide analysis of whole blood transcriptional response to community-acquired Staphylococcus aureus infection in vivo

status: Public on Apr 04 2012

city: Dallas

first: Damien

last: Chaussabel

address: 3434 Live Oak

institute: Baylor Institute for Immunology Research

summary: Analysis of transcriptional profiles in whole blood from patients with Staphylococcus aureus infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity.

overall_design: Total RNA extracted from whole blood (lysed in Tempus tubes) drawn from pediatric patients with acute community-acquired Staphylococcus aureus infection.

first: Romain

last: Banchereau

first: Octavio

last: Ramilo


title: Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression (2)

first: Alireza

last: Baradaran-Heravi

state: BC

address: 950 West 28th Avenue, Room 218

department: Medical Genetics

institute: UBC

summary: Biallelic mutations of the DNA annealing helicase SMARCAL1 (SWI/SNF-related  matrix-associated actin-dependent regulator of chromatin, subfamily a-like 1) cause  Schimke immuno-osseous dysplasia (SIOD, MIM 242900), an incompletely penetrant  autosomal recessive disorder. Using human, Drosophila, and mouse models, we show  that the proteins encoded by SMARCAL1 orthologues localize to transcriptionally active  chromatin and modulate gene expression. We also show that similar to SIOD patients,  deficiency of the SMARCAL1 orthologues alone is insufficient to cause disease in fruit  flies and mice although such deficiency causes modest diffuse alterations in gene  expression. Rather, disease manifests when SMARCAL1 deficiency interacts with genetic  and environmental factors that further alter gene expression. We conclude that the  SMARCAL1 annealing helicase buffers fluctuations in gene expression and that  alterations in gene expression contribute to the penetrance of SIOD.

overall_design: For analysis of gene expression in flies, 5.0 μg of total RNA from three biologically independent replicates was extracted from 1) yw, 2) Marcal1del/del, 3) RpII2154/FM7, and 4) RpII2154/FM7;Marcal1del/del ovaries at 20°C and from yw and Marcal1del/del at 25°C, labeled and hybridized to Affymetrix Drosophila Genome 2.0 arrays.

first: Cornelius

middle: F

last: Boerkoel


title: Microarray expression data from human renal mesangial cells (HMC) treated with a Cyclosporine A (CsA) time course.

city: Dublin

first: Sein

last: O'Connell

address: Belfield

country: Ireland

institute: University College Dublin

summary:
HMCs were treated with CsA (4.2 µM) for 0 12 and 48 hours. To exmaine global gene changes in the renal mesangium following CsA treatment in order to identify novel contributors to CsA-induced renal dysfunction
Microarray analysis was used to identify novel mechanisms of CsA nephrotoxicity in the golmerulus

overall_design: Glomerulosceroisis is a key component of overall CsA neophrotxocity. The mesangial cells of the glomerulus are an important cell type with the renal glomerulus. In order to delineate this complex process and identify novel mechanism of the disease and identify possible future therapeutic targets HMCs were treated with CsA for 0 (control) 12 or 48 hours. HMCs were treated with 4.2 µM CsA and RNA extracted and hybridised on Affymetrix  (HG-U133A) microarrays

first: Niamh

last: Tuite

first: Craig

last: Slattery

first: Michael

last: Ryan

first: Tara

last: McMorrow


title: PFT1, the MED25 subunit of the plant Mediator complex, promotes flowering through CONSTANS dependent and independent mechanisms in Arabidopsis

status: Public on Apr 03 2012

city: Ciudad de Buenos Aires

first: Sabrina

last: Iñigo

state: Buenos Aires

address: Av. Patricias Argentinas 435

country: Argentina

institute: Fundación Instituto Leloir

summary: Two aspects of light are very important for plant development: the length of the light phase or photoperiod and the quality of incoming light. Photoperiod detection allows plants to anticipate the arrival of the next season, whereas light quality, mainly the red to far-red ratio (R:FR), is an early signal of competition by neighbouring plants. phyB represses flowering by antagonising CO at the transcriptional and post-translational levels. A low R:FR decreases active phyB and consequently increases active CO, which in turn activates the expression of FT, the plant florigen. Other phytochromes like phyD and phyE seem to have redundant roles with phyB. PFT1, the MED25 subunit of the plant Mediator complex, has been proposed to act in the light-quality pathway that regulates flowering time downstream of phyB. However, whether PFT1 signals through CO and its specific mechanism are unclear. Here we show that CO-dependent and -independent mechanisms operate downstream of phyB, phyD and phyE to promote flowering, and that PFT1 is equally able to promote flowering by modulating both CO-dependent and -independent pathways. Our data are consistent with the role of PFT1 as an activator of CO transcription, and also of FT transcription, in a CO-independent manner.  Our transcriptome analysis is also consistent with CO and FT genes being the most important flowering targets of PFT1. Furthermore, comparison of the pft1 transcriptome with transcriptomes after fungal and herbivore attack strongly suggests that PFT1 acts as a hub, integrating a variety of interdependent environmental stimuli, including light quality and jasmonic acid-dependent defences.

overall_design: Two genotypes, WT (Columbia) and pft1-1 mutants. Three biological replicates for each condition (genotype X temperature combination). RNA prepared independently for each sample.

last: Inigo

first: Mariano

last: Alvarez

first: Bárbara

last: Strasser

first: Andrea

last: Califano

first: Pablo

last: Cerdan


title: miR-206 integrates multiple components of differentiation pathways to control the transition from growth to differentiation in rhabdomyosarcoma cells

status: Public on Apr 02 2012

city: Seattle

first: Janet

middle: M.

last: Young

state: WA

address: 1100 Fairview Avenue N., C3-168,  P.O. Box 19024

department: Division of Human Biology

institute: Fred Hutchinson Cancer Research Center

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

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

platform_organism:
Physcomitrium patens
Populus trichocarpa
Arabidopsis thaliana
Glycine max
Medicago truncatula
Oryza sativa
Saccharum officinarum
Sorghum bicolor
Zea mays
Caenorhabditis briggsae
Caenorhabditis elegans
Bombyx mori
Anopheles gambiae
Drosophila melanogaster
Drosophila pseudoobscura
Apis mellifera
Danio rerio
Xenopus laevis
Xenopus tropicalis
Gallus gallus
Lemur catta
Ateles geoffroyi
Lagothrix lagotricha
Macaca mulatta
Macaca nemestrina
Gorilla gorilla
Pan paniscus
Pan troglodytes
Pongo pygmaeus
Homo sapiens
Canis lupus familiaris
Sus scrofa
Bos taurus
Ovis aries
Mus musculus
Rattus norvegicus
Human betaherpesvirus 5
human gammaherpesvirus 4
Gallid alphaherpesvirus 2
Monodelphis domestica
Takifugu rubripes
Murid gammaherpesvirus 4
Human gammaherpesvirus 8
Macacine gammaherpesvirus 4
Saguinus labiatus
Schmidtea mediterranea
Tetraodon nigroviridis
Betapolyomavirus macacae

overall_design: Refer to individual Series

first: Kyle

last: MacQuarrie

first: Zizhen

last: Yao

middle: M

first: Yi

last: Cao

first: Stephen

last: Tapscott


title: miR-206 integrates multiple components of differentiation pathways to control the transition from growth to differentiation in rhabdomyosarcoma cells (Illumina)

summary: Background: Similar to replicating myoblasts, many rhabdomyosarcoma cells express the myogenic determination gene MyoD. In contrast to myoblasts, rhabdomyosarcoma cells do not make the transition from a regulative growth phase to terminal differentiation. Previously we demonstrated that the forced expression of MyoD with its E-protein dimerization partner was sufficient to induce differentiation and suppress multiple growth-promoting genes, suggesting that the dimer was targeting a switch that regulated the transition from growth to differentiation. Our data also suggested that a balance existed between various inhibitory transcription factors and MyoD activity that kept rhabdomyosarcomas trapped in a proliferative state.   Methods: Potential myogenic co-factors identified by analysis of high-throughput sequencing of chromatin immunoprecipitation experiments in normal myogenic cells were tested for their ability to drive differentiation in rhabdomyosarcoma cell culture models, and their relation to MyoD activity determined through molecular biological experiments.   Results: Modulation of the transcription factors RUNX1 and ZNF238, factors with poorly delineated roles in myogenic development, can induce differentiation in rhabdomyosarcoma cells and their activity is integrated, at least in part, through the activation of miR-206, which acts as a genetic switch to transition the cell from a proliferative growth phase to differentiation. The inhibitory transcription factor MSC also plays a role in controlling miR-206, appearing to function by occluding a binding site for MyoD in the miR-206 promoter.   Conclusions: These findings suggest that nested feed-forward circuits that proceed from MyoD, to RUNX1, to ZNF238, and finally to miR-206 function in both rhabdomyosarcomas as well as normal myogenesis to control the decision point of proliferation versus differentiation.

overall_design: Total RNA samples were collected from human RD cells transduced with lentivirus carrying RUNX1, RP58 (ZNF238), miR-206 or GFP (three biological replicates each) and allowed to differentiate for 72 hours.


title: Hyperglycemia and a Common Variant of GCKR Are Associated with the Levels of Eight Amino Acids in 9,371 Finnish Men

city: Los Angeles

first: Mete

last: Civelek

state: CA

address: 675 Charles E. Young Dr. S. MRL 3220

department: Medicine

institute: University of California Los Angeles

summary: Objective:  Insulin regulates amino acid metabolism. We investigated whether glycemia and 43 genetic risk variants for hyperglycemia/type 2 diabetes affect amino acid levels in a large population-based cohort. Subjects and Methods: A total of 9,371 non-diabetic or newly-diagnosed type 2 diabetic Finnish men from the population-based METSIM Study were studied. Proton NMR spectroscopy was used to measure plasma levels of 8 amino acids. Genotyping of 42 SNPs and mRNA microarray analysis from 200 subcutaneous adipose tissue samples were performed. Results: Increasing fasting and/or 2-hour plasma glucose levels were associated with increasing levels of alanine, valine, leucine, isoleucine, phenylalanine and tyrosine, and decreasing levels of histidine and glutamine. We also found significant correlations between insulin sensitivity (Matsuda ISI) and expression of genes regulating amino acid metabolism. Only one SNP (rs780094 in GCKR) of the 42 risk SNPs for type 2 diabetes or hyperglycemia was significantly associated with the levels of alanine, isoleucine, and glutamine. Conclusions : We observed that the levels of branched-chain, aromatic amino acids and alanine increased and the levels of glutamine and histidine decreased with increasing glycemia. These associations seemed to be mediated by insulin resistance, at least in part. GCKR rs780094 was significantly associated with several amino acids.

overall_design: Total RNA was obtained from subcutaneous fat biopsies from 200 people participating in the METSIM study (4 samples were replicated for a total of 204 arrays).

first: Alena

last: Stančáková

first: Pasi

last: Soininen

first: Antti

last: Kangas

first: Henna

last: Cederberg

first: Jussi

last: Paananen

last: Pihlajamäki

first: Lori

last: Bonnycastle

first: Mario

last: Morken

last: Boehnke

first: Päivi

last: Pajukanta

first: Aldons

last: Lusis

first: Francis

middle: S

last: Collins

first: Johanna

last: Kuusisto

first: Mika

last: Ala-Korpela

first: Markku

last: Laakso


title: Expression data from middle-aged and old Drosophila females

status: Public on Apr 01 2012

city: Leiden

first: Agnieszka

last: Doroszuk

address: Sylviusweg 72

department: Evolutionary Biology

institute: Leiden University

summary:
The mechanisms underlying natural variation in lifespan and ageing rate remain largely unknown.
We performed microarray experiment to characterise genome-wide expression patterns of a long-lived, natural variant of Drosophila melanogaster resulting from selection for starvation resistance (SR) and compare it with normal-lived control flies (C).

overall_design: We sampled adult females at two time points representing middle age (90% survival) and old age (10% survival) respectively, in three adult diets (malnutrition, optimal food, and overfeeding).

first: Martijs

last: Jonker


title: Expression data of Arabidopsis thaliana (Ler accession) phytochrome phyABCDE quintuple mutant and phyABDE quadruple mutant in response to red light, and their comparison to WT expression data

city: Davis

first: Wei

last: Hu

address: One Shields Ave.

department: Department of Molecular and Cellular Biology

institute: Univ of California at Davis

summary: Phytochromes are red/far-red light photoreceptors. We sought to test at the transcriptomic level if Arabidopsis mutants lacking all phytochromes (from phyA to phyE), or just retaining trace levels of phyC, had transcriptional response to red light exposure.

overall_design:
phyABCDE and phyABDE mutants were grown for 4 days in darkness (D), or under continuous red light at 50 µmol m-2 s-1 (R50), or in darkness followed by 2 hr of red light exposure on day 4 (DR2h).
Differentially expressed genes of the mutants in response to red light were compared to those of wild type obtained previously {Hu et al. (2009) Molecular Plant, 2: 166-182}.
Three biological replicates were employed for dark and Rc-grown samples, and 2 biological replicates for DR2h samples, thus 8 samples were used for each mutant genotype.
It needs to be pointed out that 5 of the 6 WT samples (from WT-D-2 to WT-R50-2) had previously been deposited with GEO accessions GSM226267, GSM226268, GSM226269, GSM226278 and GSM226279. Their cRNA samples were synthesized and labeled with the Affymetrix GeneChip® Expression Analysis kits (One-cycle target labeling and control reagents). They are included in this series of study for convenient comparison, with newly assigned accessions from GSM784837 to GSM784841.
The more recent GeneChip 3' IVT Express Kit (Affymetrix) was used to synthesize and label aRNA for one new WT sample (WT-D-1)(GSM784836) and all mutant samples.

first: J

middle: C

last: Lagarias


title: Dynamics of mRNA abundance and translation in response to darkness and reillumination

status: Public on Mar 31 2012

city: Riverside

first: Piyada

last: Juntawong

address: 900 University ave

department: Botany and Plant Sciences

institute: University of California Riverside

summary: Gene expression analysis of 14d-old Arabidopsis seedlings exposed to 1h darkness and 10 min reillumination after 1 h darkness to evaluate the regulation of gene expression at the level of translation.

overall_design: 12 samples, 3 conditions (1h light control, 1 h darkness treatment, 1 h darkness plus 10 min reillumination), 2 RNA pools (Total mRNA and polysomal mRNA), 2 bioreplicates

first: Julia

last: Bailey-Serres


title: Expression data from primary breast tumors (NUH)

city: Auckland

first: Cris

last: Print

address: Grafton Campus, Park Rd

country: New Zealand

institute: Auckland University

summary:
Frozen tissue specimens from primary breast tumors were collected under approved protocols and profiled using Affymetrix U133 series expression microarrays. This cohort was assembled at the National University Hospital (NUH), Singapore in 2003, and profiled at the Genome Institute of Singapore, Microarray and Expression Genomics Lab. Dr. Lance D. Miller (Wake Forest University School of medicine) directed the profiling work.
A publication describing the generation of these data is not yet available. However, these data can be used alongside other Affymetrix breast tumour data sets to form large meta-cohorts for breast cancer research, as was done in Lasham et. al. J Natl Cancer Inst. 2012 Jan 18;104(2):133-146.

overall_design:
Frozen tumor tissues comprising of >60% tumor cellularity were extracted for total RNA and hybridized on Affymetrix microarrays.
Clinical data was requested, but not provided by submitter

first: Lance

last: Miller


title: Restoration of regulatory and effector T cell balance and B cell homeostasis in systemic lupus erythematosus patients through vitamin D supplementation

status: Public on Mar 30 2012

city: PARIS

first: Nicolas

last: DERIAN

address: 15 Avenue Pitié

department: Biotherapy

summary:
Systemic lupus erythematosus (SLE) is a T and B cell-dependent autoimmune disease characterized by the appearance of autoantibodies, a global regulatory T cells (Tregs) depletion and an increase in Th17 cells. Recent studies have shown the multifaceted immunomodulatory effects of vitamin D, notably the expansion of Tregs and the decrease of Th1 and Th17 cells. A significant correlation between higher disease activity and lower serum 25-hydroxyvitamin D levels was also shown.
This preliminary study suggests the beneficial role of vitamin D in SLE patients and needs to be confirmed in randomized controlled trials.

overall_design: In this prospective study, we evaluated the safety and the immunological effects of vitamin D supplementation in 20 SLE patients with hypovitaminosis D using transcriptomic study at M0 and M2.

first: Benjamin

last: Terrier

last: Derian

first: Yoland

last: Schoindre

first: Wahiba

last: Chaara

first: Guillaume

last: Geri

first: Noel

last: Zahr

first: Kuberaka

last: Mariampillai

first: Michelle

last: Rosenzwajg

first: Wassila

last: Carpentier

first: Lucile

last: Musset

first: Jean-Charles

last: Piette

first: Adrien

last: Six

first: David

last: Klatzmann

last: Saadoun

first: Patrice

last: Cacoub

first: Nathalie

last: Costedoat-Chalumeau


title: Expression data from Drosophila  Btk29A mutant and revertant neuronal tissue

city: Huddinge

first: Hossain

last: Nawaz

state: Stockholm

address: Hälsovägen 7

department: LABMED

institute: Karolinska Institutet

summary:
In Drosophila melanogaster, Btk29A displays a dynamic pattern of expression through the embryonic to adult stages. Complete loss-of function of both splice-forms is lethal, whereas selective absence of the type 2-form reduces the adult lifespan of the fly and causes male genitalial developmental abnormalities.
Here, we investigated the role of Btk29A type 2 on a transcriptomic level in the larvae CNS and adult heads. We used samples either selectively defective in Btk29A type 2 (Btk29AficP) or flies were the Btk29A type 2 gene has been reintroduced (ficExc.1-16).

overall_design: Adult heads and larvae CNS  were dissected  for RNA extraction and hybridization on Affymetrix microarrays.

first: C

middle: I

last: Smith

first: Jessica

last: Lindvall


title: Unique signatures of estrogen independent growth of MCF-7 cells in low-estrogen versus complete estrogen depravation

city: Ann Arbor

first: Viktoriya

last: Strumba

state: MI

address: 109 Zina Pitcher place

country: USA

institute: University of Michigan

summary: Despite the success of the aromatase inhibitors (AIs) in treating estrogen receptor positive breast cancer, 15-20% of patients receiving adjuvant AIs will relapse within 5-10 years of treatment initiation. Long term estrogen deprivation (LTED) of breast cancer cells in culture has been successfully used to mimic AI-induced estrogen depletion to dissect mechanisms of AI resistance. However, we hypothesized that a subset of patients receiving AI therapy may maintain low circulating concentrations of estrogens that influence the development of endocrine resistance. We sought to expand established LTED models to account for these observations. MCF-7 cells were grown in medium with charcoal stripped serum supplemented with defined concentrations of E2 or the estrogenic androgen metabolite 3βAdiol. Cells were selected in the EC10 and EC90 of E2 or 3βAdiol, or estrogen deprived. Estrogen-independence was evaluated during selection by assessing cell growth in the absence or presence of E2 or 3βAdiol. Following >7 months of selection, estrogen-independence developed in estrogen-deprived cells and cells maintained in low concentrations of steroid hormone. Functional analyses demonstrated that estrogen-deprived and low-steroid selected cells developed estrogen-independence via unique mechanisms, independent and dependent of ERα, respectively. Estrogen-independent growth in low-steroid selected cells could be blocked by kinase inhibitors. However, these cells were completely resistant to kinase inhibition in the presence of low steroid hormone concentrations. These data offer a novel perspective on the development of resistance to AI therapy, and may yield novel approaches to treat AI-resistant tumors.

overall_design: MCF-7 cells were selected for >7months in IMEM+10% Charcoal Stripped FBS, supplmented with defined steroid hormone conditions.  Following outgrowth of estrogen-independent cells, cell lines were grown in estrogen-free conditions and gene expression analysis was performed to identify drivers of estrogen-independent growth. Cells were assessed in biological triplicates.

first: Matthew

last: Sikora

first: Marc

last: Lippman

first: Michael

last: Johnson

first: James

last: Rae


title: Cell elasticity determines macrophage function.

status: Public on Mar 29 2012

city: Boston

first: Alvin

middle: T.

last: Kho

address: 320 Longwood Avenue

department: Informatics Program

institute: Boston Children's Hospital

summary: We report that macrophage elasticity plays a dominant role in bacterial phagocytosis, release of TNF-alpha, and production of reactive oxygen species.  We show that macrophage elasticity is modulated by mechanical factors including substrate rigidity and substrate stretch. Changes in macrophage elasticity are dependent upon the degree of actin polymerization, and mediated in part through small rhoGTPase activity.  Moreover, the functional effects of macrophage elasticity are not predicted by gene expression profiles.

overall_design:
Murine RAW 267.4 macrophages were separately grown on 2 matrix stiffness levels (1200, 150000 Pascals) for 0, 2, 6, 18 hours with 3 replicate sample experiments per condition. Total RNA extracted from the cells and profiled by microarrays.
Keywords: Murine RAW 267.4 macrophage, matrix stiffness, phagocytosis, cell elasticity.

first: Naimish

middle: R

last: Patel

first: Henry

last: Koziel