title: Expression data from tumors and adjacent normal tissue from clinical oral cancer patients

status: Public on Oct 28 2017

city: Columbus

first: Steve

last: Oghumu

address: 1841 Neil Ave

country: USA

institute: Ohio State University

summary: Oral cancer kills about 1 person every hour each day in the United States and is the 6th most prevalent cancer worldwide. In this study we utilized existing microarray data from a prior oral cancer study to examine the role of chronic pro-inflammatory mediators in oral carcionogenesis by comparing gene expression in oral tumors with adjacent non-tumor oral tissue from the same patient

overall_design: Oral tumors and adjacent non-involved oral tissue were obtained from oral squamous cell carcinoma patients (N = 6) enrolled in a Phase 0 clinical trial study (ClinicalTrials.gov ID NCT01465776) approved by the Internal Review Board at the Ohio State University Wexner Medical Center. Gene regulation was determined by comparisons of mRNA expression in tumor tissue relative to adjacent non-tumor tissue from the same patient

first: Thomas

last: Knobloch

first: Christopher

last: Weghorst


title: Early-life gene expression in neurons modulates lasting epigenetic states. [RNA-Seq]

status: Public on Oct 19 2017

city: Dallas

first: Hume

last: Stroud

state: TX

address: 5323 Harry Hines Blvd

institute: UT Southwestern

type: Expression profiling by high throughput sequencing

summary: In mammals during the early postnatal period the environment plays a critical role in promoting the final steps in neuronal development. While epigenetic factors are thought to contribute to this process, the underlying molecular mechanisms remain poorly understood. Here we show that in the brain during early life the DNA methyltransferase DNMT3A transiently binds across transcribed regions of lowly expressed genes, and its binding specifies the pattern of DNA methylation at CA sequences (mCA) within these genes. We find that DNMT3A occupancy and mCA deposition within the transcribed regions of genes is negatively regulated by gene transcription and may be modified by early-life experience. Once deposited, mCA is bound by the methyl-DNA-binding protein MECP2 and functions in a rheostat-like manner to fine-tune the cell type-specific transcription of genes that are critical for brain function.

overall_design: Indrops single nuclei RNA-seq on mouse corticies

first: William

last: Renthal

first: Lisa

last: Boxer

first: Michael

middle: E

last: Greenberg


title: Aging, Dementia, and TBI Study

status: Public on Oct 16 2017

city: Seattle

first: Jeremy

last: Miller

state: WA

address: 615 Westlake Ave N

institute: Allen Institute for Brain Science

summary:
The Aging, Dementia and Traumatic Brain Injury Study is a detailed neuropathologic, molecular and transcriptomic characterization of brains of control and TBI exposure cases from a unique aged population-based cohort from the Adult Changes in Thought (ACT) study.  This study was developed by a consortium consisting of the University of Washington, Kaiser Permanente Washington Health Research Institute, and the Allen Institute for Brain Science, and was supported by the Paul G. Allen Family Foundation.  This freely available resource (http://aging.brain-map.org/) presents a systematic and extensive data set of study participant metadata, quantitative histology and protein measurements of neuropathology, and RNA sequencing (RNA-seq) analysis of hippocampus and neocortex. Specific methodological details are available on the “Documentation” tab at http://aging.brain-map.org/.  Included in this data set are normalized RNA-Seq FPKM files used for analysis in "Neuropathological and transcriptomic characteristics of the aged brain", published in eLife.  Other processed data files as well as sample and donor meta-data and QC metrics are available at http://aging.brain-map.org/download/index

Controlled access to raw data files is available via https://www.niagads.org/datasets/ng00059

overall_design: In total, 376 samples collected from cortical grey (parietal and temporal) and white matter (parietal) and hippocampus from a total of 107 brains are presented in this resource (one of the 377 samples from the original resource was not included in analyses for the manuscript).  This study includes 55 participants of the ACT study self-reporting TBI with loss of consciousness, along with 55 individuals matched for age, sex, and year of death who did not report a TBI with loss of consciousness (three donors were removed as outliers prior to performing the analysis).

middle: A

first: C

middle: D

last: Keene

first: Ed

middle: S

last: Lein


title: Phospholipase Cγ pathway-dependent mTOR signaling controls IL-7-mediated   early B cell development

status: Public on Sep 25 2017

city: Memphis

first: Geoffrey

last: Neale

state: TN

address: 262 Danny Thomas Place

department: Hartwell Center

institute: St Jude Childrens Research Hospital

summary: We examined the global gene expression profile of PLCγ1/PLCγ2 double-deficient CLPsand B cell progenitors by RNA-seq analysis.

overall_design: CLPs (Lin-IL-7R+) and B cell progenitors (B220+IgM-IL-7R+) were sorted from PLCγ1-/-PLCγ2-/- and control mice, and subjected to RNA-seq analysis. 3 repricates of each population from each genotype.

first: Mei

last: Yu

first: Yuhong

last: Chen

first: Hu

last: Zeng

first: Yongwei

last: Zheng

first: Guoping

last: Fu

first: Wen

last: Zhu

first: Ulrich

last: Broeckel

first: Praful

last: Aggarwal

first: Amy

last: Turner

first: Cliff

last: Guy

first: Hongbo

last: Chi

first: Renren

last: Wen

first: Demin

last: Wang


title: Glycosylation-related gene expression in the mucus-secreting gastrointestinal cell line HT29-MTX-E12 in response to infection by Helicobacter pylori

status: Public on Sep 21 2017

city: Galway

first: Michael

last: Cairns

address: University Road

department: NCBES

country: Ireland

institute: NUI Galway

summary:
The HT29 derivative cell line HT29-MTX-E12 (E12) produces an adherent mucus layer predominantly of the gastric MUC5AC mucin when grown on transwells. This mucus layer supports Helicobacter pylori survival in culture. E12 cells were infected with H. pylori and the transcriptome of infected and uninfected E12 were compared. Also included for comparison was the HT29 parent cell line grown on transwells.
The study focused on glycosylation related genes as these regulate the structures that have a major role to play in pathogen-host cell interaction.

middle: T

first: Ananya

last: Gupta

first: Julie

last: Naughton

first: Marian

last: Kane

first: Marguerite

last: Clyne

first: Lokesh

last: Joshi


title: De novo MYC addiction as an adaptive response of cancer cells to CDK4/6 inhibition

status: Public on Sep 15 2017

city: Barcelona

first: Míriam

last: Tarrado-Castellarnau

address: Av. Diagonal 643

country: Spain

institute: Universitat de Barcelona

summary:
Cyclin-dependent kinases (CDK) are rational cancer therapeutic targets fraught with the development of acquired resistance by tumor cells. Through integrated fluxomics and transcriptomics approaches, we show that the inhibition of CDK4/6 causes enhanced metabolism of glucose, glutamine and amino acids, a metabolic reprogramming directed by the MYC transcription factor. Upon inhibition of CDK4/6, MYC is stabilized and its accumulation induces an upregulation of the mTOR pathway and increased glutamine metabolism and production of α-ketoglutarate, a prolyl hydroxylase substrate that triggers HIF1α hydroxylation and degradation. These MYC-driven adaptations to CDK4/6 inhibition render cells highly sensitive to inhibitors of mTOR and glutaminase and to hypoxia, revealing that drug resistance can mechanistically promote the emergence of new vulnerabilities that can be exploited therapeutically.
We used microarrays to detail the global programme of gene expression underlying inhibition of CDK4 and CDK6.

overall_design: Cells were transfected with a mix (siRNA CDK4/6) containing siRNA against CDK4 and siRNA against CDK6 or with a mix (siRNA Control) containing Non-Targeting Control Pool siRNA  and Silencer Select Negative Control siRNA.

first: Tarrado-Castellarnau

last: Miriam

first: Tarragó-Celada

last: Josep

first: Pedro

last: de Atauri

first: Marta

last: Cascante


title: Discovery and validation of a gene expression profile for human islet integrity and transplant functionality

status: Public on Sep 14 2017

city: La Jolla

first: Sunil

last: Kurian

state: CA

address: 10550 N Torrey Pines Road

department: Molecular and Experimental Medicine

institute: The Scripps Research Institute

summary: There is growing evidence that transplantation of cadaveric human islets is an effective therapy for type 1 diabetes. However, gauging the suitability of islet samples for clinical use remains a challenge. We hypothesized that islet quality is reflected in the expression of specific genes. Therefore, gene expression in 59 human islet preparations was analyzed and correlated with diabetes reversal after transplantation in diabetic mice. Analysis yielded 262 differentially expressed probesets, which together predict islet quality with 83% accuracy. Pathway analysis revealed that failing islet preparations activated inflammatory pathways, while functional islets showed increased regeneration pathway gene expression. Gene expression associated with apoptosis and oxygen consumption showed little overlap with each other or with the 262 probeset classifier, indicating that the three tests are measuring different aspects of islet cell biology. A subset of 36 probesets surpassed the predictive accuracy of the entire set for reversal of diabetes, and was further reduced by logistic regression to sets of 14 and 5 without losing accuracy. These genes were further validated with an independent cohort of 16 samples. We believe this limited number of gene classifiers in combination with other tests may provide complementary verification of islet quality prior to their clinical use.

overall_design: Microarray profiles of 59 human islet preparations were compared between three data sets using class comparisons, network and biological function analyses. Specific genes were validated by quantitative PCR and immunopathology. Clinical findings were also compared.

middle: M


title: Distinct signature in liver and gut clock revealed by a ketogenic diet

status: Public on Sep 18 2017

city: Irvine

first: Yu

last: Liu

state: California

address: UCI

department: Computer Science

institute: University of California, Irvine

summary: The circadian clock orchestrates rhythms in physiology and behavior, allowing the organism to adapt to daily environmental changes. Recently, efforts have been made to unravel the connection between the circadian clock and metabolism and to understand how the peripheral clock in different organs coordinates circadian responses to maintain metabolic homeostasis. It is becoming clear that diet can influence diurnal rhythms, however, the molecular mechanisms responsible for alterations in daily oscillations and how tissue-specific clocks interpret a nutritional challenge are not well understood. Here, we reveal tissue-specific circadian plasticity in response to a ketogenic diet (KD) in both the liver and intestine and a remarkable deviation within these two tissues following subsequent carbohydrate supplementation. KD caused a dramatic change in the circadian transcriptome in both liver and intestine in a tissue-specific fashion. In particular, both the amplitude of clock genes as well as specific BMAL1 recruitment was profoundly altered by KD while the intestinal clock was devoid of such plasticity. While PPARG nuclear accumulation was circadian in both tissues, it showed substantial phase specificity as did downstream targets. Finally, the gut and liver clocks had distinct responses to carbohydrate supplementation to KD composition, suggesting a higher plasticity in the ileum whose gene expression was almost restored to control baseline. For the first time our results demonstrate how nutrients modulate clock function in a tissue-specific manner, suggesting that a food stress arouses unique circadian molecular signatures in distinct peripheral tissues.

overall_design:
We used microarray to quantify expression levels of circadian genes under different diet regime in liver and gut, which is quantified in terms of total RNA.
All starting total RNA samples were quality assessed prior to beginning target preparation/processing steps by running out a small amount of each sample (typically 25-250 ng/well) onto a RNA 6000 Nano LabChip that was evaluated on an Agilent Bioanalyzer 2100 (Agilent Technologies, Palo Alto, CA). Microarray analysis was performed at the UCI Genomics High-Throughput Facility, University of California Irvine, as already described in Eckel-Mahan et al. 2013.

first: Mari

last: Murakami

first: Paola

last: Tognini

first: Kristin

middle: L

last: Eckel-Mahan

first: John

last: Newman

first: Eric

last: Verdin

first: Pierre

last: Baldi

first: Paolo

last: Sassone-Corsi


title: Comparasion of DNA methylomes of human CD11b+ cells from healthy donors (HD) peripheral blood and CD11b+ cells isolated from ascitic fluid (a) or peripheral blood (b) from ovarian cancer patients

status: Public on Sep 11 2017

city: Badalona, Barcelona

first: Esteban

last: Ballestar

state: N/A = Not Applicable

address: Ctra de Can Ruti, Camí de les Escoles s/n

institute: Josep Carreras Research Institute (IJC)

type: Methylation profiling by genome tiling array

summary: The methylation profiles of bisulfite-modified DNA of human CD11b+ cells from healthy donors (HD) were compared with CD11b+ cells isolated from ovarian cancer patients (blood or ascitic fluid) using the Infinium HumanMethylation850 BeadChips (Illumina, Inc., San Diego, CA,). This platform allows the interrogation of >850,000 methylation sites per sample at single-nucleotide resolution, and comprises an average of 17 CpG sites per gene in the 99% of RefSeq genes. 96% of CpG islands are covered, with additional coverage in CpG island shores and the regions flanking them. The samples were hybridized in the array following the manufacturer’s instructions.

overall_design: Total DNA isolated by standard procedures from  isolated CD11+ cells.

first: Javier

last: Rodríguez-Ubreva

first: Francesc

last: Català-Moll

first: Natasa

last: Obermajer

first: Damiana

last: Álvarez-Errico

first: Ricardo

middle: N

last: Ramirez

first: Carlos

last: Company

first: Roser

last: Vento-Tormo

first: Gema

last: Moreno-Bueno

first: Robert

middle: P

last: Edwards

first: Ali

last: Mortazavi

first: Pawel

last: Kalinski


title: RANBP6 silencing in HEK293 cells

status: Public on Nov 01 2017

city: Madrid

first: Massimo

last: Squatrito

address: Calle Melchor Fernandez Almagro 3

institute: Spanish National Research Center (CNIO)

summary: Expression data from HEK293 cells expressing a doxcycline-inducible RANBP6 shRNA

overall_design: Expression data from HEK293 RANBP6 shRNA cells


title: Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells [HG-U133_Plus_2]

status: Public on Oct 14 2017

city: Houston

first: Scott

middle: Andrew

last: Ochsner

address: One Baylor Plaza

department: Molecular and Cellular Biology

institute: Baylor College of Medicine

summary:
Glucocorticoid (GC)- sensitive cells are killed by receptor (GR)-filling concentrations of GC for a sufficient time.
We used 2 closely related clones ( sensitive, 1 resistant) from the CEM line of ALL cells to test the hypothesis that at this early pre-apoptosis time, a distinct set of regulated genes would be found in the sensitive clones, with cross-talk to other significant pathways

overall_design:
CEM C1-15(resistant) is a subclone of resistant clone CEM C1.  CEM C7-14 is a subclone of sensitive clone CEM C7.  C1 and C7 were cloned from the original CEM ALL line.  Samples were obtained 3 hr after addition of 10E-6 M dexamethasone (Dex) to triplicate cultures, RNA extracted and analyzed for transcript expression levels

**Please note that the submitter was unable to locate the raw data CEL files. Thus raw data is not included in the current records.**

first: M

last: Webb

first: Aaron

last: Miller

first: Tamara

last: Howard

first: Betty

middle: H

last: Johnson

first: Sergei

last: Chumakov

first: Yuriy

last: Fofanov

first: Trang

last: Nguyen-Vu

first: C

middle: Y

last: Lin

first: E

middle: B

last: Thompson


title: Anti-leukemic effects of glucocorticoids in childhood acute lymphoblastic leukemia: conserved transcriptional pathway to cell cycle arrest but not to cell death

status: Public on Sep 22 2017

city: Bolzano

first: Johannes

last: Rainer

address: Via A. Volta 21

department: Institute for Biomedicine

country: Italy

institute: Eurac Researc

summary: Glucocorticoids (GCs) cause cell cycle arrest and cell death in malignant lymphoblasts and constitute a principal component in the treatment of childhood acute lymphoblastic leukemia (chALL). To address the molecular mechanism of the anti-leukemic GC effects, we performed microarray-based whole-genome expression profiling of lymphoblasts from 46 patients undergoing systemic GC mono-therapy and combined these data with clinical information (e.g., molecular genotype, reduction in peripheral blood lymphoblasts, GC bioactivity in the patient's blood) using differential gene expression with GO analyses, regression modeling correlating transcriptional with clinical response, and an iterative elastic net approach to address combinatorial effects of gene expression and regulation. Our analysis revealed that, although there are a number of common response genes, the transcriptional response to GC in vivo varies considerably in the different molecular subtypes of this disease. Regarding the anti-leukemic response, repression of mRNA for key regulators of G2/M transition was commonly observed in all subtypes whereas we failed to observe a common transcriptional control of apoptosis genes. Although sets of genes were identified which in combination appear to contribute to the apoptotic response, the data as a whole suggest that GC-induced cell death does not result from conserved transcriptional regulation of the apoptotic machinery itself but might rather result from a wide spread deregulation of gene expression.

overall_design:
For differential expression analysis, M-values (log2 fold change values) were calculated for each patient comparing the 6 or 24 hour gene expression profile to the gene expression profile prior to treatment start (0h time point). Differential expression analysis was performed on these M-values using the moderated t-test from limma employing two different linear models, one including a factor for the time point, thus identifying differentially expressed genes after 6 or 24 hours of GC treatment (common GC response), and one with an additional factor for the chALL subtype, thus identifying differentially expressed genes after 6 or 24 hours in each subtype (sub-type specific response).

Description of sample characteristics: treatment time point: time point in hours relative to initiation of GC mono-therapy; age: age of the patient at day of diagnosis; sex: gender; ALL subtype by clustering: ALL subtype determined by clustering based on the gene expression profile and probe sets specific for the various subtypes of ALL; ALL subtype for analysis: subtype assignment used in the analysis; prednisone poor responder: clinical indicator whether the patient responded to the first week of GC therapy; hyb year: year in which the microarray was generated; normalization set: defines the sets in which the microarrays were normalized, arrays with set of type reference were used to define the reference vectors for frozen RMA (and affinity parameters for GCRMA background adjustment), all other microarrays were normalized using the parameters estimated in the reference set.

first: Tatsiana

last: Aneichyk

first: Daniel

last: Bindreither

first: Armin

last: Kroesbacher

first: Nikola

last: Mueller

first: Bernhard

last: Meister

first: Roman

last: Crazzolara

first: Georg

last: Mann

first: Renate

last: Panzer-Gruemayer

first: Reinhard

last: Kofler

first: Stephan

last: Geley


title: Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells

first: Scott

last: Ochsner

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

overall_design: Refer to individual Series


title: Treatment of advanced liver fibrosis in HIV- and HCV-infected adults with simtuzumab, a monoclonal antibody against lysyl oxidase-like 2: Results of a 6-month open-label safety trial

status: Public on Sep 08 2017

city: Hamilton

first: Dan

last: Sturdevant

state: MT

address: 903 S 4th street

department: NIAID

institute: NIH

summary: Chronic liver injury can result in fibrosis that may progress over years to end-stage liver disease. The most effective antifibrotic therapy is treatment of the underlying disease, however when this is not possible, interventions to reverse fibrosis are needed. We conducted an open-label pilot trial to study the safety and tolerability of simtuzumab, a monoclonal antibody directed against lysyl oxidase-like 2 (LOXL2) enzyme, in patients with advanced liver disease from hepatitis C virus (HCV), human immunodeficiency virus (HIV), or HCV-HIV co-infection. 18 patients with advanced liver fibrosis received simtuzumab 700mg IV every 2 weeks for 22 weeks. There were no discontinuations due to adverse events. No significant change was seen in hepatic venous pressure gradient or liver biopsy fibrosis score after treatment. Exploratory transcriptional and protein profiling using paired pre- and post-treatment liver biopsies, serum, and whole blood identified upregulation of TGFβ3 and IL-10 pathways with treatment. In summary, simtuzumab was well tolerated in HCV- and HIV-infected patients with advanced liver disease. Modulation of TGFβ3 and IL-10 pathways as a result of simtuzumab treatment merits investigation in future trials.

overall_design: Paired liver biopsy of pre-treatment (PRE) versus post-treatment (POST), and paired blood PRE and POST, in 12 participants.

first: Eric

middle: G

last: Meissner

first: Mary

last: McLaughlin

first: Lindsay

last: Matthews

first: Ahmed

last: Gharib

first: Ralph

last: Sinkus

first: Kimmo

last: Virtaneva

first: Stephen

middle: F

last: Porcella

first: David

last: Kleiner

first: Colleen

last: Hadigan

first: Henry

last: Masur

first: Theo

last: Heller

first: Joseph

last: Kovacs

first: Shyam

last: Kottilil

first: Caryn

last: Morse


title: Sam68-mediated disruption of CBP/β-catenin neoplastic transcriptional programming allows selective targeting of human cancer stem cells

status: Public on Oct 10 2017

first: Mickie

last: Bhatia

state: Ontario

address: 1200 Main Street West

department: Stem Cell and Cancer Research Institute (SCC-RI)

country: Canada

institute: McMaster University

summary: Increasing evidence suggests that cancer arises from cells that are capable of initiating and sustaining neoplastic tissue growth, termed cancer stem cells (CSCs). Of central scientific and clinical relevance, cells with CSC properties are enriched for chemo- and radiation resistance and therefore may represent a population of cells that must be therapeutically targeted to prevent cancer recurrence/relapse 1. Human CSCs were first isolated in neoplastic hematopoietic tissue that manifests leukemias such as adult acute myeloid leukemia (AML) 2. AML stem cells represent a benchmark model of human CSC biology, ultimately motivating foundational studies leading to the identification of CSCs from solid tumours such as breast and colon 3. Independent of tissue type, a consistent feature of CSCs is their uncontrolled self-renewal capacity and differentiation blockade that have been commonly related to aberrant activation of pro-oncogenic events such as dysregulation of CBP/p300 transcriptional regulation involving β-catenin 4. However, the transcriptional networks involving CBP/p300/β-catenin complex have been shown to be equally critical to maintain normal stem cell (SCs) self-renewal for tissue homeostasis and regeneration 5. Here, we identify Sam68 as a distinct target that affords the ability to uniquely regulate CBP mediated transcription in human CSCs. Using a small molecule that targets Sam68, we reveal that shifting its affinity for CBP disrupts CBP/β-catenin complexes, leading to immediate changes in histone H3 (K14 and K18) acetylation. Chemical targeting of Sam68 induced global changes in transcriptional programs of patient AML cells involving apoptosis and differentiation and was able to uniquely reduce neoplastic self-renewal of human CSCs in an in vivo model of patient specific acute myeloid leukemia (AML). Our study establishes an approach whereby the CBP/β-catenin transcriptome can be uniquely targeted via Sam68 based vulnerability of CSCs that impacts neoplastic differentiation and self-renewal.

overall_design: AML MNCs were injected via tail vein into sublethally irradiated NSG adult mice. Transplanted mice were treated IP daily for 10 days with 100 mg CWP/kg body weight starting 2 weeks after transplantation. Vehicle control-treated transplanted mice were injected as described above with 100 mL saline solution/kg body weight.  Engrafted-AML blasts treated with vehicle or CWP were sorted based on the co-expression of CD45 and CD33, and absence of CD19 and CD3 using a FACSAria II (BD). Total RNA from purified populations was extracted and amplified as described previously (Shojaei et al., 2005). Amplified-labeled RNA was hybridized to HG-U133Plus v2.0 chip.

first: Yannick

last: Benoit

first: Ryan

middle: R

last: Mitchell

first: Ruth

last: Risueno

first: Eva

last: Szabo

first: Masakatsu

last: Eguchi

first: Michelle

last: Jones

first: Allison

last: Boyd

first: Lili

last: Aslostovar

first: Zoya

last: Shapovalova

first: Monica

last: Graham

first: Angelique

last: Schnerch

first: Uyen

last: Dang

first: Aline

last: Fiebig-Comyn

first: Michael

last: Trus

first: Tony

middle: J

last: Collins

first: Anargyros

last: Xenocostas

first: Brian

last: Leber


title: Effects of leptin on gene transcription of human epidermal keratinocytes

status: Public on Sep 01 2017

city: Seoul

first: Minsoo

last: Noh

address: 1 Gwanak-ro, Gwanak-gu

department: Pharmacy

country: South Korea

institute: Seoul National University

summary: Subcutaneous fat adipocytes and dermal adipocytes produce leptin. Association of leptin with cutaneous would healing is known, however, the response of human epidermal keratinocytes to leptin has not unclear in a molecular level. In order to get biological insights on the role of leptin in epidermal physiology, the genome scale transcriptional response of normal human keratinocytes to leptin was investigated.

overall_design: Normal human keratinocytes (NHKs) were treated with 10 ng/ml of leptin for 24 hours and harvested for total RNA extraction and hybridization on Affymetrix Human GeneChip 133 2.0 microarrays.


title: Single cell RNA-seq analysis of head and neck cancer

status: Public on Nov 30 2017

city: Rehovot

first: Itay

last: Tirosh

address: Herzl 234

country: Israel

institute: WEIZMANN INSTITUTE OF SCIENCE

summary: To understand the diversity of expression states within head and neck cancers, we profiled 5902 single cells from 18 patients with oral cavity tumors by single cell RNA-seq

overall_design:
Tumors were disaggregated, sorted into single cells, and profiled by Smart-seq2.
-------------------------------------------------------
Authors state that "We are currently unable to provide the raw data  due to privacy concerns, but will have the raw data available once  we obtain permission from our institution."

first: Sid

last: Puram

first: Anuraag

last: Parikh


title: DNA methylation of human cancer cell lines and normal cells.

city: Chuo-ku

first: Naoko

last: Iida

state: Tokyo

address: 5-1-1 Tsukiji

country: Japan

institute: National Cancer Center in Japan.

summary: DNA methylation in cancer cell lines and normal cells.

overall_design: Bisulphite converted DNA from the cell lines were hybridised to the Illumina Infinium 450k Human Methylation Beadchip


title: General characterization of HNSCC cell lines

status: Public on Oct 03 2017

city: Baltimore

first: Elana

middle: Judith

last: Fertig

state: MD

address: 670 W. Baltimore Street, 3rd floor

department: Institute for Genome Sciences

institute: University of Maryland, Baltimore

summary: Profiling gene expression in a panel of 14 HNSCC cell lines

overall_design: 28 total RNA collected from a panel of 14 HNSCC cell lines.


title: Comparative transcript profiling of EBNA2 target gene expression in CBF1 proficient and deficient DG75 cells

city: Munich

first: Bettina

last: Kempkes

address: Marchioninistr. 25

department: AGV

country: Germany

institute: HMGU

summary:
Epstein-Barr virus (EBV) infection converts resting human B cells into permanently growing lymphoblastoid cell lines (LCLs). The viral Epstein-Barr virus nuclear antigen 2 (EBNA2) plays key role in this process. It preferentially binds to B cell enhancers and establishes a specific viral and cellular gene expression program in LCLs. The cellular DNA binding factor CBF1/CSL serves as a sequence specific chromatin anchor for EBNA2. The ubiquitous expression of this highly conserved protein raises the question whether additional cellular factors might determine EBNA2 chromatin binding selectively in B cells. Here we used CBF1 deficient B cells to identify cellular genes up or downregulated by EBNA2 as well as CBF1 independent EBNA2 chromatin binding sites. Both, CBF1 independent EBNA2 target genes and chromatin binding sites are less frequent than CBF1 dependent EBNA2 functions. CBF1 independent EBNA2 binding sites are highly enriched for EBF1 binding motifs. We show that EBNA2 binds to EBF1 in CBF1 proficient and deficient B cells and requires EBF1 to bind to CBF1 independent binding sites. Our results identify EBF1 as a co-factor of EBNA2 which conveys B cell specificity to EBNA2.
In order to test, if EBNA2 can exert any functions in the absence of its DNA adaptor CBF1, a microarray based genome wide screen for EBNA2 target genes in DG75 B cells that are either proficient (wt) or deficient (ko) for CBF1 was performed. CBF1 deficient DG75 cells (SM224.9) cells had been generated by gene targeting using homologous recombination in the somatic B cell line DG75. Both cell lines, the CBF1 proficient DG75 parental cell line and the CBF1 deficient somatic knock-out cell line constitutively express an estrogen receptor (ER) hormone binding domain EBNA2 fusion protein (ER/EBNA2). ER/EBNA2 is retained in the cytoplasm of the cell but is rapidly activated and translocated to the nucleus in response to estrogen. For expression profiling, DG75, DG75 CBF1 ko (SM224.9), DG75 ER/EBNA2 CBF1 wt (SM295 D6) and DG75 ER/EBNA2 CBF1 ko (SM296 D3) cells were cultured in estrogen supplemented media for 24 h, total cellular RNAs were harvested and processed for the hybridization of gene arrays.
The cellular system used for this study has been published: Maier S, Santak M, Mantik A, Grabusic K, Kremmer E, Hammerschmidt W, et al. A somatic knockout of CBF1 in a human B-cell line reveals that induction of CD21 and CCR7 by EBNA-2 is strictly CBF1 dependent and that downregulation of immunoglobulin M is partially CBF1 independent. Journal of Virology. 2005 Jul;79(14):8784-92. PubMed PMID: 15994772.

overall_design: Gene expression profiling of EBNA2 induced target genes by Affymetrix microarrays

first: Florian

last: Erhard

first: Sybille

last: Thumann


title: Epigenetic mechanisms underlie the crosstalk between growth factors and a steroid hormone [methylation I]

status: Public on Sep 24 2017

first: Yehoshua

last: Enuka

department: Biological Regulation

institute: Weizmann Institute of Science

summary: Growth factors (GFs) suppression by steroid hormones  recurs in embryology and is co-opted in pathology. While studying mammary cell migration, which is stimulated by GFs and antagonized by glucocorticoids (GCs), we found that GCs inhibit positive feedback loops activated by GFs and stimulate the reciprocal negative loops. Although no alterations in DNA methylation accompany the transcriptional events instigated by either stimulus, forced demethylation of distal regions broadened the repertoire of inducible genes. Our data indicate that the crosstalk involve transcription factors like p53 and NF-kB, along with reduced pausing (and traveling) of RNA polymerase II (RNAPII) at the promoters (and bodies) of GF-inducible genes. In addition, while GFs hyper-acetylated chromatin at unmethylated promoters and enhancers of genes involved in motility, GCs hypo-acetylated the corresponding regions. In conclusion, stably unmethylated genomic regions that encode feedback regulatory modules and differentially recruit RNAPII and acetylases/deacetylases underlie suppression of growth factor signaling by glucocorticoids.

overall_design: DNA methylation – time course of EGF (up to 8 hours)


title: Whole blood RNA sequencing of current and former cigarette smokers

status: Public on Sep 05 2017

city: Boston

first: Margaret

last: Parker

state: MA

address: 181 Longwood Ave

department: Medicine

institute: Brigham and Women's Hospital

summary: Purpose: The purpose of this study was to describe transcriptomic changes between current and former smokers using differential gene expression and differential exon usage

overall_design:
Whole blood from 515 subjects (229 current smokers and 286 former smokers) were RNA sequenced. Raw read data will be submitted to dbGaP.
--------------------------
Submitter states "Raw read data will be submitted to dbGaP."

first: Peter

last: Castaldi


title: Gene expression and DNA methylation profiling for HEK-293T cells transfected with GFP and DMEΔ

status: Public on Sep 20 2017

first: Jin Hoe

last: Huh

address: Gwanak-gu

department: Dept Plant Science


title: Gene expression data for HEK-293T cells transfected with GFP control and plant derived DNA demethylase DMEΔ

summary: Expression profiles of human embryonic kidney (HEK)-293T cells expressing a GFP (293T-GFP) or a truncated form of Arabidopsis DEMETER (DME) 5-methylcytosine (5mC) DNA glycosylase (293T-DMEΔ) analyzed on an Affymetrix Human Genome U133 Plus 2.0 Array Platform. These array data revealed differentially expressed genes (DEGs) between the 293T-GFP cells (without direct 5mC excision activity) and 293T-DMEΔ cells (with artificially implemented direct 5mC excision activity).

overall_design: To investigate whether DMEΔ induces gene expression, GFP- and DMEΔ-expressing in HEK-293T cells were collected 48h after transfection by flow cytometry, and RNA were hybridized to Human Genome U133 Plus 2.0 Array

first: Young

last: Mok

first: Jin


title: Identify genes modulated by gemcitabine and/or GNE-783 in HT-29 tumors in vivo

city: South San Francisco

first: Matthew

last: Brauer

address: 1 DNA Way

department: Bioinformatics

institute: Genentech, Inc.

summary: Identified genes that were up- or down-regulated in HT-29 xenograft tissue in response to the indicated treatments.

overall_design: Animals were administered 60 mg/kg gemcitabine or vehicle, and 24 hours later were administered 25 mg/kg GNE-783 or vehicle. Tumors were harvested 24 hours later.

first: Kristin

last: Zimmerman

first: Thomas

last: O'Brien


title: A model of exposure to extreme environmental heat uncovers the human transcriptome to heat stress

city: Riyadh

first: Musa

last: Gabere

address: Kashmalaan

country: Saudi Arabia

institute: King Abdullah International Medical Research Center,  NGHA

summary: The molecular mechanisms by which individuals subjected to environmental heat stress either adapt or develop heat-related complications are not well understood. We analysed the changes in blood mononuclear gene expression patterns in human volunteers exposed to an extreme heat in a sauna (temperature of 78 ± 6 °C).

overall_design: Fifteen male and female volunteers were subjected to heat stress, and PBMCs were analyzed from three time points, namely: before exposure (T0), at the end of heat exposure (T1), and 1 hour after the end of heat stress (T2).

first: M

first: A

last: Bouchama

first: S

last: Al Mahri

last: Hussein

last: Abdullah

last: Mohammad

last: Aziz


title: Expression data from human hepatocellular carcinoma tissues and the correponding non-cancerous tissues

city: Shanghai

first: Zhuoan

last: Cheng

address: No.25/Ln2200 Xie-Tu Road

country: China

institute: Shanghai Cancer Insitute

summary:
To identifythe the functional roles and the pathophysiological contributions of coding genes and noncoding RNAs in human hepatic carcinogenesis, we analysed the differenial expression of genes and noncoding RNAs in hepatocellular carcinoma tissues and the corresponding non-cancerous tissues.
We used microarrays to detail the global programme of gene expression in human hepatocellular carcinomas and correponding non-cancerous tissues.

overall_design: Total RNA from 14 pairs hepatocellular carcinoma tissues and correponding non-cancerous tissues were isolated and purified. Five micrograms of total RNA from each sample were used to synthesize double-stranded complementary DNA (cDNA), and then amplified and labeled with biotin and hybridized to the GeneChip Human Genome U133 Plus 2.0 Array

first: Wenxin

last: Qin

first: Haojie

last: Jin

first: Hui

last: Wang


title: Identification of mRNAs modulated by the HOXB7-MEK signaling cascade

status: Public on Sep 13 2017

city: Nankoku

first: Keisuke

last: Taniuchi

address: Kohasu

institute: Kochi Medical School

summary: Transcripts upregulated or downregulated by HOXB7-MEK signaling  were identified for use on the microarray using the Affymetrix GeneChip WT PLUS Reagent Kit in comparison with HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid and treated with MEK inhibitor, and HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid but not treated with MEK inhibitor.

overall_design: We endeavored to identify factors and pathways regulated by HOXB7-MEK signaling and to obtain leads regarding the mechanism underpinning the observed phenotypic changes by performing cDNA microarray analysis.


title: The DNA methylation profiles of CD14+ monocytes, dendritic cells and myeloid-derived suppressor cells

first: Esteban

last: Ballestar

address: Ctra de Can Ruti, Camí de les Escoles s/n

institute: Josep Carreras Research Institute (IJC)

summary: The methylation profiles of bisulfite-modified DNA of human CD14+ monocytes were compared with derived immature dendritic cells (GM-CSF/IL-4 ), myeloid-derived suppressor cells (GM-CSF/IL-4/PGE-2), EP2 antagonized myeloid-derived suppressor cells (GM-CSF/IL-4/PGE-2/ PF 04418948 5 µM), EP4 antagonized myeloid-derived suppressor cells (GM-CSF/IL-4/PGE-2/ L-161,982 5 µM) and EP2 + EP4 antagonized myeloid-derived suppressor cells (GM-CSF/IL-4/PGE-2/PF 04418948 5 µM /L-161,982 5 µM)  using the Infinium HumanMethylation450 BeadChips (Illumina, Inc., San Diego, CA,). This platform allows the interrogation of >485,000 methylation sites per sample at single-nucleotide resolution, and comprises an average of 17 CpG sites per gene in the 99% of RefSeq genes. 96% of CpG islands are covered, with additional coverage in CpG island shores and the regions flanking them. The samples were hybridized in the array following the manufacturer’s instructions.

overall_design: Total DNA isolated by standard procedures from CD14+ cells (total monocytes, MOs) corresponding to six sets of samples of monocytes (MOs), derived immature DCs, myeloid-derived suppressor cells, EP2 antagonized myeloid-derived suppressor cells, EP4 antagonized myeloid-derived suppressor cells and EP2 + EP4 antagonized myeloid-derived suppressor cells      (DCS and MDSCs).

first: Javier

last: Rodríguez-Ubreva

first: Francesc

last: Català-Moll

first: Nataša

last: Obermajer

first: Damiana

last: Álvarez-Errico

first: Ricardo

last: Ramirez

first: Carlos

last: Company

first: Roser

last: Vento-Tormo

first: Robert

last: Edwards

first: Ali

last: Mostazavi

first: Pawel

last: Kalinski


title: DNA methylation profiling for HEK-293T cells transfected with GFP and DMEΔ

first: Jin Hoe

last: Huh

summary: Methylome data obtained from human embryonic kindey (HEK)-293T cells expressing a GFP (293T-GFP) or a truncated form of Arabidopsis DEMETER (DME) 5-methylcytosine (5mC) DNA glycosylase (293T-DMEΔ) analyzed on a Human Methylation 450K BeadChip platform (Illumina). These methylation array data revealed genome-wide DNA methylation patterns of the 293T-GFP cells (without direct 5mC excision activity) and 293T-DMEΔ cells (with artificially implemented direct 5mC excision activity).

overall_design: Bisulfite converted DNA from the 2 samples were hybridised to the Illumina HumanMethylation 450k BeadChip

first: Young

last: Mok

first: Jin


title: ExpertMIX stratification of molecular profiles and clinical disease severity of RRMS patients

status: Public on Sep 10 2017

city: Cambridge

first: Jadwiga

last: Bienkowska

address: 45 Fayette Str Apt 3

institute: BiogenIdec

summary: Whole blood expression was profiled in Relapsing Remitting Multiple Sclerosis patients

overall_design: Identifying patients subgroups with similar molecualr and clinical profiles

first: Norm

last: Allaire

first: Jaya

last: Goyal


title: Transcriptome of the septic shock after treatment by activated protein C (Xigris)

city: Illkirch/Strasbourg

first: Wolfgang

last: Raffelsberger

address: 1 rue Laurent Fries

department: DBGS

country: France

institute: IGBMC

summary:
Septic shock by pneumopathy was studied in prospective way in 20 patients before and after respective treatment by activated protein C (Xigris). Initial blood samples were taken within 12 hours of diagnosis and the resulting transcritomes were compared to samples drawn after respective treatment.
keywords: patient cohort study, septic shock, transcription-profile, blood

overall_design: In total 20 patients were tested before and after specific treatment.

first: Pascal

last: Bilbault

first: Thomas

last: Lavaux

first: Estelle

last: Zink

first: Xavier

last: Delabranche

first: Feraht

last: Meziani

first: Marie

last: Gaub

first: Pierre

last: Oudet

first: Francis

last: Schneider


title: Gene expression of peripheral blood mononuclear cells from adults with sickle cell disease (UIC cohort)

city: Chicago

first: Zhengdeng

last: Lei

state: IL

address: 1853 W Polk St

department: Research Resources Center

institute: University of Illinois at Chicago

summary:
Sickle cell disease is associated with systemic complications, many associated with either severity of disease or increased risk of mortality. We sought to identify a circulating gene expression profile whose predictive capacity spanned the spectrum of these poor outcomes in sickle cell disease.
The Training cohort consisted of patients with SCD who were prospectively recruited from the University of Illinois. The Testing cohort consisted of a combination of patients prospectively seen at two separate institutions including the University of Chicago and Howard University

overall_design: The gene expression of PBMC from 172 sickle cell disease patients at UIC were analyzed

first: Ankit

last: Desai

first: Roberto

last: Machado


title: Expresion data from primary retinal pigment  epithelium (RPE) and immortalized RPE

status: Public on Sep 07 2017

city: Setagaya

first: Takuya

last: Kuroda

address: 1-18-1 Kamiyoga

department: Division of cell-based therapeutic products

institute: National Institute of Health and Sciences

summary:
We used microarrays to detail the global gene expression of primary RPE and immortalized RPE.
We investigated highly expression genes in immortalized RPE.

overall_design: We classified primary RPE (commercially available human fetal RPE, Lonza) and  immortalized RPE (ARPE-19, ARPE19/HPV-16 and h1RPE7)

first: T

first: S

last: Yasuda

first: Y

last: Sato


title: Gene expression of peripheral blood mononuclear cells from adults with sickle cell disease

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

overall_design: Refer to individual Series


title: Comparison of ox-BS-450k 5-hydroxymethylcytosine and BS-450k 5-methylcytosine profiles in the human placenta

status: Public on Sep 12 2017

city: L'Hospitalet de Llobregat, Barcelona

first: Jose Ramon

last: Hernandez

address: Av. Gran Via de l'Hospitalet 199-203

department: Cancer Epigenetics and Biology Program (PEBC)

institute: Institut d'Investigació Biomèdica de Bellvitge (IDIBELL)

summary: Bisulphite (BS) and oxidative bisulphite (oxBS) converted DNA from 4 normal human placentas were hybridized to the Illumina HumanMethylation450 Beadchip v1.2, obtaining the BS and oxBS DNA methylation profiles across approximately 450,000 CpGs. By using the oxBS treatment, the selective chemical oxidation of 5-hydroxymethylcytosine (5hmC) to 5-formylcytosine (5fC) and the deamination of the latter to uracil during the BS conversion allowed the quantification of independent 5-methylcytosine (5mC) and 5hmC methylation levels at every single CpG. In consequence, this data set characterizes the genome-wide distribution of 5hmC in the human placenta offerring a high-confidence list of intervals enriched for 5hmC in this tissue.

overall_design: Bisulphite and oxidative bisulphite converted DNA from 4 human placenta samples were hybridised to the Illumina HumanMethylation450 BeadChip v1.2

first: Jose

first: David

last: Monk


title: ESR1 mutations affect anti-proliferative responses to tamoxifen through enhanced cross-talk with IGF signaling

status: Public on Sep 04 2017

city: Houston

first: Suzanne

last: Fuqua

state: Texas

address: 1 Baylor Plaza

institute: Baylor College of Medicine

summary: The rediscovery of estrogen receptor (ESR1) mutations in metastatic breast cancer is current clinical scenario. We have modeled the three most frequent ESR1 mutations using stable lentiviral vectors in human breast cancer cell lines, and determined that they confer relative resistance to tamoxifen (Tam) in a cell-type specific manner due to distinct epigenetic changes. Resistance was only observed with concomitant engagement and activation of the insulin growth factor signaling pathway (IGF1R). The ESR1 mutants also exhibited enhanced binding with insulin growth factor receptor beta (IGF1Rβ). The selective estrogen degrader, fulvestrant, significantly reduced the anchorage-independent growth of ESR1 mutant-expressing cells, while the combination treatment with the mTOR inhibitor everolimus, restored Tam sensitivity. Since we detected relatively high frequencies of these three mutations in primary breast tumors, our results suggest that clinical targeted sequencing of both primary and metastatic tumors may be justified and comination therapies considered.

overall_design: 2 cell lines: MCF7C and ZR75; 2 genotypes: WT or Y537S mutation;  2 treatments: Control or Tamoxifen; 23 samples in total, 8 groups

middle: A

first: Luca

last: Gelsomino

first: Guowei

last: Gu

first: Yassine

last: Rechoum

first: Amanda

last: Beyer

first: Sasha

last: Pejerrey

first: Anna

last: Tsimelzon

first: Tao

last: Wang

first: Kenneth

last: Huffman

first: Andrew

last: Ludlow

first: Sebastiano

last: Andò


title: The BTK Inhibitor CC-292 shows activity in Mantle Cell Lymphoma and synergizes with Lenalidomide and NIK Inhibitors depending on NFκB mutational status

city: Barcelona

first: Patricia

last: Pérez-Galán

state: Barcelona

address: Centre Esther Koplowitz, Hemato-oncology dept, Rosello 149-153, 2nd floor

department: Hemato-oncology

institute: IDIBAPS

summary:
Mantle Cell lymphoma (MCL) were treated with the BTK inhibitor 1mM CC-292 for 48h
We used microarrays to uncover the mechanisms underlying CC-292 activity in Mantle Cell lymphoma (MCL)

overall_design: Global RNA expression was done in two MCL cell lines treated in vitro with CC-292 for 48h

last: Vidal-Crespo


title: Expression data in T-ALL cell lines after TOX knockdown

city: Charlestown

last: Langenau

state: Massachusetts

address: 149 13th Street, Room 6027

institute: Massachusetts General Hospital

summary: T-ALL is an aggressive malignancy of thymocyte. We identified a collaborative oncogenic driver, TOX (Thymocyte Selection Associated HMG box) that negatively modulates the non-homologous end joining by directly interacting to KU70/KU80.

overall_design: CCRF-CEM and HPB-ALL T-ALL cell lines were transduced with shRNA against TOX (2 different shRNA) or scramble shRNA. Also untransduced T-ALL cells were used as controls.

first: Riadh

last: Lobbardi


title: Gene expression profile of A549 cells cultured with normal 2D condition and xenografted tumor tissue

city: Shiraoka

first: Ayako

last: Otani

state: Saitama

address: 1470 Shiraoka

department: Medical Materials group

institute: Nissan Chemical Industries

summary:
Preclinical cancer drug discovery efforts have employed two-dimensional (2D)-cell-based assay models, which fail to forecast in vivo efficacy and contribute to a lower success rates of clinical approval.  Three-dimensional (3D) cell culture models are recently expected to bridge the gap between 2D and in vivo models. We compared between A549 cells cultured in ordinal 2D condition and xenografted tumor tissue.
Gene microarrays were used to observe the global gene expression in A549 cells cultured with petri dish (2D, control) or xenografted tumor tissue and identified distinct classes of up or down-regulated genes.

overall_design: A549 cells were cultured in with petri dish (2D).  5 × 10^6 cells in 100 μL PBS was injected subcutaneously into one or both scapulars of 7-8 week old male BALB/cAJcl-nu/nu mice. The tumors were harvested within 21 days.

last: Aihara


title: Transcriptomic analysis of Caco-2 cells following exposure to VTEC isolates derived from diverse origins

city: Dublin 4

first: Marion

middle: Teresa

last: Ryan

address: Belfield

department: Veterinary Sciences

institute: University College Dublin

summary:
This project has two goals. Firstly, to compare the gene expression profiles of Caco cells following exposure to Verocytotoxigenic E. coli0157:H7 (VTEC) isolates from food animals (bovine, ovine, porcine) and human in an effort to assess the invasive and toxigenic potential of isolates of different origin. All sources contain the common virulence and type 3 secretory system genes.
Secondly, to compare the gene expression profiles of Caco-2 cells following exposure to VTEC isolates that contain (positive) or do not contain (negative) the genes of the type 3 secretory system (TTSS).

overall_design: Eight groups (TTSS positive), four replicates (32 arrays in total):1. Control x 4, 2. Human x 4, 3. Ovine x 4, 4. Bovine x 4, 5. Porcine x 4, 6. International Reference x 4, 7. TTSS_NEG_Human x 4, 8.TTSS_NEG_Ovine x 4

first: T

last: Sweeney

first: C

last: Kennedy


title: T cell zone resident macrophages silently dispose of apoptotic cells in the lymph node

status: Public on Aug 21 2017

city: Illkirch

first: Doulaye

last: Dembele

department: Biopuces

summary: Dendritic cells (DC) are the most potent antigen-presenting cells of the immune system. In lymph nodes (LN), they are also believed to dispose of apoptotic cells, a critical function usually achieved by macrophages (Mφ) in other tissues. We report a population of tolerogenic Mφ located in the T cell zone of LN. T zone Mφ (TZM) are long lived Mφ seeded after birth and slowly replaced by blood monocytes. We show that TZM but not DC act as the only professional scavengers clearing apoptotic cells in the LN T cell zone. Importantly, we demonstrate that TZM prevent the capture of apoptotic cells by DC and the associated potential noxious activation of T cell immunity. We thus propose a new model in which efferocytosis and T cell activation are uncoupled processes handled by TZM and DC respectively.

overall_design: Microarray of  lymph node resident macrophages (TZM), lymph node CD8a+ DC and microglia sorted from CX3CR1 gfp+/- mice. 3 replicates for each population.

first: Myriam

last: Baratin

first: Marc

last: Bajénoff


title: Expression profile of Rhabdomyosarcoma (RMS) cells after Vismodegib treatment

first: Ana

last: Almazán

address: Passeig Vall d'Hebron 119-129

institute: VHIR

summary: A cDNA microarray was performed to identify pathways differentially regulated between untreated and Vismodegib-treated cells.

overall_design: Three RMS cell lines were analyzed: RD, RH4 and RH30. Cells were treated for 48 hours with 50µM Vismodegib and total RNA was extracted. Control plates were treated with equal volumes of vehicle (DMSO). A total of six samples were analyzed in this study.


title: Identify genes modulated by a 5 uM 30-minute pulse dose of gemcitabine

first: Matthew

last: Brauer

summary: Identified genes that were up- or down-regulated in HT-29 cells in response to gemcitabine

overall_design: HT-29 cells were treated with a 30-minute pulse dose of 5 uM gemcitabine. Cells were harvested 24 hours later

first: Kristin

last: Zimmerman

first: Thomas

last: O'Brien


title: Extracellular vesicle role in Chronic Lymphocytic Leukemia B-cells defined by microarray analysis

status: Public on Aug 20 2017

city: anderlecht

first: Emerence

last: Crompot

state: Bruxelles

address: 808 route de lennik

country: Belgium

institute: Jules Bordet Institute - ULB

summary: Interactions between Chronic Lymphocytic Leukemia B-cells (CLL B-cells) and the microenvironment (ME) play a major function in the physiopathology of CLL. Extracellular vesicles (EVs) (composed of exosomes and microparticles) have been shown to play an important role in cell communication. EVs, purified by ultracentrifugation from bone marrow mesenchymal stromal cells (BM-MSC) culture, were added to CLL B-cells.  Microarray study highlighted 805 differentially expressed genes between CLL-B-cells cultured with and without EVs. Of these, CCL3/4, EGR1/2/3, MYC (involved in BCR pathway) were increased while pro-apoptotic genes like HRK were decreased. We showed for the first time the potential of EVs alone to induce gene expression modifications in CLL B-cell, notably in BCR and apoptosis pathways. We concluded that a substantial part of communication between CLL B-cells and BM-ME is mediated through EV.

overall_design: CLL B-cells obtained from 3 patients were treated in vitro with extracellular vesicles from bone marrow mesenchymal stromal cells (or nothing as a negative control) for 24 hours. Their effects on gene expression were thereafter studied using Affymetrix technology

first: Michael

last: Van Damme

first: Karlien

last: Pieters

first: Laurence

last: Lagneaux

first: Basile

last: Stamatopoulos


title: Identify genes modulated by gemcitabine and/or GNE-783

address: 1 DNA Way

institute: Genentech, Inc.

summary: Identified genes that were up- or down-regulated in HT-29 cells in response to the indicated treatments.

overall_design: HT-29 cells were treated with a 30-minute pulse dose of 1 uM gemcitabine followed by 1 uM GNE-783. All cells were harvested 24 hours later


title: Transcriptome of the septic shock

first: Wolfgang

last: Raffelsberger

type:
Expression profiling by array
Third-party reanalysis

summary:
Septic shock by pneumopathy was studied in prospective way in 20 patients and compared to normal blood. Blood samples were taken within 12 hours of diagnosis and the resulting transcritomes were compared to 42 normal control samples (selected samples from series GSE10715, GSE12711, GSE16728 and GSE7400).
keywords: patient cohort study, septic shock, transcription-profile, blood

overall_design: In total 20 patients were tested before specific treatment and compared to 42 control samples.

first: Pascal

last: Bilbault

last: Lavaux

first: Estelle

last: Zink

first: Xavier

last: Delabranche

first: Feraht

last: Meziani

first: Marie

last: Gaub

first: Pierre

last: Oudet

first: Francis

last: Schneider


title: CHK1 inhibition following gemcitabine treatment

last: Brauer


title: Transcript profiling of mouse 4T1 tumors grown in preirradiated vs. nonirradiated mammary tissue

status: Public on Aug 31 2017

city: Basel

first: Tim

last: Roloff

address: Maulbeerstrasse 66

department: Functional Genomics

country: Switzerland

institute: FMI

summary: The present study was designed to identify genes induced by irradiation in the 4T1 breast cancer model mimicking aggressive local relapse after radiotherapy. For this purpose, we obtained the transcriptomes of 4T1 tumors grown in either preirradiated (IRR+4T1) or non-irradiated (4T1) mammary tissue.

overall_design: Primary tumors were initiated by orthotopic injection of 4T1 (ATCC; CRL-2539) mammary carcinoma cells into BALB/c mice (Charles River Laboratories) as described (1). To investigate the effect of mammary tissue irradiation on gene expression, the fourth mammary gland was either pretreated with a single dose of 20 Gy X-ray irradiation or left untreated before implanting 4T1 tumor cells (1, 2). Tumor tissue samples were collected, flash-frozen and homogenized in RLT buffer using a Dispomix Drive (Medic Tools). Total RNA was isolated using the RNeasy Mini Kit (Qiagen), converted into labeled cDNA and hybridized to Affymetrix GeneChip Mouse Gene 1.0 ST arrays. RMA-normalized expression values were calculated with the affy package from Bioconductor 2.4 (3), and differentially expressed genes were identified using moderated t-statistics calculated with the empirical Bayes method as implemented in the Bioconductor limma package (4). To be considered as differentially expressed between tumors grown in preirradiated (IRR+4T1) and nonirradiated (4T1) mammary tissue, genes had to pass the filters: P-value ≤ 0.05, a log2 fold change ≥ 0.4 and a log2 average expression value ≥ 4.0.  References:  1. Kuonen F, Laurent J, Secondini C, Lorusso G, Stehle JC, Rausch T, et al. Inhibition of the Kit ligand/c-Kit axis attenuates metastasis in a mouse model mimicking local breast cancer relapse after radiotherapy. Clin Cancer Res 2012;18:4365-74.  2. Monnier Y, Farmer P, Bieler G, Imaizumi N, Sengstag T, Alghisi GC, et al. CYR61 and αVβ5 integrin cooperate to promote invasion and metastasis of tumors growing in preirradiated stroma. Cancer Res 2008;68:7323-31.  3. Gentleman R, Carey V, Bates D, Bolstad B, Dettling M, Dudoit S, et al. Bioconductor: open software development for computational biology and bioinformatics. Genome Biol 2004;5:R80.  4. Smyth GK, Speed T. Normalization of cDNA microarray data. Methods 2003;31:265-73.

first: Maria

last: Asparuhova

first: Stephane

last: Thiry

first: Ruth

last: Chiquet-Ehrismann


title: A new 3D culture system to identify disease-relevant genes in colorectal cancer [Microarray expression]

status: Public on Aug 30 2017

city: Nashville

first: Shilin

last: Zhao

address: 2200 Pierce Ave, PRB building 571

department: Center for Quantitative Sciences

institute: Vanderbilt University

summary: It is increasingly appreciated that properties of cultured epithelial cells differ dramatically in 2D compared to 3D, and the latter more faithfully recapitulates in vivo behavior. By studying a battery of human colorectal cancer (CRC) cell lines in type-1 collagen, we have found that HCA-7 cells form colonies with two distinctive and persistent morphological and functional properties. We observed predominantly single-layered polarized cysts (cystic colonies, CC) and a smaller fraction displaying disorganized solid masses (spiky colonies, SC) that were highly invasive in vivo. Despite overall genomic similarity, CC and SC exhibited distinct and dynamic patterns of gene expression in 3D.

overall_design: In type-1 collagen culture, a human colorectal cancer cell line, HCA-7, forms colonies with two distinct morphologies, cystic colonies (CC) and spiky colonies (SC). CC and SC were isolated and grown in 3D collagen in 12-well dishes using 50,000 cells/ml. On day 5, 10, or 15, total RNA was extracted from the middle and microarray analysis was performed in Affymatrix 133 Plus 2.0 array. So there were total of six samples performed (SC1 Day 5, 10, 15 and CC3 day 5, 10, 15)

first: Cunxi

last: Li

first: Bhuminder

last: Singh

first: Ramona

last: Deal

first: Haiting

last: Ma

first: Alina

last: Starchenko

first: Will

last: Fry

first: Yang

last: Wang

first: Ginger

last: Milne

first: Gregory

middle: D

last: Ayers

first: Mary

middle: K

last: Washington

last: Yeatman

first: Oliver

last: Mcdonald

first: Qi

last: Liu

first: Robert

last: Coffey


title: Expression data from human primary cumulus cells culture (hCC)

status: Public on Aug 29 2017

city: Montpellier

first: Said

last: Assou

address: 80, av. Augustin Fliche

department: Institute for Regenerative Medecine and Biotherapy

institute: University Hospital of Montpellier, Inserm

summary:
The cumulus cells niche that surrounds the oocyte is essential for its maturation and presumably for the oocyte to acquire its competence to confer pluripotency. The cells cultured from the human oocyte cumulus niche (hCC) could be used as feeders for the propagation of human pluripotent stem cells in vitro.
We used microarrays to establish the molecular portrait of the hCC at different passages

overall_design: Cumulus cells were dissociated mechanically from the oocyte and cultured for a long period. Affymetrix Human Genome U133 Plus 2.0 DNA chips were performed to analyze the transcriptome of hCC at different passages (P3, P6 and P9).  The Affymetrix 3’ IVT express protocol was used to prepare cRNA (one-cycle amplification). The gene expression data were extracted using Affymetrix Expression Console software.

first: Ounissa

last: Aït-ahmed

first: Samir

last: Hamamah


title: Trajectories of DNA hydroxymethylation across human brain development

status: Public on Aug 25 2017

city: Oxford

first: Helen

last: Spiers

address: Keble Road

country: United Kingdom

institute: University of Oxford

summary: Epigenetic processes play a key role in orchestrating transcriptional regulation during the development of the human central nervous system. We previously described dynamic changes in DNA methylation occurring during human fetal brain development, but other epigenetic processes operating during this period have not been extensively explored. Of particular interest is DNA hydroxymethylation (5hmC), a modification that is enriched in the human brain and hypothesized to play an important role in neuronal function, learning and memory. In this study, we quantify DNA hydroxymethylation across the genome of 71 human fetal brain samples spanning 23 to 184 days post-conception.

overall_design:
DNA modifications (DNA methylation (5mC) and DNA hydroxymethylation (5hmC)) were assessed in 71 human fetal brain samples (36 male; 36 female), spanning 23 to 184 days post-conception (DPC). Two pre-treatments, BS and oxBS conversion, and two Illumina 450K arrays were run for each sample. DNA modification and DNA methylation beta values were generated, and a DNA hydroxymethylation value calculated from these measures.

Please note that the 'hydroxy_GEO_matrix.csv' contains the hydroxy data produced by subtracting the oxBS data from the BS data and, thus the data column headers in the 'hydroxy_GEO_matrix.csv' correspond to the BS-pretreatement sample titles [GSM2467039-GSM2467109]

first: Eilis

last: Hannon

first: Leonard

middle: C

last: Schalkwyk

first: Nicholas

last: Bray

first: Jonathan

last: Mill


title: Expression data from SET knockdown R1 embryonic stem cells

status: Public on Aug 26 2017

city: Jerusalem

first: Raghu

last: Edupuganti

address: 2-543, Silberman Building

department: Dept. of Genetics

institute: The Hebrew University

summary: We used microarrays to identify the gene expression changes after SET knockdown in ESCs and 4 day RA differentiated ESCs

overall_design: Actively growing ESCs and 4d RA differentiated ESCs were harvested and RNA was extracted immediately.

first: Eran

last: Meshorer


status: Public on Aug 15 2017

city: Giessen

first: Marek

last: Bartkuhn

state: Hessen

address: Aulweg 132

department: Biomedical Informatics and Systems Medicine

institute: Justus-Liebig-University Giessen

summary:
Genome-wide DNA-methylation profiles of human lung cancer cell lines and normal lung cells were generated by Infinium bead chip technology
DNA methylation patterns of over 480,000 CpG sites were analyzed in normal human bronchial epithelial cells (NHBEC) and three non small cell lung cancer cell lines (NSCLC: A427, A549 and H322) using bisulfite-based Illumina 450K BeadChip arrays

overall_design: Three lung cancer cell lines (A549, A427 and H322), normal bronchial ephitelial cells (NHBEC)

first: Tobias

last: Zimmermann

first: Reinhard

last: Dammann


title: Skeletal muscle biopsies of patients with myotonic dystrophy (DM) and non-DM neuro-muscular disorders

first: Mario

last: Sirito

state: TX

address: 1515 Holcombe blvd

department: Cancer Genetics

institute: M. D. Anderson Cancer Center

summary:
Skeletal muscle biopsies from DM1, DM2, idiopathic DM (DMx), and non-DM NMD patients were compared to those from normal individuals, with focus on MEF2 and MEF2-related genes.

Keywords: 7 diseases and 2 normal (fetal and adult) groups

overall_design: Skeletal muscle biopsies from 10 DM1 biopsies, 20 DM2 biopsies, 16 DMx (DM-like, no DMPK or ZNF9 expansion), 5 BMD (Becker Muscular Dystrophy), 1 MC-AD (Myotonia Congenita-Autosomal Dominant), 3 DMD (Duchenne Muscular Dystrophy), 4 TMD (Tibial Muscular Dystrophy), 3 Normal Fetal and 6 Normal individuals

first: Ralf

last: Krahe


title: Smoking-induced Up-regulation of AKR1B10 Expression in the Airway Epithelium of Healthy Individuals

city: New York

first: Yael

last: Strulovici-Barel

state: NY

address: 1300 York Avenue

department: Department of Genetic Medicine

institute: Weill Cornell Medical College

summary: The aldokatoreductases (AKRs) represent a gene superfamily that code for monomeric, soluble NAD(P)H-dependent oxidoreductases that mediate elimination reactions. AKR1B10, an AKR that functions to eliminate retinals, has been observed to be upregulated in squamous metaplasma and non small cell lung cancer, and has been suggested as a diagnostic marker specific to tobacco-related carcinogenesis. In the context of the link of smoking and lung cancer and the enhanced expression of AKR1B10 expression in lung cancer, we hypothesize that enhanced expression of AKR1B10 may be initiated in healthy smokers, prior to the development of any evidence of lung cancer. For this purpose, expression of AKR1B10 was assessed at the mRNA level using microarrays in the large airway epithelium (21 healthy nonsmokers, 31 health smokers) and small airway epithelium (51 healthy nonsmokers, 58 healthy smokers) obtained by fiberoptic bronchoscopy and brushing, as well as assessment in a subset of this population by TaqMan PCR and in endobronchial biopsies by Western analysis and immunohistochemistry. Compared to healthy nonsmokers, ARK1B10 mRNA levels were markedly upregulated in both the large and small airway epithelium of healthy smokers (large airway microarray p<0.0001, small airway p<0.0001; TaqMan large airway, p<0.02, small airway p<0.01). Consistent with the mRNA data, AKR1B10 protein was significantly upregulated in the airway epithelium of healthy smokers as assessed by Western analysis and by immunohistochemistry, with AKR1B10 expressed in both differentiated and basal cells of the normal epithelium. Finally, cigarette smoke extract mediated up-regulation of AKR1B10 in airway epithelial cells in vitro. Thus, smoking per se mediates up-regulation of AKR1B10 expression in the airway epithelium of healthy smokers with no evidence of lung cancer. In the context of these observations, and the link of AKR1B10 to the metabolism of retinals and to lung cancer, the smoking-induced up-regulation of AKR1B10 may be an early process in the multiple events leading to the develop of lung cancer.

overall_design: Affymetrix arrays were used to assess the expression of AKR1B10 gene expression data in large airway and small airway epithelium obtained by fiberoptic bronchoscopy of 21 healthy non-smokers and 31 healthy smokers (large airways) and 51 healthy non-smokers and 58 healthy smokers (small airways).

first: Rui

last: Wang

first: Guoqing

first: Barbara

last: Ferris

first: Jacqueline

last: Salit

first: Neil

last: Hackett

first: Ronald

last: Crystal


title: Guanabenz effect on activated GM-CSF DCs

city: Marseille

first: Philippe

last: Pierre

address: Campus Luminy - case 906

institute: CIML - CNRS - INSERM

summary:
Guanabenz is an FDA approved drug for hypertension. It has been shown also to be an inhibitor of GADD34, the stress-inducible cofactor of PP1. GADD34 has been shown to play a key role in controlling cytokine production in MEFs and dendritic cells.
A microarray-based mRNA transcription analysis was used to compare the transcriptional response of GM-CSF DCs, activated with poly I:C or Proteus mirabilis, in presence or absence of 50µM Guanabenz.

overall_design: GM-CSF DCs were left untreated or were activated for 8h and 16h with poly I:C (lipofected or soluble) or Proteus mirabilis (with the bacteriostatic Chloramphenicol) . Their RNA content was extracted with a commercial kit for RNA extraction. Three independent experiments were performed.

first: Clarisse

last: Bourbon-Caillet

first: Jessica

last: Perego


title: Gene expression signature of Anagrelide in megakaryocytes

status: Public on Aug 16 2017

city: Cardiff

first: Lee

middle: Ryan

last: Butcher

address: Llandaff, Campus, Western Avenue, Llandaff

institute: Cardiff Metropolitan University

summary:
Anagrelide is a cytoreductive agent used to lower platelet counts in essential thrombocythemia. Although the drug is known to selectively inhibit megakaryopoiesis, the molecular mechanism accounting for this activity has not been elucidated.
In order to gain an insight into the mechanism of action of this drug we used microarrays to obtain a global gene expression signature of anagrelide

overall_design: CD34+ human hematopoietic cells from three different donors (biological replicates 1, 2 & 3) were treated ex vivo for four days with anagrelide  (TPO-ANA) or  with an equivalent amount of vehicle (TPO-DMSO) while growing under megakaryocyte differentiation conditions. Total RNA was then extracted with RNeasy reagent and subjected to gene expression profiling on Affimetrix Human Genome U133 Plus 2.0 oligonucleotide chips.

first: Maninder

last: Ahluwalia

first: Jorge

last: Erusalimsky


title: Cancer-specific retargeting of BAF complexes by a prion-like domain [ATAC-Seq]

status: Public on Aug 24 2017

city: Boston

first: Sowmya

last: Iyer

department: Pathology

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Alterations in the function of transcriptional regulators can orchestrate oncogenic programs that are critical for the transformation and survival of cancer cells. Here we show that the BAF chromatin remodeling complex, which is mutated in over 20% of human tumors, interacts with EWSR1, a member of the FET family of proteins containing prion-like domains that are frequent partners in oncogenic fusions with transcription factors. In Ewing sarcoma, characterized by the EWS-FLI1 fusion, we find that the BAF complex is recruited by EWS-FLI1 to tumor specific enhancers at GGAA microsatellite repeats and contributes to the activation of target genes. This process depends on tyrosine residues that are necessary for the aggregation properties of the EWSR1 prion-like domain and is a neomorphic feature of EWS-FLI1 compared to the wild type ETS transcription factor FLI1. Furthermore, fusion of short fragments of the EWSR1 prion-like domain to FLI1 is sufficient to recapitulate EWS-FLI1-mediated gene expression. Our studies demonstrate that the aggregation properties of prion-like domains can retarget chromatin regulatory complexes to establish and maintain oncogenic gene expression and proliferation.

overall_design:
ATAC-seq for mesenchymal stem cells (MSC). EWS-FLI1, wild-type FLI1 and the mutant proteins EWS(YS37)-FLI1, SYGQ2-FLI1 and BAF47-FLI1 were expressed in MSCs with lentiviral expression vectors.

Raw data not provided for primary cells due to patient privacy concerns. Submitter states that the raw data for these samples will be submitted to dbGaP.

first: Gaylor

last: Boulay

first: Miguel

last: Rivera


title: Embryonic signature distinguishes pediatric and adult rhabdoid tumors from other SMARCB1-deficient cancers

status: Public on Aug 13 2017

city: Paris

first: Wilfrid

last: Richer

address: 26 rue d'Ulm

institute: Institut Curie

summary: We used microarrays to compare gene expression profilings in various SMARCB1-deficient tumors.

overall_design: [human mRNA] 16 RT, 16 SD-NRT (8 Epithelioid Sarcomas, 3 Undifferentiated Chordomas and 5 Renal Medullary Carcinomas), 37 SMARCB1 deficient tumors.

first: Franck

last: Bourdeaut

first: Julien

last: Masliah Planchon


title: Pilot open label clinical trial of oral ruxolitinib in patients with alopecia areata

status: Public on Aug 23 2017

city: Iowa City

first: Ali

last: Jabbari

state: IA

address: 200 Hawkins Dr, 40025 PFP

institute: University of Iowa

summary:
This goal of these studies were to examine gene expression profiles of skin from patients with alopecia areata undergoing treatment with oral ruxoltinib.
Microarray analysis was performed to assess changes in gene expression in affected scalp skin.

overall_design: Twelve patients were recruited for this study.  Scalp skin biopsies were performed at baseline and at twelve weeks following the initiation of 20 mg BID ruxolitinib PO.  In addition, biopsies were taken prior to twelve weeks of treatment in some cases.  Biopsies from three healthy controls were also included in the dataset.

first: Jane

middle: E

last: Cerise

first: Angela

middle: M

last: Christiano


title: Expression data from Daxx knockout MEFs

status: Public on Aug 22 2017

city: philadelphia

first: Xianxin

last: Hua

state: PA

address: 421 Curie BLVD

department: Department of Cancer Biology

institute: University of Pennsylvania Perelman School of Medicine

summary:
Neuroendocrine tumors (NETs) often harbor loss-of-function mutations in Daxx gene. Daxx interacts with several partners to regulate cellular processes and gene expression.
We used microarrays to detail the global gene expression change in Daxx knockout MEFs and identified up-regulated genes during this process.

overall_design: Daxx knockout mouse embryonic fibroblasts complemented with vector or Daxx were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain downstream target genes regulated by Daxx.

first: Zijie

last: Feng


title: Neuromedin U promotes a malignant phenotype in luminal breast cancer involving Naked 2 (NKD2) modulated WNT signalling

city: Aachen

first: Bernd

last: Denecke

state: NRW

address: Pauwelsstrasse 30

department: IZKF Aachen

institute: RWTH Aachen University

summary:
Neuromedin U (NMU), which is thought to contribute to putative metastasis processes in various tumor entities, was identified as being up-regulated in breast cancer. Therefore, we aimed to uncover the role of NMU in breast cancer subtypes deciphering for the first time NMU-driven signalling pathways and downstream targets.
Stable gain-of-function in vitro models were generated  to decipher the biological role of NMU in breast cancer cells. To uncover underlying signalling pathways and key molecules affected by NMU in the luminal-like SKBR3 model, microarray analysis was carried out.

overall_design: Gene expression analysis of stably transfected SKBR3 NMU and mock clones was carried out using the GeneChip® Human Gene 2.0 ST Array (Affymetrix, Santa Clara, CA, USA) in independent triplicates. Total RNA was isolated using the Trizol method and quantified (Nanodrop). RNA quality was assessed using RNA 6000 Nano Assay with the 2100 Bioanalyzer (Agilent, Santa Clara, CA, USA). Samples, each 300 ng total RNA, for the GeneChip® Human Gene 2.0 ST Arrays were prepared and hybridized to the arrays according to the Ambion whole-transcript expression and the Affymetrix whole-transcript terminal labeling and control kit manuals. Processed samples were hybridized to the GeneChip® Human Gene 2.0 ST Arrays at 45 °C for 16 h with 60 rpms, washed and stained on a Fluidics Station 450 (program: FS450 0002) and scanned on a GeneChip® Scanner 3000 7G (both Affymetrix). Raw image data were analyzed with Affymetrix® Expression Console™ Software (Affymetrix, USA), and gene expression intensities were normalised and summarized with robust multiarray average algorithm

first: Stefan

last: Garczyk

first: Natalie

last: Klotz

first: Sabrina

last: Szczepanski

first: Wiebke

last: Antonopoulos

first: Saskia

last: von Stillfried

first: Ruth

last: Knüchel

first: Michael

last: Rose

first: Edgar

last: Dahl


title: Initiation of aberrant DNA methylation patterns and heterogeneity in precancerous lesions of human HCC

city: Rochester

first: Keith

last: Robertson

state: Minnesota

address: 200 1st St SW

department: Molecular Pharmacology & Experimental Therapeutics

institute: Mayo Clinic

summary: Infinium 450k data from three HCV-infection patients. Ten cirrhotic nodules were isolated from each patient for genome-wide DNA methylation analysis. One case had an incedental tumor that was also processed.

overall_design: 31 total samples processed from DNA isolated from FFPE liver tissue

first: Ryan

last: Hlady


title: The transcription factor Tcf1 ensures the development and cytotoxic function of NK cells by limiting the expression of Granzymes [Affymetrix]

city: Lausanne

first: Paolo

last: Angelino

address: Quartier Sorge, Bâtiment Génopode

department: BCF

institute: SIB Swiss Institute of Bioinformatics

summary: The transcription factor Tcf1 plays an essential role for the development of NK cells, however, its precise role for NK cell development, maturation and function is poorly understood. Here we show that distinct domains of Tcf1 direct bone marrow progenitors towards the NK cell lineage and mediate lineage commitment and NK cell expansion, and that Tcf1 downregulation is required for terminal NK cell maturation. Impaired NK cell development in the absence of Tcf1 is explained by increased cell death due to excessive expression of Granzyme family proteins, which results in NK cell self-destruction. In addition, excessive Granzyme B expression leads to target cell induced NK cell death and consequently reduced target cell killing by NK cells lacking Tcf1. Mechanistically, Tcf1 prevents excessive Granzyme B expression by binding to a newly identified enhancer element upstream of the Granzyme B locus. These data identify an unexpected requirement to limit the expression of cytotoxic effector molecules for lymphocyte development.

overall_design: Total RNA was isolated from flow-sorted bone marrow mNK cells (CD3- CD19- CD122+ NK1.1+ DX5+) from Tcf7+/+ (WT) and Tcf7-/- (KO) mice, and cDNA was synthesized, amplified and triplicate samples were hybridized to Affymetrix GeneChip Mouse Gene 1.0 ST array.

first: Jasmine

last: Gehrig

first: Werner

last: Held


title: Expression data from rheumatoid arthritis synovial macrophages

status: Public on Aug 10 2017

first: Lionel

middle: B.

last: Ivashkiv

address: 535 East 70th Street

institute: Hospital for Special Surgery

summary: Macrophages from RA synovial fluids were compared to primary human monocyte-derived macrophages.

overall_design: Freshly isolated RA synovial macrophages and control macrophages cultured with M-CSF for 3 days were obtained at Hospital for Special Surgery using a protocol approved by the HSS Institutional Review Board. De-identified discard specimens were obtained under a partial waiver of consent. Microarray analysis was performed at Boehringer Ingelheim Pharmaceuticals Inc. using the Affymetrix platform according to the manufacturer’s instructions.

first: Karen

last: Berg

first: Adedayo

last: Hanidu

first: Jun

last: Li

first: Gerald

last: Nabozny


title: Small molecules increase direct neural conversion of human fibroblasts

city: Lund

first: Shamit

last: Soneji

address: Solvegatan 19

country: Sweden

institute: BMC

summary: Time course micro array experiment  to identify transcriptional changes in response to exposure of hFLs to different combinations of small molecules during direct neuronal reprogramming

overall_design: hFL1 cells were transduced with conversion factors Ascl1, Brn2a and Myt1L and five days after transduction, transgene expression was activated by doxycycline. On day 3 of transgene expression, MEF medium was replaced by N2B27 medium plus small molecules, depending on the condition. Ascl1 expression was linked to GFP so that all GFP pos cells were FACS isolated at different times of exposure to small molecules (or N2B27 medium in transgene only groups). Post FACS, cells were lysed and total RNA was extracted and used as input for micro array experiments.

first: Malin

last: Parmar

first: Ulrich

last: Pfisterer

first: Stefan

last: Lang


title: Mining the Human Urine Proteome for Monitoring Renal Transplant Injury

city: San Francisco

first: Minnie

last: Sarwal

state: CA

address: 500 Parnassus Ave

institute: UCSF

summary:
Gene expression data was analyzed to map with urine proteomics data
gene expression data from kidney biopsies from kidney transplant  patients with and without acute rejection, chronic allograft nephropathy and BK virus nephritis was used to study gene expression changes during acute rejection, chronic allograft nephropathy and bk virus nephropathy. Samples labeled STA16, STA22, STA14, and STA18 were included in the CAN vs no-CAN analysis as no-CAN samples as they also qualified as non-CAN samples.

overall_design: The study was to identify transplant injury markers using proteomics. We used gene expression data to evaluate intersection of transcriptome and proteome.

first: Tara

last: Sigdel

first: Anyou

last: Wang


title: Gene expression-based, individualized outcome prediction for RUNX1T1 Knock-down treated ECFCs

status: Public on Aug 17 2017

city: Taipei

first: Ko-Hsun

last: Liao

state: Taipei

address: No. 155, Sec. 2, Linong St., Beitou District,

department: Institute of Microbiology and Immunology

country: Taiwan

institute: National Yang-Ming University

summary: Individualized outcome prediction classifiers were successfully constructed through expression profiling of RUNX1T1 mediated.

overall_design: In the study presented here, the ECFCs from cord blood treated RUNX1T1 knock-down or shRNA and analyzed by microarray.

first: Oscar

last: Lee


title: Pharmacologic inhibition of the menin-MLL interaction blocks progression of MLL leukemia in vivo

city: Gaithersburg

first: Jingya

state: Maryland

address: 1 Medimmune Way

country: USA

summary: Chromosomal translocations affecting Mixed Lineage Leukemia (MLL) gene result in acute leukemias resistant to therapy. The leukemogenic activity of MLL fusion proteins is dependent on their interaction with menin, providing basis for therapeutic intervention. Here we report development of novel, highly potent and orally bioavailable small molecule inhibitors of the menin-MLL interaction, MI-463 and MI-503, show their profound effects in MLL leukemia cells and substantial survival benefit in mice models of MLL leukemia. Finally, we demonstrate efficacy of these compounds in primary samples derived from MLL leukemia patients. Overall, we demonstrate for the first time that pharmacologic inhibition of the menin-MLL interaction represents an effective treatment for MLL leukemias in vivo and provide advanced molecular scaffold for clinical lead identification.

overall_design: MV4;11 human MLL leukemia cells were treated with the menin-MLL inhibitor MI-389

first: Jolanta

last: Grembecka

first: Tomasz

last: Cierpicki

first: Trupta

last: Purohit


title: Molecular subtypes of metastatic colorectal cancer are predictive of patient response to chemo and targeted therapies (part 2)

city: Montpellier Cedex 5

first: Pierre

last: Martineau

address: 208 Rue des Apothicaires

department: IRCM

institute: Inserm

summary: We report that previously described molecular subtypes of colorectal cancer are associated with the response to therapy in patients with metastatic disease. We also identified a patient population with high FOLFIRI sensitivity, as indicated by their 2.7-fold longer overall survival when treated with FOLFIRI, as first-line regimen, instead of FOLFOX. Our results demonstrate the interest of molecular classifications to develop tailored therapies for patients with metastatic colorectal cancer.

overall_design: The COSIVAL cohort was a retrospective multicenter study involving 6 French hospitals (CHU Trousseau - Tours, Hôpital Purpan - Toulouse, Hôpital Central - Nancy, Hôpital Dupuytren - Limoges, Hôpital Ambroise Paré – Boulogne Billancourt, Hopital de Lille ) and 2 comprehensive Cancer Centers (ICM, Montpellier; Institut Bergonié, Bordeaux)  and contained 68 patients

first: Maguy

last: Del Rio

first: Caroline

last: Mollevi


title: Molecular subtypes of metastatic colorectal cancer are predictive of patient response to chemo and targeted therapies

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

overall_design: Refer to individual Series


title: Mesenchymal stromal cells in platelet lysate versus fetal calf serum

status: Public on Aug 11 2017

first: Wolfgang

last: Wagner

address: Pauwelsstrasse 20

department: Helmholtz Institute for Biomedical Engineering


title: Molecular subtypes of metastatic colorectal cancer are predictive of patient response to chemo and targeted therapies (part 1)


title: Clear cell renal cell carcinoma (ccRCC) samples

status: Public on Aug 08 2017

city: Singapore

first: Min Han

last: Tan

state: Sinagpore

address: 31 Biopolis Way,

country: Singapore

institute: Institute of Bioengineering and Nanotechnology

summary:
To select signatures of ccRCC, 265 ccRCC samples were obtained from the Van Andel Research Institute.
Gene expression profiles of  265 samples were determined using the HG-U133_Plus_2 platform.

overall_design: For this study, Total RNA from 265 ccRCC tumor samples were hybridised to the Affymetrix HG-U133_Plus_2  microarrays.

first: Xiaona

last: Wei

first: Min

middle: H


title: Evaluation of Niacinamide effects on murine primary macrophage transcriptional regulation and cell cycle progression.

status: Public on Aug 21 2017

first: Julien

last: Maurizio

address: Centre d’Immunologie de Marseille-Luminy

institute: INSERM

summary: Murine MafB/c-MAF double KO (Maf-DKO) primary macrophages are known for their unlimited non-tumorigenic self-renewal ability (Aziz et al., 2009). In an in vitro screen for cytokines and small molecules we identified Niacinamide (NAM) a potent inhibitor of their proliferative potential characterized by a reversible cell cycle arrest.

overall_design: The aim of the project is to identify the transcriptional network established in Maf-DKO macrophages upon Niacinamide (NAM) treatment., during an early (1 hour) and a late (10 hours) response phases.

first: M

last: Sieweke

first: J

first: F

last: Imperatore


title: Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs with in vivo activity in hematological malignancies [array]

city: Pamplona

first: Xabier

last: Agirre

state: Navarra

address: Pio XII, 55

department: Oncology

country: Spain

institute: CIMA

summary: The indisputable role of epigenetics in cancer and the fact that epigenetic alterations can be reversed have favored development of epigenetic drugs. In this study, we have design and synthesize potent novel, selective and reversible chemical probes that simultaneously inhibit the G9a and DNMTs methyltransferase activity. In vitro treatment of hematological neoplasia (Acute Myeloid Leukemia-AML, Acute Lymphoblastic Leukemia-ALL and Diffuse Large B-cell Lymphoma-DLBCL) with the lead compound CM-272, inhibited cell proliferation and promoted apoptosis, inducing interferon stimulated genes and immunogenic cell death. CM-272 significantly prolonged survival of AML, ALL and DLBCL xenogeneic models. Our results represent the discovery of first-in-class dual inhibitors of G9a/DNMTs and establish this chemical series, as a promising therapeutic tool for unmet needs in hematological tumors.

overall_design: Transcriptome analysis of AML cell lines before and after treatment with a dual inhibitor against G9a and DNMTs.

first: Edurne

last: San José-Eneriz

first: Victor

last: Segura

first: Felipe

last: Prósper


title: Impact of short-term high fat diet regimen on hepatic transcriptome

status: Public on Aug 01 2017

first: Maria

middle: M.

last: Mota

address: Av. Prof Egas Moniz

country: Portugal

institute: IMM Lisboa

summary:
We used microarrays to unveil the gene expression alterations upon short-term HFD administration
We found that short-term HFD administration impacts hepatic lipid biosynthesis and redox status

overall_design: Pairwise comparison between  RD and HFD. 3 biological replicates of each condition were used.

first: Vanessa

last: Zuzarte-Luís

first: Céline

last: Carret


title: Epigenetic mechanisms regulate FOXP1 expression in CD4+ T cells

city: Gosselies

first: Martin

last: Bizet

address: Rue Adrienne Bolland, 8

institute: Université Libre de Bruxelles

summary:
Genome-scaled profiling of naive and memory CD4+ T cells in activated and resting state.
Differential methylation can be observed between resting naïve and memory cells at cg related to FOXP1 gene.

overall_design: Bisulphite converted DNA from the 12 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

first: Soizic

last: Garaud

first: Florence

last: Roufosse

first: Pushpamal

last: De Silva

first: Jean-Nicolas

last: Lodewyckx

first: Hugues

last: Duvillier

first: Sarah

last: Dedeurwaeder

first: Francoise

last: Bex

first: Francois

last: Fuks

first: Martine

last: Piccart

first: Karen

last: Willard-Gallo


title: DNA methylation analysis in women with fibromyalgia

city: Campinas

first: Mariana

last: Maschietto

state: São Paulo

address: Rua Márcia Mendes, 619

department: Research Center

country: Brazil

institute: Boldrini Children's Hospital

summary: FM is a complex syndrome with physiological, genetics and environmental factors involved. It can present changes in functional neuroimaging, in cortical excitability measurements performed by transcranial magnetic stimulation and in grey matter density. Similarly, it has been shown that patients with FM have abnormal autonomic control, inflammatory profile and dysfunctional hypothalamic–pituitary–adrenal axis leading to disruptive sleep and fatigue. We characterized clinical and neurophysiological parameters and peripheral blood DNA methylation profiles of patients with FM and compared them to sex and age matched healthy controls. We hypothesized that these exploratory analyses could provide mechanistic insights into the pathophysiology of FM and possibly contribute to the future development of biological markers of diagnosis.We showed that patients with fibromyalgia have different (mainly hypo-) methylated CpG sites related to genes implicated in immune system and response to external stress pathways and that this methylation profile is related to a dysfunctional connectivity in pain network, adding evidence to consider fibromyalgia as a DOHAD disorder.

overall_design: Bisulphite converted DNA from 47 samples were hybridised to the Illumina Infiniun 450k Human Methylation Beads following manufacture's protocols.

first: Helena

last: Brentani

first: Daniel

last: Ciampi


title: NF2 disruption by genomic rearrangments drives a subset of radiation induced meningiomas

status: Public on Jul 29 2017

city: PITTSBURGH

first: SAMEER

last: AGNIHOTRI

state: Pennsylvania

address: Rangos Research Center, 7th Floor, ROOM 7126, 530, 45th Street

department: MacFeeters-Hamilton Brain Tumour Centre

institute: University of Pittsburgh

summary: Genome wide DNA methylation profiling of spontaneous meningiomas and meningiomas from patients who had received radiotherapy for previous medical condition. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs. Samples include 18 radiation induced meningiomas and 19 spontaneous meningiomas.

overall_design: Bisulphite converted DNA from the 37 samples were hybridized to the Illumina Infinium 450k Human Methylation Beadchip

first: Gelareh

last: Zadeh

first: Kenneth

last: Aldape


title: The AP-1 transcription factor FOSL1 causes melanocyte reprogramming and transformation

status: Public on Aug 02 2017

city: Wuerzburg

first: Susanne

middle: Elma

last: Kneitz

address: Biozentrum, Am Hubland

department: Physiologigcal Chemistry

institute: University of Wuerzburg

summary: The MAPK pathway is activated in the large majority of melanomas and is the subject of several therapeutic approaches. Under normal conditions, it quickly raises the so-called immediate early response, which encompasses the transient transcription of several genes belonging to the AP-1 transcription factor family. Under pathological conditions such as consistent MAPK pathway overactivation due to oncogenic alterations occurring in melanoma, these genes are permanently expressed. The consequences of a permanent expression of these genes are currently unknown.

overall_design: Here, we show that FOSL1 is the main immediate early AP-1 member induced by melanoma oncogenes. We first examined its role in established melanoma cells, and found that FOSL1 is involved in melanoma migration as well as cell proliferation and anoikis-independent growth, which is mediated by the gene product of its target gene HMGA1, a multipotent chromatin modifier. As FOSL1 expression is increased in melanomas compared to nevi, we investigated the effect of enhanced FOSL1 expression on melanocytes and found that FOSL1 is able to reprogram them by shifting the balance between MITF and AXL and re-enforcing pro-tumorigenic trancription factors MYC, E2F3 and AP-1. This results in the enhancement of growth-promoting processes such as ribosome biogenesis and pyrimidine metabolism and eventually causes the transformation of melanocytes into malignant tumors.

first: Meierjohann

last: Svenja

first: Maurus

last: Katja

first: Geiger

last: Fabienne

first: Hufnagel

last: Anita

first: Graf

last: Saskia

first: Berking

last: Carola

first: Heinemann

last: Anja

first: Paschen

last: Annette

first: Kneitz

last: Susanne

first: Stigloher

last: Christian

first: Geissinger

last: Eva

first: Otto

last: Christoph

first: Bosserhoff

first: Schartl

last: Manfred


title: Effect of TLR2 coactivation on Naïve CD4+ T cells  differentiation and function

status: Public on Aug 04 2017

city: Cleveland

first: Ahmad

middle: Faisal

last: Karim

state: OH

address: 2109 Adelbert road; BRB 1010B

institute: Case Western Reserve University

summary:
We have recently demonstrated that mycobacterial ligands engage Toll like receptor 2 (TLR2) on CD4+ T cells and up-regulate T-cell receptor (TCR) triggered- Th1 responses in vitro and in vivo.
To extend our previous studies on the role of TLR2 in the regulation of T-cell function and differentiation, we compared the gene expression profile of mouse CD4+ T cells co-stimulated via CD28 or TLR2. Unlike CD28 co-stimulation, TLR2 co-engagement with CD3 triggered the regulation of a very discrete set of genes. Unexpectedly, naïve CD4+ T- cells co-stimulated via TLR2 showed a significant up-regulation of Il9 mRNA compared to cells co-stimulated via CD28.

overall_design: Mouse CD4+ T cells were co-stimulated via CD28 or TLR2 in addition to CD3 at two different timepoints i.e. 24hrs and 48 hrs. Total RNA were extracted from each treatment conditons and used for hybridization on Affymetrix microarrays.

first: Roxana

last: Rojas

first: Scott

last: Reba


title: DNA Methylation Barcodes in Human Fetal Tissues and Human Induced Pluripotent Stem Cells II

status: Public on Jul 26 2017

city: Leiden

first: Roderick

last: Slieker

address: PO Box 9600

department: Medical Oncology

country: Netherlands

institute: Leiden University Medical Center

summary: Here we assessed the genome-scale DNA methylation in multiple tissues and derived iPSs using the Illumina 450k array.

overall_design: Comparison of DNA methylation of  fetal human tissues at mutiple timepoints

first: R

first: M

middle: S

last: Roost

first: B

middle: T

last: Heijmans

first: S

last: Chuva de Sousa Lopes


title: DNA Methylation Barcodes in Human Fetal Tissues and Human Induced Pluripotent Stem Cells


title: Lineage-specific transcription factors regulate DNA methylation dynamics during hematopoietic development [Methylation]

city: Yokohama

first: Takahiro

last: Suzuki

state: Kanagawa

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

department: Center for Integrative Medical Sciences

institute: RIKEN

summary: DNA methylation is a major epigenetic modification for gene silencing and is dramatically altered spatiotemporally during cellular development. However, the roles of DNA methylation dynamics and regulation in cellular development remain unclear. The present analyses of DNA methylome dynamics during hematopoietic development suggest that DNA demethylation pre-defines the gene expression potential of terminal differentiation-specific genes at the progenitor cell stage and is regulated by lineage-specific transcription factors (TFs). Demethylation of majority of hypo-methylated CpGs in terminally differentiated cells occurs during the progenitor cell stage and is associated with rapid upregulation of terminal differentiation-specific genes. Accordingly, TF overrepresentation analyses indicated that lineage-specific TFs regulate DNA demethylation. The present experiments show that RUNX1 induces site-directed active DNA demethylation by recruiting DNA demethylation enzymes. Collectively, the present data indicate an integrated system of DNA methylation and gene expression during cellular development.

overall_design: Bisulphite converted DNA from the 6 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip.

first: Yuri

last: Shimizu

first: Erina

last: Furuhata

first: Shiori

last: Maeda

first: Mami

last: Kishima

first: Hajime

last: Nishimura

first: Yoshihide

last: Hayashizaki

first: Harukazu