title: RUNX1-Mediated Binding Site Directed DNA Demethylation is a Novel Mechanism of Hematopoietic Gene Activation.

summary: RUNX1 (also known as AML1) is a key transcription factor for definitive hematopoietic stem cell development and following hematopoietic cell linage specifications, in which chromatin- or epigennome-mediated regulation by RUNX1, particularly regulation of DNA methylation status, is proposed to be involved in addition to its direct gene expression regulation. However, how RUNX1 regulates DNA methylation status and its role in the hematopoiesis remain to be elucidated. Here we first demonstrated that RUNX1 induces RUNX1 binding site directed DNA demethylation across the whole genome. HaloTag-based pull-down assay revealed associations of RUNX1 with active DNA demethylation related proteins such as TET, TDG or GADD45A, suggested that the RUNX1-mediated DNA demethylation is active DNA demethylation mechanism. Additional combinatorial overexpression of TET and TDG enlarged the RUNX1-mediated DNA demethylation, supporting what RUNX1-mediated DNA demethylation is active DNA demethylation.  These results strongly suggested that RUNX1-mediated DNA demethylation is achieved by recruiting those proteins involved in active DNA demethylation.  Finally, we found that the RUNX1-mediated demethylation predominately targets and activates hematopoietic genes whose promoter regions are demethylated during hematopoiesis. Collectively, our insight suggested that RUNX1-mediated binding site directed DNA demethylation is a novel mechanism of hematopoietic gene activation.

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


title: Histone variant H3F3A promotes lung cancer cell migration through intronic regulation.

status: Public on Aug 12 2017

city: Goyang

first: Seong-min

last: Park

address: Ilsan-ro

country: South Korea

institute: NCC

summary:
Although several somatic single nucleotide variations in histone H3.3 have been investigated as cancer drivers, other types of aberrations have not been well studied. Here, we demonstrate that overexpression of H3F3A, encoding H3.3, is associated with lung cancer progression and promotes lung cancer cell migration by activating metastasis-related genes. H3.3 globally activates gene expression through the occupation of intronic regions in lung cancer cells. Moreover, H3.3 binding regions show characteristics of regulatory DNA elements. We show that H3.3 is deposited at a specific intronic region of GPR87, where it modifies the chromatin status and directly activates GPR87 transcription. The expression levels of H3F3A and GPR87, either alone or in combination, are robust prognostic markers for early stage lung cancer, and may indicate potential for the development of treatments involving GPR87 antagonists. Our results demonstrate that intronic regulation by H3F3A may be a target for the development of novel therapeutic strategies.
We performed microarray-based global gene expression analysis of H3F3A-overexpressing and H3F3A knockdown A549 cells.

overall_design: Examination of mRNA expression in H3F3A-overexpressing and H3F3A knockdown A549 cells.

first: Eun-Young

last: Choi

first: Youn-Jae

last: Kim


title: Gene expression profiling of marginal zone B-cell lymphomas and variants

status: Public on Jul 24 2017

city: Ulm

first: Karlheinz

last: Holzmann

address: Helmholtzstreet 8/1

department: Medical Faculty

country: Germany

institute: Ulm University

summary: Large cell lymphomas of the gastrointestinal tract are currently regarded as diffuse large B-cell lymphomas despite a more favourable clinical outcome and a lower aggressiveness compared to other nodal and extranodal DLBCL. We compared gene expression profiles of 28 gastrointestinal marginal zone B-cell lymphomas and variants with several other B-cell lymphoma entities such as Burkitt’s lymphoma, nodal DLBCL, follicular lymphoma, mantle cell lymphoma, primary mediastinal B-cell lymphoma and normal B-cell populations. Based on a subset of NF-kappaB target genes, partitioning and hierarchical cluster algorithms were used which led to comparable results. The different B-cell subsets, the Burkitt’s lymphoma, and the small cell lymphomas formed distinct groups, respectively. The DLBCL were subdivided into one group containing only DLBCL samples, one subset clustered together with the PMBL samples, and another one together with the blastic variants of MZBL. These results implicate that extranodal blastic MZBL represent a distinct subgroup of DLBCL.

overall_design:
Affymetrix arrays were performed according to the manufacturer's directions on RNA extracted from cryopreserved tumor samples.
Gene expression analysis on Affymetrix HG U133 plus 2.0 arrays was performed for 2 gastric follicular lymphoma, 8 small cell MALT lymphomas, 9 large cell areas of Composite lymphomas and 13 large cell variants.

first: Lucia

last: Flossbach

first: Thomas

middle: F

last: Barth


title: African American esophageal squamous cell carcinoma expression profile reveals loss of detox networks

status: Public on Aug 15 2017

city: Bethesda

first: Kory

middle: R

last: Johnson

state: MD

address: 10/3B01, 9000 Rockville Pike

department: DIR IT & Bioinformatics

country: USA

institute: NINDS/NIH

summary: Esophageal carcinoma is the third most common gastrointestinal malignancy worldwide and is generally unresponsive to therapy.  African Americans have an increased risk for esophageal squamous cell cancer (ESCC), the subtype that shows marked variation in geographic frequency. To identify key genes involved in ESC carcinogenesis in African Americans we conducted microarray expression profiling and found a significant dysregulation of genes encoding stress response and drug-metabolizing enzymes, mainly in NRF2 pathway. The involvement of NRF2 mediated oxidative damage represent a key step in the evolution of African American ESCC. Loss of activity of these enzymes would confer increased sensitivity of esophageal cells to xenobiotics, such as alcohol and tobacco smoke, and may account for the high incidence of ESCC in this ethnic group. The differential expression profile also indicates an inflammatory component and tissue regeneration in ESCC tumorigenesis. Together, these findings suggest a remarkable interplay of genetic and environmental factors in the pathogenesis of African American ESCC.

overall_design: Fourteen paired Human biopsy specimens collected from African Americans diagnosed with Esophageal Squamous Cell Carcinoma (ESCC).  Seven of the fourteen specimens represent ESCC while the remaining represent paired healthy tissue.

first: Hayriye

middle: V

last: Erkizan

first: Leema

last: Peddareddygari

first: Svetlana

last: Ghimbovschi

first: Deepa

last: Karkera

first: Gregory

last: Trachiotis

first: Houtan

last: Adib

first: Rafael

last: Gorospe

first: Sevilla

last: Detera-Wadleigh

first: Robert

middle: G

last: Wadleigh

first: Eric

middle: P

last: Hoffman


title: Expression data from liver, muscle and fat tissue of children with end stage liver disease

status: Public on Jul 31 2017

city: London

first: Matthew

last: Arno

state: LONDON

address: 150 Stamford Street

department: Genomics Centre

country: United Kingdom

institute: King's College London

summary:
Cachexia, described as a syndrome of weight loss, muscle wasting, fat loss and insulin resistance has been described in patients with chronic liver disease. Whereas extensive work is being done to delineate these molecular pathways in adult patients with chronic liver or other disease, very little is known about these pathways in children with chronic liver disease.
We used microarrays to detail the global programme of gene expression underlying the metabolic processes of cachexia in children with end stage liver disease udergoing liver transplantion. We included tissue from patients with Crigler-najjar syndrome as controls. We were able to identify distinct classes of differentially regulated genes related to these processes.

overall_design:
9 liver,  11 muscle (rectus abdominis) and 11 subcutaneous fat tissue samples were collected at the time of liver tranplantation from 11 patients with end stage liver disease as well as 2 liver, 2 muscle and 2 fat samples from 2 children with Crigler-Najjar syndrome serving as controls.

Please note that 2 of the (end stage liver disease) patients did not give good quality Liver RNA so were not processed onto microarrays.

BA = Biliary atresia
BC = Biliary cirrhosis
NSC = Neonatal sclerosing cholangitis
a1AT = Alpha-1-antitrypsin deficiency

first: Eirini

last: Kyrana


title: Pre-processing method comparison on Illumina HumanMethylation450 BeadChips array

status: Public on Aug 02 2017

city: Toronto

first: Yu-Jia

last: Shiah

state: Ontario

address: MaRS Centre 661 University Avenue Suite 510

department: Informatics and Bio-computing

country: Canada

institute: Ontario Institute for Cancer Research

type: Methylation profiling by genome tiling array

summary: This study is trying to provide guildeline on how to identify the most optimal pre-processing method for  Illumina HumanMethylation450k BeadChips array on prostate cancer dataset.

overall_design: In total, we have methylation profiles for 310 samples (corresponding to 202 unique samples). Out of the 202 unique samples, 71 samples were repeated twice, 14 samples repeated three times, 3 samples repeated four times.

first: Paul

middle: C

last: Boutros

last: Bristow

first: Michael

last: Fraser


title: DNA methylation of mesenchymal stromal cells in platelet lysate versus fetal calf serum

status: Public on Aug 11 2017

city: Aachen

first: Wolfgang

last: Wagner

address: Pauwelsstrasse 20

department: Helmholtz Institute for Biomedical Engineering

institute: RWTH Aachen University

summary: Culture medium of mesenchymal stromal cells (MSCs) is usually supplemented with either human platelet lysate (HPL) or fetal calf serum (FCS). Many studies have demonstrated that proliferation and cellular morphology is influenced by these additives – hence they may favor outgrowth of specific subpopulations, thereby affecting the heterogeneous composition of MSCs. We have isolated and expanded human bone marrow derived MSCs in parallel with HPL or FCS for two passages. In HPL the proliferation was significantly higher and cells reflected more spindle-shaped morphology. In contrast, global DNA-methylation profiles did not reveal any significant differences. None of the CpGs revealed significant differences between MSCs that were cultured in HPL versus FCS if the analysis was corrected for multiple testing (limma-adjusted P-value of <0.05). These results indicate that there is no systematic bias for specific subpopulations of MSCs by using either HPL or FCS.

overall_design: Illumina Infinium 450k Human Methylation Beadchip analysis of Mesenchymal stromal cells after 2 passages under HPL or FCS supplementation.

first: Eduardo

last: Fernandez-Rebollo

first: Birgit

last: Mentrup

first: Regina

last: Ebert

first: Julia

last: Franzen

first: Giulio

last: Abagnale

first: Torsten

last: Sieben

first: Per

last: Hofmann

first: Björn

last: Rath

first: Franz

last: Jakob


title: Comparison of the DNA methylation profiles of CD14+ monocytes from human peripheral blood with derived macrophages (MACs) and osteoclasts (OCs) obtained by exposure with M-CSF and M-CSF/RANKL, respectively, for 5 and 20 days

status: Public on Jul 19 2017

city: Badalona, Barcelona

first: Esteban

last: Ballestar

state: N/A = Not Applicable

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

country: Spain

institute: Josep Carreras Research Institute (IJC)

summary: The methylation profiles of bisulfite(BS)- and oxidative-BS-modified DNA of human CD14+ monocytes were compared with derived macrophages (MACs) and osteoclasts (OCs) following M-CSF and M-CSF/RANKL incubation for 5 and 20 days, 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 three sets of samples of monocytes (MOs) and derived MACs and OCs following incubation with M-CSF or M-CSF/RANKL for 5 and 20 days.

first: Antonio

last: Garcia-Gomez

first: Tianlu

last: Li

first: Martin

last: Kerick

first: Francesc

last: Català-Moll

first: Natalia

last: Comet

first: Javier

last: Rodríguez-Ubreva

first: Lorenzo

last: de la Rica

first: Miguel

last: Branco

last: Martín


title: Expression data from early stage CRC patients' tumors [Affymetrix]

city: Singapore

first: Steve

last: Rozen

address: 8 College Road

country: Singapore

institute: Duke-NUS

summary: This study was conducted in order to identify biomarkers for a prognostic gene expression signature for metastases in early stage CRC.

overall_design: Expression profiles from 100 metastasis negative and 50 metastasis positive early stage CRC tumors were obtained.

first: Yee-Syuen

last: Low

first: Christopher

last: Blöcker

first: Iain

middle: B

last: Tan

first: Steven

first: Peh-Yean

last: Cheah


title: Comparative gene expression in adult SVZ-neurospheres neuronally differentiated under standard conditions and upon PARP1 inhibition

status: Public on Jul 17 2017

city: Frankfurt

first: Dorothea

last: Schulte

address: Heinrich Hoffmann Str. 7

department: Neurology (Edinger Institute)

institute: Goethe University Hospital, Frankfurt

summary: The relevance of DNA-dependent poly-ADP ribose production for neuronal differentiation of adult stem- and progenitor cells from the SVZ was studied. To identify genes whose up- or downregulation during neuronal differentiation requires the activity of poly-ADP-Ribosylase (PARP) 1 or 2, SVZ-derived adult neurosphere cultures were differentiated in the presence or absence of Olaparib.

overall_design: Freshly isolated stem- and progenitor cells from the SVZ of adult mice were neuronally differentiated by transduction of Pax6. Two treatment regimes were compared: i) standard conditions ii) pharmacological inhibition of PARP1 and PARP2 by 100nM Olaparib in 0.01% DMSO.

first: Claudia

last: Döring


title: An FFPE-based prognostic signature to predict metastasis in stage I/II microsatellite stable colorectal cancer

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

overall_design: Refer to individual Series


title: Expression data from xenografted human leukemia cells comparing leukemic cells engrafted in the central nervous system (CNS) to leukemic cells derived from bone marrow (BM)

first: Hans

middle: A

last: Kestler

address: Albert-Einstein-Allee 11

department: Research Group Bioinformatics and Systems Biology

institute: University of Ulm

summary:
CNS leukemia is still the major obstacle in treating childhood acute lymphoblastic leukemia (ALL). We have used our NOD/SCID/huALL xenotransplantation model to identify molecular pathways leading to the infiltration of leukemic cells into the CNS compartment.
We analysed gene expression differences of leukemic cells isolated from CNS and BM of CNS-positive samples using a microarray approach to detect expression differences between different infiltrated compartments.

overall_design: We xenotransplanted primary leukemic cells into NOD/SCID mice by tail vein injection. When moribund, mice were sacrificed and total RNA was prepared from human leukemia cells isolated from CNS and BM, which subsequently have been subjected to hybridization on Affymetrix microarrays.

first: Vera

last: Muench

first: Luca

last: Trentin

first: Julia

last: Herzig

first: Salih

last: Demir

first: Felix

last: Seyfried

first: Johann

middle: M

last: Kraus

first: Rolf

last: Koehler

first: Geertruy

last: te Kronnie

first: Klaus-Michael

last: Debtain

first: Lueder

middle: H

last: Meyer


title: BECon: A tool for interpreting DNA methylation findings from blood in the context of brain

status: Public on Aug 01 2017

city: Vancouver

first: Michael

middle: S.

last: Kobor

state: BC

address: 950 West 28th Avenue

department: Medical Genetics

institute: Centre for Molecular Medicine and Therapeutics / University of British Columbia

summary: Tissue differences are one of the largest contributors to variability in the human DNA methylome. Despite the tissue specific nature of DNA methylation, the inaccessibility of human brain samples necessitates the frequent use of surrogate tissues such as blood, in studies of associations between DNA methylation and brain function and health. Results from studies of surrogate tissues in humans are difficult to interpret in this context, as the connection between blood-brain DNA methylation is tenuous and not well documented. Here we aimed to provide a resource to the community to aid interpretation of blood based DNA methylation results in the context of brain tissue. We used paired samples from 16 individuals from three brain regions and whole blood, run on the Illumina 450K Human Methylation Array to quantify the concordance of DNA methylation between tissues. From these data we have made available metrics on: the variability of CpGs in our blood and brain samples, the concordance of CpGs between blood and brain, and estimations of how strongly a CpG is affected by cell composition in both blood and brain through the web application BECon (Blood-Brain Epigenetic Concordance; https://redgar598.shinyapps.io/BECon/). We anticipate that BECon will enable biological interpretation of blood based human DNA methylation results, in the context of brain.

overall_design: This cohort consist of genomic DNA extracted from 18 whole blood, 18 Broadman Brain Area 7, 18 Broadman Brain Area 10 and 16 Broadman Brain Area 20 samples, bisulphite converted and hybridized to the Illumina Infinium HumanMethylation450 Beadchip for genome wide DNA methylation profiling.

first: Rachel

middle: D

last: Edgar

first: Meaghan

middle: J

last: Jones

last: Meaney

first: Gustavo

last: Turecki

middle: S


title: The HDAC inhibitor Panobinostat (LBH589) exerts in vivo anti-leukaemic activity against in MLL-rearranged Acute Lymphoblastic Leukaemia and involves the RNF20/RNF40/WAC – H2B ubiquitination axis

status: Public on Jul 12 2017

city: Padova

address: Via Giustiniani, 3

department: Department of Women's and Children's Health

country: Italy

institute: University of Padova

summary: We demonstrate the in vivo efficacy of the histone deacetylase inhibitor Panobinostat (LHB589) against MLL-rearranged ALL using xenograft mouse models of MLL-rearranged ALL cell lines and primary patient cells. Panobinostat monotherapy showed strong anti-leukaemic effects, extending survival and reducing overall disease burden. Comprehensive molecular analyses in vitro showed the anti-leukaemic activity in MLL-rearranged ALL to involve depletion of H2B ubiquitination via suppression of the RNF20/RNF40/WAC E3 ligase complex.

overall_design: Gene expression was measured using  Affymetrix platform in 4 distinct cell lines treated or untreated in vitro with Panobinostat  at 5 nM for 24 hours. Four independent biological replicates were carried out.

first: Patricia

last: Castro

first: Ronald

last: Stam


title: Increasing of antitumor effect of decitabine against classical Hodgkin lymphoma (cHL) by targeting decitabine-activated pro-survival pathways

first: Alexey

last: Ushmorov

department: Institute of Physiological Chemistry

summary: We found that 5-Aza-dC/decitabine induces various prosurvival pathways (JAK-STAT-, NFkB-, MEK/ERK- and PI3K/AKTpathway) in cHL cell lines. Inhibition of these pathways with specific small molecular weight inhibitors potentiates the antitumor effect of 5-Aza-dC.

overall_design: L1236 and L428 cells were treated with 1µM of 5-Aza-dC for 24h and were then washed out. After additional 72 h incubation in normal medium, total RNA was isolated with RNeasy mini kit (QIAGEN). Microarray analyses were performed using 200 ng of total RNA as starting material and 5.5 µg ssDNA per hybridization (GeneChip Fluidics Station 450; Affymetrix, Santa Clara, CA). The total RNAs were amplified and labeled following the Whole Transcript (WT) Sense Target Labeling Assay (http://www.affymetrix.com). Labeled ssDNA was hybridized to Human Gene 1.0 ST Affymetrix GeneChip arrays (Affymetrix, Santa Clara, CA). The chips were scanned with an Affymetrix GeneChip Scanner 3000 and subsequent images analyzed using Affymetrix® Expression Console Software (Affymetrix). Probe level data were obtained using the robust multichip average (RMA) normalization algorithm.

first: Tatjana

last: Swerev

first: Thomas

last: Wirth


title: Expression profiling of H4 cells expressing a Myc tagged aSyn construct

city: Zagreb

first: Fran

last: Borovecki

address: Salata 2

department: Center for Translational anc Clinical Research

country: Croatia

institute: University of Zagreb School of Medicine

summary: The aim of the present study was to identify and confirm gene expression differences in control H4 cells and WT asyn expressing H4 cells, one of the cell-based models of Parkinson`s disease. DNA microarray gene expression was performed in two samples of control H4 cells and in two samples expressing WT asyn, along with bioinformatics analysis of retrieved data.

overall_design: Total RNA was extracted from two samples of H4 control cells and two samples of WT asyn expressing H4 cells (myc-tagged), labeled and hybridized to Human Genome U133 PLUS 2.0 arrays.


title: Epigenome analysis of DNA from umbilical cord blood (UCWBC) in CCCEH birth cohort

city: Cincinnati

first: Shuk-mei

last: Ho

state: OH

address: 160 Panzeca Way

department: Environmental Health

institute: University of Cincinnati

summary: Genome wide DNA methylation profiling of 152 umbilical cord blood samples from CCCEH birth cohort. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in cord blood samples

overall_design: Bisulphite converted DNA from the 152 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip


title: transcriptional profiling of mouse full thickness skin of PPARgamma null mice

city: Lausanne

first: Federica

last: Gilardi

address: chemin de la Vulliette 4

department: University Center of Legal Medicine

country: Switzerland

institute: University of Lausanne

summary: PPARgamma null (PpargΔ/Δ) mice present a generalized lipoatrophy and a dramatic skin phenotype, characterized by delayed hair morphogensis and the appearance, at adult age, of severe inflammatory infiltration. To investigate the molecular mechanisms underlying the delayed hair morphogenesis observed in PpargΔ/Δ mice, we used microarrays to detail the global program of gene expression in full thickness skin of PpargΔ/Δ mice and respective control mice at embryionic stage E17.5.

overall_design: We examined 2 experimental groups: PpargΔ/Δ and control mice at E17.5. For each experimental group we analysed the transcriptional profile of 4 individual RNA from full thickness skin.

first: Greta

last: Paola

first: Giordano

last: Attianese

first: Chiara

last: Sardella

first: Carine

last: Winkler

first: Barbara

last: Toffoli

first: Béatrice

last: Desvergne


title: DNA methylation in human DIP2C knockout cancer cells

city: Uppsala

first: Chatarina

last: Larsson

address: Rudbeck Laboratory

department: Immunology, Genetics and Pathology

country: Sweden

institute: Uppsala University

summary: Aim: The disco-interacting protein 2 homolog C (DIP2C) gene is an uncharacterized gene found mutated in breast and lung cancers. We want to understand the role of DIP2C in tumor development.   Methods: We engineered human DIP2C knockout cell systems by genome editing, and studied these to identify cellular processes affected by gene knockout. We used the Illumina HumanMethylation 450k beadchip array to identify methylation sites affected by the loss of DIP2C.  Results: Inactivation of DIP2C triggered changes in cell morhpology, growth, gene expression and DNA methylation. Differential methylation at promoters was found inversly correlated with gene expression changes.

overall_design: We engineered DIP2C knockout RKO colorectal cancer cells by rAAV-mediated gene targeting. Parental RKO cells, two homozygous knockout and two heterozygous knockout cell lines were analyzed using the Illumina HumanMethylation 450k beadchip array to investigate if DNA methylation patterns are altered in knockout cells.

first: Tobias

last: Sjöblom


title: A gene expression profiling to predict recurrence of advanced tongue squamous cell carcinoma (TSCC): Discovery and external validation

city: Kashiwanoha, kashiwa

first: Tomohiro

last: Enokida

country: Japan

institute: National Cancer Center Hospital East

summary: Though several approaches for improving therapy have been carried out, the prognoses of TSCC patients still remains poor. Furthermore, biological markers, which are able to distinguish patients at high risk of recurrence has not been sufficiently explored. In this study, we identified and validated the 30-specific genes for predicting TSCC patiens prognosis. In addition, the gene expression profiling data was successfully converted to protein expression profiling data.

overall_design: Global gene expression analysis was performed on 26 clinicopathologically homogeneous advanced TSCC tissue samples using cDNA microarray. We then identified 30-predictive genes associated with recurrence and created formula to predict the individual patients’ prognosis. The validation study to examine whether the genes expression pattern enable to predict prognosis was perfomerd in another publicly available three cohorts of microarray data set.

first: Satoshi

last: Fujii

first: Mari

last: Takahashi

first: Youichi

last: Higuchi

first: Tetsuro

last: Wakasugi

first: Tomoko

last: Yamazaki

first: Ryuichi

last: Hayashi

first: Atsushi

last: Ohtsu

first: Makoto

last: Tahara


title: Genome-wide DNA methylation analysis of psoriatic and normal skin tissues

status: Public on Jul 07 2017

city: Hefei

first: Fusheng

last: Zhou

address: No 96 Meishan Road, Hefei, China

country: China

institute: Anhui Medical University

summary: Genome wide DNA methylation profiling of psoriatic (PP), paired uninvolved psoriatic (PN) and normal skin tissues (NN). The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 485,000 CpGs in 135 PP, 41PN and 62 NN tissues which were obtained from those who underwent skin biospsies. We not only revealed a genome-wide methylation level pattern for psoriasis, but also identified a strong association between the skin-specific DNAm of 9 DMS and psoriasis.

overall_design: Bisulphite converted DNA from the 217 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.2

first: Xuejun

last: Zhang


title: Gene and MicroRNA expression data from lymphoblastoid cell lines from patients with bipolar disorder

status: Public on Jul 04 2017

city: Paris

first: Jeverson

last: Moreira

address: 4 Avenue de l'Observatoire

country: France

institute: INSERM

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

platform_organism:
Homo sapiens
synthetic construct


title: VLX60 characterization II

first: Mårten

last: Fryknäs

address: Akademiska sjh ingång 61

department: Medical sciencies

institute: Uppsala university

summary: Microarray based mRNA profiling was used to identify the mechanism of action for the small molecule VLX60.

overall_design: HCT116 cells were treated with the drug candidate VLX50 or VLX60 for 6h prior to RNA isolation

first: Marten

last: Fryknas


title: Stromal Repair via Long-term Engraftment of Primary Bone Marrow Stroma Improves Hematopoietic Stem Cell Transplantation

status: Public on Jul 02 2017

first: Jean-Paul

last: Abbuehl

department: ISREC

institute: Ecole Polytechnique Federale de Lausanne

overall_design: Purified CD45‐Ter119‐CD73+ CD105‐ and CD45‐Ter119‐CD73+ CD105+ cells were directly sorted on lysis buffer with FACS Aria 2 in triplicate.

first: Joerg

last: Huelsken


title: Genome-wide DNA methylation patterns in CD4+ T from rheumatoid arthritis

status: Public on Jul 29 2017

city: Shanghai

first: Dongyi

last: He

address: Changning District

department: Department of Rheumatology

institute: Shanghai Guanghua Hospital of Integrated Traditional and Western Medicine

summary:
Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints involved with genetic and epigenetic aberrant. Recent evidence found more and more importance of the epigenetic contribution, especially the DNA methylation, to the pathogenesis of rheumatoid arthritis. To understand the extent and nature of dysregulated DNA methylation in rheumatoid arthritis T cells, we performed a genome-wide DNA methylation study in CD4+ T cells in 12 rheumatoid arthritis patients compared to 12 matched normal healthy controls. [Methods and Result] Cytosine methylation status was quantified with Illumina methylation 450K microarray (HM450K, 485512 CpG sites). We identified 810 hypomethylated and 392 hypermethylated CG sites in RA CD4+ T cells compared to normal controls, representing 383 and 785 genes hypermethylated and hypomethylated in RA patients (P<3.4*10-7).  Cluster analysis based on significantly differential methylated loci showed distinct separation between RA and normal controls. Gene ontology analysis showed alternative splicing (P=1.2*10-7, FDR) and phosphoprotein (1.7*10-2, FDR) were significantly aberrant in RA patients, indicating the abnormal of transcript alternative splicing and protein modification mediated by DNA methylation might play important role in the pathogenesis of rheumatoid arthritis. What’s more, the result showed human leukocyte antigen (HLA) region was frequently hypomethylated in RA patients, including HLA-DRB6, HLA-DQA1 and HLA-E, however, HLA-DQB1 showed different methylation profiles with significant hypermethylation in CpG island region and hypomethylation in CpG shelf region. Outsite of the MHC region, the most hypermethylated genes in RA included HDAC4, NXN, TBCD and TMEM61 while the most significant hypomethylated genes included ITIH3, TCN2, PRDM16, SLC1A5 and GALNT9. [Conclusion] Genome-wide DNA methylation patterns revealed significant DNA methylation change in CD4+ T cells from patients with rheumatoid arthritis.
12 rheumatoid arthritis and 12 matched health individuals

overall_design: Bisulphite converted DNA from the CD4+ T cell extracted from Rheumatoid arthritis 12 patients and age, gender, race matched 12 normal controls were hybridized to the Illumina Illumina HumanMethylation450 BeadChip arrays

first: Shicheng

last: Guo


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

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 at multiple timepoints using the Illumina 450k array.

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

first: R

first: M

last: Roost

first: L

last: van Iperen

first: H

middle: E

last: Suchiman

first: E

middle: W

last: Tobi

first: F

last: Carlotti

last: de Koning

first: P

last: Slagboom

first: B

middle: T

last: Heijmans

first: S

last: Chuva de Sousa Lopes


title: Asbestos-associated genome-wide DNA methylation changes in lung cancer

city: Bron

first: Hector

last: Hernandez-Vargas

state: Rhone

address: 36 bis Rue de la Batterie

institute: Genomics Consulting

summary: Genome-wide DNA methylation study in lung cancer and paired normal lung with well-documented asbestos exposure

overall_design: 28 fresh-frozen lung cancer samples and their corresponding microscopically normal peripheral lung tissues were used for bead array methylation analyses. Six additional non-tumor control lung tissues were processed and analyzed in parallel. Samples (tumor, tumor-adjacent, and control tissues.) were analyzed according to asbestos exposure. Asbestos exposure was based on pulmonary fiber counts and occupational history.

last: Kettunen


title: Prospective randomized doubleblind assessment of transcriptome modulation by hydrocortisone in severe burn shock

city: Lyon

first: Julien

last: Textoris

address: Hôpital Edouard herriot - Pavillon P; 5 place d'Arsonval

department: Medical Diagnostic Discovery Department (MD3)

institute: bioMérieux

summary: Rationale: Despite shortening vasopressor use in shock, hydrocortisone administration remains controversial, with potential harm on the immune system. Few studies assessed hydrocortisone  impact on the transcriptional response in shock, and we are lacking data in burns.   Objectives: To assess the hydrocortisone-induced transcriptional modulation in severe burn shock, particularly on the immune response.  Methods: We collected whole blood samples (n= 117) during a randomized controlled trial assessing the efficacy of hydrocortisone administration on burn shock. Using whole genome microarrays, we first compared burn patients from the placebo group (n=15) to healthy volunteers (n=13) to describe the transcriptional modulation induced by burn shock over the first week. Then we compared burn patients randomized for either hydrocortisone administration (n=15) or placebo (n=15) to assess hydrocortisone-induced modulation.  Measurements and Main Results: Study groups were similar in terms of severity and major outcomes, but shock duration (significantly reduced in the hydrocortisone group). Many genes (n=2250) were differentially expressed between burn patients and healthy volunteers, with 85% of them exhibiting a profound and persistent modulation over seven days. Interestingly, we showed that hydrocortisone enhanced the shock-associated repression of adaptive, but also innate immunity.   Conclusions: We found that the initial host response to burn shock encompasses a wide and persistent modulation of gene expression, with profound modulation of pathways associated with metabolism and immunity. Importantly, hydrocortisone administration may worsen the immunosuppression associated with severe injury. These data should be taken into account in the risk ratio of hydrocortisone administration in patients with inflammatory shock.

overall_design: Prospective randomized double blind study comparing hydrocortisone administration to placebo (NaCl 0.9%). Whole blood samples were collected at inclusion (S1, before treatment administration), one day after (S2, one day after treatment administration), and at a median of 120h (S3, 120h after treatment administration) and 168h (S4, 168h after treatment administration). 13 healthy volunteers (HV) were sampled to provide control for the microarray experiments.

first: Jonathan

last: Plassais

first: Fabienne

last: Venet

first: Marie-Angélique

last: Cazalis

first: Diane

last: Le Quang

first: Alexandre

last: Pachot

first: Guillaume

last: Monneret

first: Sylvie

last: Tissot


title: ASCL1 defines differentiation-competent GBM cells and directs neoplastic cells towards neuronal fate

status: Public on Jul 21 2017

city: Toronto

first: Paul

last: Guilhamon

state: ON

address: 686 Bay Street

institute: SickKids

type: Genome binding/occupancy profiling by high throughput sequencing

summary: We identified a subgroup of patient-derived glioblastoma (GBM) cells that express high levels of the neurogenic transcription factor, ASCL1, which predicts response to pharmacological inhibition of the Notch signaling pathway. Treatment of ASCL1hi GBM cells with a Notch signaling inhibitor induced a change in cell fate from neoplastic to neuronal. Importantly, acquisition of the neuronal fate was accompanied by a reduction in tumorigenic potential. Loss of ASCL1 in GBM cells rendered cells no longer responsive to Notch signaling inhibition and we determined ASCL1 is required for the competency of GBM cells to undergo neuronal differentiation. Enforced ASCL1 expression directed GBM cells towards a neuronal cell fate reminiscent of terminal differentiation. RNA-seq analysis of GBM cells treated with the Notch signaling inhibitor reveals neuronal target gene activation is associated with increased stoichiometric levels of ASCL1, suggesting threshold levels of ASCL1 in GBM cells governs neuronal differentiation. We demonstrate that neoplastic cells which retain expression of key neurogenic programs can have their fates redirected towards terminal differentiation. Directed fate specification to neuronal cell types by exploiting latent neurogenic programs may be a strategy to treat a subset of GBM patients. Our findings therefore highlight the potential of differentiation therapy for a subset of molecularly defined GBMs.

overall_design:
Glioblastoma cells were profiled for open chromatin using ATAC-seq (total = 11 samples).
Raw data files (fastq) are under controlled access. Contact the Princess Margaret Cancer Centre Genomics Core/University Health Network (geneservice@pmgenomics.ca) for access using the identifiers and file names outlined in the Sample records.

first: Nicole

middle: I

last: Park

first: Xiaoyang

last: Lan

first: Mathieu

last: Lupien

first: Peter

last: Dirks


title: Meta-Analysis of Autism Cortical Transcriptome Reveals Discordant Region-Specific Changes   Linked to Radial Glia and Inhibitory Interneurons

status: Public on Jul 01 2017

city: Miami

first: Dmitry

last: Velmeshev

state: FL

address: 1501 NW 10th ave, BRB 629

department: Psychiatry

institute: Universtiy of Miami

summary: DNA methylation analysis of the prefrontal cortex samples from autistic patients and neurologically normal controls

overall_design: 18 samples (9 autism and 9 controls) were analyzed using Illumina HumanMethylation450 BeadChip

first: Emilia

last: Mazza


title: DNA methylation profiling of signet ring cell colorectal cancer

city: Cambridge

first: Muhammad

middle: Abdullah

last: Alvi

address: Addenbrooke's site

institute: University of Cambridge

summary: Identification of molecular subtypes of colorectal signet ring cell carcinoma based on differences in DNA methylation.

overall_design: Using discovery (n=26) and validation (n=18) cohorts, a comprehensive analysis of DNA methylation was carried out using Illumina infinium450k arrays.

first: Manuel

last: Salto-Tellez


title: DNA Methylation Profiling and Transcriptomic Changes in Signet Ring Cell Colorectal Cancer

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

overall_design: Refer to individual Series


title: Genome-wide single base resolution profiling of 5-methylcytosine in human breast tissue

status: Public on Jun 29 2017

city: Hanover

first: Kevin

middle: Crowley

last: Johnson

state: NH

address: 72 College Street

department: Epidemiology

institute: Geisel School of Medicine at Dartmouth College

summary: The underlying biological mechanisms through which epidemiologically defined breast cancer risk factors contribute to disease risk remain poorly understood. Here we investigated the impact cancer risk factors have on the normal breast epigenome by analyzing DNA methylation genome-wide (Infinium 450K array) in cancer-free women. We tested the relation of established breast cancer risk factors with DNA methylation adjusting for potential variation in cell-type proportions.

overall_design: Non-diseased breast tissue (n=18) DNA was subjected to bisulfite conversion with an input of 4ug per sample using the TrueMethyl® kit v.1.1 (Cambridge Epigenetix) protocol optimized for Illumina HumanMethylation450 arrays.


title: Deconvolution of whole blood DNA methylomes reveals immune cell type-specific differential methylation in Multiple Sclerosis

status: Public on Jun 30 2017

city: Parkville

first: Andrew

middle: David

last: Fox

state: VIC

address: 30 Royal Parade

department: MS Division

country: Australia

institute: The Florey Institute of Neuroscience and Mental Health

summary: Whole blood is a highly convenient and informative tissue from which to sample DNA and RNA in epigenomic and functional genomic studies, but it is comprised of multiple distinct cell types and this complexity significantly impairs our ability to interpret downstream differential methylation and/or differential expression results. In this multiple sclerosis (MS)-focused study we utilised an application of current statistical deconvolution methods to interrogate whole blood DNA methylation data thereby enabling the methylome of several immune cell types to be analysed independently. Methylome profiling on cell type-purified blood samples revealed optimal CpG sets for use as robust immune cell markers in the statistical deconvolution process. We show that it is possible to identify differentially methylated (DM) loci in a cell type specific manner using statistical deconvolution. Finally, we demonstrate that deconvolution improved the biological relevance and interpretability of our DM results, significantly enhancing concordance of the identified DM loci with loci previously shown to be genetically or epigenetically associated with MS.

overall_design: Case-Control design with whole blood methylomes of 14 healthy controls and 13 Multiple Sclerosis affected cases (1 failed bisulphite conversion) assayed. In addition, 8 of the healthy controls also have cell-type purified samples of neutrophils, CD4+ T cells, CD8+ T cells, NK cellsa, B cells and monocytes individually assayed.

first: Judith

last: Field

first: Melissa

last: Gresle

first: Laura

first: Louise

last: Laverick

first: Helmut

last: Butzkueven

first: Trevor

last: Kilpatrick


title: DNA methylation during HepaRG hepatocyte differentiation

status: Public on Jul 22 2017

first: Hector

last: Hernandez-Vargas

summary:
During embryonic development DNA methylation is highly dynamic, although less is known about the stability and fine-tuning of DNA methylation at later stages of differentiation. To understand the role of DNA methylation during hepatocyte differentiation, we profiled approximately 450k methylation sites at different time points in the progression from hepatoblast to hepatocyte stages using the bipotent liver progenitor HepaRG cell line.
Progressive demethylation of HNF4A P1 was highly correlated with increased expression of the shorter isoforms of HNF4A. In addition, the absence of cell division at later stages of differentiation and the increased expression of TET1 and TET2 transcripts indicates that a process of active demethylation is taking place at this specific locus. These data suggest that liver progenitors are poised for targeted demethylation at specific genomic locations involved in terminal stages of hepatocyte differentiation.

overall_design: HepaRG cells were seeded in culture six-well plates using William’s Medium E and incubated at 37°C, 5% CO2. The medium was renewed every 3 days. Once a maximal confluence was reached (85 to 100%), culture medium was supplemented with EGF (90 ng/mL) during 1 week then with EGF and 2% dimethyl sulfoxide (DMSO) for another week to stimulate HepaRG cells differentiation. Both EGF and DMSO were kept thereafter until final differentiation (week 4).


title: DNA methylation-based immune response signature improves patient diagnosis in multiple cancers (TOP Cohort)

status: Public on Jul 16 2017

city: Gosselies

first: Martin

last: Bizet

address: Rue Adrienne Bolland, 8

country: Belgium

institute: Université Libre de Bruxelles

summary:
Breast cancer (BC) is one of the most common and deadliest malignancies in women worldwide. Tumor immune response is increasingly recognized to be associated with better clinical outcome in breast and other cancers. However, the quantitative evaluation of the tumor immune response by measuring tumor-infiltrating lymphocytes (TILs) remains challenging, since it relies on subjective measurements, which are limited in accuracy and reproducibility.
In this study, we sought to identify a set of DNA methylation markers (MeTIL signature) that better recapitulate the evaluation of TILs and their impact on long-term outcome in BC. We showed that the MeTIL score measures TIL distributions in a more robust and sensitive manner than conventional pathological TIL counts and that this translates into better prediction of survival and response to chemotherapy in BC. We demonstrated that the MeTIL score can be determined in low amounts of DNA from FFPE tumor tissue by bisulfite pyrosequencing allowing for the fast and cost-efficient evaluation of TILs in the clinical setting.

overall_design: Bisulphite converted DNA of  58 samples from the TOP Cohort were hybridized to the Illumina Infinium 450k Human Methylation Beadchip

first: Jana

last: Jeschke

first: Christine

last: Desmedt

first: Emilie

last: Calonne

first: Sarah

last: Dedeurwaerder

first: Soizic

last: Garaud

first: Alexander

last: Koch

first: Denis

last: Larsimont

first: Roberto

last: Salgado

first: Gert

last: Van den Eynden

first: Karen

last: Willard Gallo

first: Gianluca

last: Bontempi

first: Matthieu

last: Defrance

first: Christos

last: Sotiriou

first: François

last: Fuks


title: DNA methylation-based immune response signature improves patient diagnosis in multiple cancers


title: DNA methylation-based immune response signature improves patient diagnosis in multiple cancers (Cohort 1)

overall_design: Bisulphite converted DNA of the 118 samples from the Cohort 1 were hybridized to the Illumina Infinium 450k Human Methylation Beadchip


title: IFNγ influences epithelial anti-viral responses via histone methylation of the RIG-I promoter

status: Public on Jun 26 2017

city: London

first: Akul

last: Singhania

address: 1 Midland Road

institute: The Francis Crick Institute

summary: This in-vitro study suggests the inflammatory environment of naive epithelial cells can induce epigenetic modulation of innate immune responses at the level of histone methylation and potentially lead to long-term impacts on anti-viral immunity.

overall_design:
Investigate the epigenetic effects of cytokine priming on innate immune response genes in the airways epithelium.
AALEB cells were treated with interferon-gamma (IFNγ), infected with RSV, both, or neither. Two replicates each.

first: C

last: Spalluto

first: Tom

last: Wilkinson


title: Expression data in HT1080 cells treated with cMyc-shRNA or non-targeting control shRNA

first: Ping

last: Gao

state: Anhui

address: Huangshan Road 443

department: Innovation Center for Cell Biology

institute: School of Life Science, University of Science and Technology of China

summary: cMyc is a master regulator of transcription in growing cells. Here, we used microarray to study global transcriptomic expression of cMyc knockdown HT1080 cells to investigate cMyc- regulated gene expression.

overall_design: Human fibrosarcoma HT1080 cells were transfected with cMyc shRNA or non-targeting control shRNA followed by RNA extraction and hybridization on Affymetrix GeneChip Human Gene 2.0 ST array.

first: Gongwei

last: Wu

first: Mengqiu

last: Yuan

first: Huafeng

last: Zhang


title: IFNγ-dependent tissue immune homeostasis is co-opted in the tumor microenvironment

first: Sanjay

last: Prakadan

state: MA

address: 77 Massachusetts Ave, E25-356

institute: Massachusetts Institute of Technology

type: Expression profiling by high throughput sequencing

summary:
Homeostatic programs maintain equilibrium between immune protection, and selftolerance. Such mechanisms impact autoimmunity and tumor formation, respectively. How tissue homeostasis is maintained, and impacts tumor surveillance is unknown. Here we identify that mononuclear phagocytes share conserved programming during homeostatic differentiation, and entry into tissue. IFNγ is necessary and sufficient to induce these transcripts, revealing a key instructive role. Remarkably, homeostatic and IFNγ-dependent programs enrich across primary human tumors, including melanoma, and stratify metastatic melanoma survival. Single-cell RNA-sequencing reveals enrichment of these modules in monocytes and DCs in human metastatic melanoma. Suppressor-of-cytokine-2 (SOCS2), a highly conserved transcript in this program is induced by IFNγ, and expressed in mononuclear phagocytes infiltrating primary melanoma. SOCS2 limits DC adaptive anti-tumoral immunity and T cell priming in vivo, indicating a critical regulatory role. Our findings link homeostasis in peripheral tissue to anti-tumoral immunity and escape, revealing coopting of tissue-specific immune development in the tumor microenvironment.
The raw FASTQ sequence files are being deposited in dbGAP.

overall_design: Single-cell RNA sequencing experiments of human patient-derived monophagocytes, including BDCA1+, BDCA3+ and monocyte-derived cells.

first: Alex

middle: K

last: Shalek


title: Gene expression signature and mitochondrial DNA copy number variation in ulcerative colitis patients

city: Bunkyo-ku

first: Toshiaki

last: Watanabe

state: Tokyo

department: Department of Surgical Oncology

institute: University of Tokyo

summary: Specimens were obtained from non-neoplastic colorectal mucosa for RNA ayalysis. Samples were obtained either from surgically resected specimens or during surveillance coloscopy. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays.The correlation between mtDNA CNV and mitochondria-related gene expressions were investigated.

overall_design: Thirty patients who underwent surgical resection or surveillance coloscopy were included in this study. The copy number of mitochondria DNA was measured by absolute quantification using QuantStudio SD digital PCR system. Samples were classified into mtDNA-Low and mtDNA-High at the median.

first: Takashi

last: Kobunai

first: Etsuko

last: Sakamoto

first: Eriko

last: Hashimoto


title: Gene expression of AML cell lines (HL60, KG1a, MOLM14 and U937) untreated or treated with metformin

status: Public on Jun 25 2017

city: Strassen

first: Tony

last: KAOMA

address: 1 A-B Rue Thomas Edison

department: Quantitative Biology Unit

country: Luxembourg

institute: Luxembourg Institute of Health

overall_design: Four human acute myeloid leukemia cell lines (KG1a, U937, HL60 and MOLM14) were grown and treated with electron transfer chain complex I inhibitor (metformin, 10mM) during 24 hours for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain gene signature specific of high oxidative phsophorylation function.

first: Sarah

last: Scotland

first: Estelle

last: Saland

first: Jean-Emmanuel

last: Sarry

last: Kaoma


title: Effects of smoke and smokeless tobacco products on gene expression and cellular pathways in oral cavity cells

status: Public on Jun 23 2017

city: Memphis

first: Quynh

last: Tran

state: TN

address: 262 Danny Thomas Place, C4029, Mail Stop 250

department: Pathology

institute: St. Jude Children's Research Hospital

summary: Tobacco exposure has been established to be a major risk factor for developing oral squamous cell carcinoma (OSCC). The purpose of this study is to identify potential biomarkers to distinguish the biological effectsof combustible tobacco products from that of non-combustible tobacco products using normal human gingival epithelial cells (HGEC), non-metastatic (101A) and metastatic (101B) OSCC cell lines.

overall_design: We performed microarray-based gene expression profiling and combined with Gene Set Enrichment Analysis (GSEA) to determine a set of genes that showed common biological pathways in human oral cavity cells when when exposed to cigarette smoke total particulate matter (TPM), whole-smoke conditioned media (WS-CM), smokeless tobacco extract in complete artificial saliva (ST/CAS), or nicotine (NIC) alone.

first: G

middle: L

last: Prasad


title: Expression data from liver of obese patients

status: Public on Jul 11 2017

city: Lille

first: Lefebvre

last: Philippe

address: Bld Pr Jules Leclerc

institute: Inserm

summary:
Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of histological findings, from simple steatosis to steatohepatitis (NASH), the latter presenting a higher risk of cardiovascular and kidney diseases, type 2 diabetes and end-stage liver disease. NAFLD is seen as the hepatic manifestation of the metabolic syndrome and affects up to 70-80% of obese patients. There are currently no approved pharmacological therapies for NASH, thus the only option is lifestyle intervention or bariatric surgery in order to lose weight and to improve insulin resistance. Although surgical intervention has allowed collections of liver biopsies, transcriptomic data from livers are still scarce and especially follow-up data to evaluate the impact of weight loss intervention on the liver. Therefore we studied hepatic transcriptomic data in a large cohort of obese patients assessed for presence of NASH at baseline and 1 year follow-up.
Patients visiting the obesity clinic of the Antwerp University Hospital for a problem of being overweight (BMI above 25 to 29.9 kg/m²) or obese (BMI above 30 kg/m²) were prospectively recruited and underwent a hepatic work-up. Patients were excluded from further analysis in case of significant alcohol consumption (>20 g/day), history of bariatric surgery, diagnosis of another liver disease, pre-existing diabetes. Patients who were, however, diagnosed with de novo diabetes at baseline or at follow-up were not excluded. If NAFLD was suspected, liver biopsy was proposed. For patients undergoing bariatric surgery (BS), a liver biopsy was proposed regardless of the criteria. Patients were reassessed after 1 year. Liver biopsy was performed percutaneously (16G Menghini) or peri-operatively (14G Tru-Cut). The different histological features of NAFLD were assessed using the NASH Clinical Research Network (NASH CRN) Scoring System. The presence of NASH was defined according to Chalasani et al. necessitating the combined presence of steatosis, ballooning and lobular inflammation.

overall_design: Microarray data were obtained for 152 patients at baseline (44 no NASH, 104 NASH, 4 undefined) and 79 patients (54 no NASH, 22 NASH, 3 undefined) at 1 year follow-up (38 diet restriction [Diet], 41 bariatric surgery [BS]). When paired (baseline - follow-up) samples were available, the number in brackets in Sample name indicates the baseline number of the same patient.

first: Sven

last: Francque

first: An

last: Verrijken

first: Luc

last: Van Gaal

first: Philippe

last: Lefebvre

first: Bart

last: Staels


title: EWS-FLI1 represses Rho-actin signaling via MRTFB/YAP-1/TEAD perturbation in Ewing Sarcoma [Affymetrix]

status: Public on Jul 06 2017

city: Vienna

first: Maximilian

last: Kauer

address: Zimmermannplatz 10

department: Molecular Biology

country: Austria

institute: CCRI, St.Anna Children Cancer Research Institute

summary: Ewing Sarcoma (EwS) is a EWS-FLI1- fusion driven pediatric bone cancer with high metastatic potential. Cellular plasticity, typically regulated via the Rho-pathway, is a prerequisite for metastasis initiation. Here we interrogated the role of the Rho transcriptional effectors MRTFA/B in EwS. We find MRTFB transcriptional function strongly repressed by EWS-FLI1. Under EWS-FLI1-low (knock-down) conditions, MRTFB is activated and antagonizes global EWS-FLI1-dependent transcription. Furthermore, ChIP-Seq revealed strong overlaps in MRTFB and EWS-FLI1 chromatin occupation, especially for EWS-FLI1 suppressed-(anticorrelated) genes. Enrichment of TEAD binding motifs in these shared genomic binding regions, and overlapping transcriptional footprints of MRTFB and TEAD1-4 perturbation led us to propose synergy between MRTFB and TEAD in the regulation of EWS-FLI1 suppressed-anticorrelated genes. Finally, we find F-actin assembly to be already perturbed in our EwS model, F-actin polymerization is perturbed by EWS-FLI1 in our model cell line, however,but pharmacological inhibition of actin polymerization still reduced expression serum-induced expression of MRTFB/YAP-1/TEAD target genes. In summary our data support a model of indirect and direct EWS-FLI1-driven perturbation of MRTFB/YAP-1/TEAD target gene regulation .

overall_design:
combined knockdown of MRTFA, MRTFB and EWS-FLI1 in A673/TR/shEF EwS cells under serum-starved or serum-induced conditions (4 samples/replicate: 2 replicates total)
8 different conditions: starved/SI transfected with sh-NS (control) or sh-MKL1/2 (MRTFA/B) and -/+ doxycycline

first: Anna

last: Katschnig

middle: O

first: Raphaela

last: Schwentner

first: Eleni

last: Tomazou

first: Cornelia

middle: N

last: Mutz

first: Markus

last: Linder

first: Maria

last: Sibilia

first: Javier

last: Alonso

first: Dave

last: Aryee

first: Heinrich

last: Kovar


title: DNA methylation-based immune response signature improves patient diagnosis in multiple cancers (Cohort 2)

first: Martin

last: Bizet

overall_design: Bisulphite converted DNA of the 119 samples from the Cohort 2 were hybridized to the Illumina Infinium 450k Human Methylation Beadchip

first: Jana

last: Jeschke

first: Christine

last: Desmedt

first: Emilie

last: Calonne

first: Sarah

last: Dedeurwaerder

first: Soizic

last: Garaud

first: Alexander

last: Koch

first: Denis

last: Larsimont

first: Roberto

last: Salgado

first: Gert

last: Van den Eynden

first: Karen

last: Willard Gallo

first: Gianluca

last: Bontempi

first: Matthieu

last: Defrance

first: Christos

last: Sotiriou

first: François

last: Fuks


title: Gene expression data from lymphoblastoid cell lines from patients with bipolar disorder

city: Paris

first: Jeverson

last: Moreira

address: 4 Avenue de l'Observatoire

institute: INSERM

summary:
Bipolar disorder (BD) (1% of the general population) is a major affective disorder characterized by recurrent manic and depressive episodes and associated with considerable burden and costs. Lithium (Li) is the first line treatment for relapse prevention in bipolar disorders with many patients who remain asymptomatic for several years (even decades). In addition, it is the only psychoactive drug that has demonstrated efficacy in suicide prevention. However a large proportion of patients is experiencing very high relapse rates (overall between 70 and 80% relapse, 2 years after a major episode).  Li mechanism of action is rather complex and still not fully understood despite extensive studies. In order to explore potential lithium effects on global gene and miRNAs expression, we initiated a study in cell-lines from excellent responders (ER) and non-responders (NR) bipolar patients
Briefly, long-term treatment response to lithium was evaluated using a validated scale “Retrospective Criteria of Long-Term Treatment Response in Research Subjects with Bipolar Disorder” , also known as the Alda scale. In our sample we analyzed dichotomous phenotypes for lithium response:  patients with total score (TS) higher or equal to 7, characterized as ER; and  patients with TS lower than 2, characterized as NR according to the literature.

overall_design: The study was performed in lymphoblastoid cell-lines (LCL) form BD patients recruited among French Centre Expert Bipolaire Network. LCLs from ER (n=4) and NR (n=4) were incubated for 4 days with or without LiCl (1mM) and mRNA profiling using Affymetrix™ microarrays was performed.

first: Cindie

last: Courtin

first: Nicolas

last: Cagnard

first: Pierre

middle: A

last: Geoffroy

first: Emmanuel

last: Curis

first: Bellivier

last: Frank

first: Cynthia

last: Marie-Claire


title: Genome-wide DNA methylation profiling of prostate specimens from a clinical trial of genistein supplementation prior to prostatectomy.

city: Atlanta

first: Carlos

last: Moreno

state: GA

address: Michael Street

department: Pathology & Laboratory Medicine

country: USA

institute: Emory University

summary: To identify molecular effects of genistein on DNA methylation in prostate cancer, we compared DNA methylation profiles of genistein-treated tumors with placebo-treated samples. There were 156 probes with significantly increased methylation in placebo-treated cases versus normal tissues that were not significant between genistein-treated cases and normal tissues, suggesting that genistein may have had some demethylation effects. These 156 probes corresponded to at least 92 separate genes including ADCY4, ALOX12, HAAO, LRRC4, NEU1, RAPGEFL1, and WNT7B.These findings highlight the effects of genistein on global changes in DNA methylation in prostate cancer and its effects on molecular pathways involved in prostate tumorigenesis.

overall_design: We analyzed prostate tissue samples from a clinical trial, which was a randomized, placebo-controlled, double-blind Phase 2 study on Norwegian patients with localized prostate cancer who received 30 mg synthetic genistein or placebo capsules daily for 3-6 weeks before radical prostatectomy. We investigated the DNA methylation levels of prostate tumor samples from 10 patients who received genistein and 10 patients who received placebo. Four adjacent normal prostate tissue samples were also analyzed.

first: Aud

last: Svindland


title: Comprehensive Analysis of the DNA Methylome of Human Cutaneous Melanoma

city: L'Hospitalet del Llobregat

first: Sebastian

last: Moran

state: Barcelona

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

department: PEBC

institute: IDIBELL

type: Genome variation profiling by genome tiling array

summary: Novel screening techniques are allowing the depiction of the portraits of molecular alterations across cancer types, enabling a better understanding of the progression mechanisms and providing new therapeutic targets. Here, we performed an unbiased genome-wide DNA methylation analysis to interrogate the epigenetic events characterizing melanoma progression and prognosis, on a discovery cohort of clinical specimens. Our data underscores the importance of epigenetic regulation in triggering metastatic dissemination through the inactivation of central cancer-related pathways. Inactivation of cell-adhesion and differentiation programs unleashes malignant dissemination, and subsequent activation of inflammatory and immune system programs impairs anti-tumoral defense pathways. Moreover, we identify several markers of tumor progression previously unrelated with melanoma, and determined a survival prognostic signature with potential clinical applicability. All findings were validated in independent clinical cohorts and cross-correlated with publicly available databases, highlighting the relevance of the identified DNA methylation alterations for melanoma progression.

overall_design: Three different cancer types Nevi, metastatic melanoma, primary melanoma

first: Miguel

last: Vizoso

first: Jasper

last: Wouters

first: Manel

last: Esteller


title: Prostate specimens from a clinical trial of genistein supplementation prior to prostatectomy

type:
Expression profiling by array
Methylation profiling by array

overall_design: Refer to individual Series


title: Acquired resistance with epigenetic alterations under long-term anti-angiogenic therapy for hepatocellular carcinoma

first: Kaoru

last: Mogushi

address: 2-1-1 Hongo

department: Intractable Disease Research Center

institute: Juntendo University

summary: Anti-angiogenic therapy is initially effective for several solid tumors including hepatocellular carcinoma (HCC); however, they finally relapse and progress, resulting in poor prognosis. We here established in vivo drug-tolerant subclones of human HCC cells by long-term treatment with vascular endothelial growth factor receptor (VEGFR) inhibitor and serial transplantation in immunocompromised mice (total 12 months), and then compared them with the parental cells in molecular and biological features. Gene expression profiles elucidated a G-actin monomer binding protein thymosin β 4 (Tβ4) as one of the genes enriched in the resistant cancer cells relative to the initially sensitive ones. Highlighting epigenetic alterations involved in drug resistance, we revealed that Tβ4 could be aberrantly expressed following demethylation of DNA and active modification of histone H3 at the promoter region. Ectopic overexpression of Tβ4 in HCC cells could significantly enhance sphere-forming capacities and infiltrating phenotypes in vitro, and promote growth of tumors refractory to the VEGFR mutltikinase inhibitor sorafenib in vivo. Clinically, sorafenib failed to improve the progression-free survival in patients with Tβ4-high HCC, indicating that Tβ4 expression could be available as a surrogate marker of susceptibility to this drug. This study suggests that Tβ4 expression triggered by epigenetic alterations could contribute to the development of resistance to anti-angiogenic therapy by the acquisition of stemness, and that epigenetic control might be one of the key targets to regulate the resistance in HCC.

overall_design: The human HCC cell line HuH7 was obtained from the Human Science Research Resources Bank (Osaka, Japan). Microarray analysis was performed to compare gene expression patterns between the parental (HuH7-F0) and drug-resistant cells (HuH7-F6 and -F12). The expression levels of 119 genes were more than four-fold upregulated in HuH7-F6 cells while those of 2199 genes in HuH7-F12.

first: Yoshiteru

last: Ohata

first: Shu

last: Shimada

first: Yoshimitsu

last: Akiyama

first: Keisuke

last: Nakao

first: Satoshi

last: Matsumura

first: Arihiro

last: Aihara

first: Yusuke

last: Mitsunori

first: Daisuke

last: Ban

first: Takanori

last: Ochiai

first: Atsushi

last: Kudo

first: Shigeki

last: Arii

first: Minoru

last: Tanabe

first: Shinji

last: Tanaka


title: Gene expression of MYB wild type and MYB knockdown myeloproliferative K11bL cells

status: Public on Jun 19 2017

city: Durham

first: Wenbin

last: Wei

address: Stockton Road

department: Biosciences

country: United Kingdom

institute: Durham University

summary:
Low levels of MYB promote the development of myeloproliferative neoplasm (MPN). The cell type identified that can transplant the MPN phenotype has been identified as expressing KIT, CD11b and low levels of lineage markers (K11bL).
We sought to identify changes in gene expression between wild type and MYB knockdown K11bL cells to identify potential targets of MYB that play a role in the establishment of MPN.

overall_design: 4 week old male wild type and MYB knockdown mice (three mice per group) were sacrificed and Kit+CD11b+Lin-Low (K11bL) cells were sorted by FACS from their bone marrow. RNA was extracted and hybridised on Affymetrix microarrays.

first: Mary

last: Clarke

first: Giacomo

last: Volpe

first: Lozan

last: Sheriff

first: Carl

last: Ward

first: Stephanie

last: Dumon

first: Paloma

last: Garcia

first: Jon

last: Frampton


title: Expression data of runners participating in an ultra-marathon trail

city: Barcelona

first: Alexandre

last: Perera

address: Pau Gargallo 5

department: ESAII

institute: Universitat Politecnica de Catalunya

summary:
An ultra-marathon trail (UMT) represents a significant physical and psychological effort. However, little is known about the gene expression response to an UMT although this approach has been explored in shorter races.
The objective is to identify the affected pathways in response to an 82km UMT considering a genome-wide analysis. Such response is interpreted as a global effect and as a sum of independent sources identified through an Independent Component Analysis.

overall_design: Peripheral blood samples were extracted from 16 runners before and after their participation (12 out of the initial 16) in the Cavalls del Vent ultra trail (2012 edition). RNA was isolated from them and hybridized on Affymetrix microarrays.

first: Maria

last: Maqueda

first: Emma

last: Roca

first: Daniel

last: Brotons

first: Jose

middle: M

last: Soria


title: Xenobiotic transporter gene expression in isolated lactating and non-lactating human mammary epithelial cells

city: Pittsburgh

first: Philip

middle: E.

last: Empey

state: PA

address: 3501 Terrace Street

department: Pharmacy & Therapeutics

institute: University of Pittsburgh School of Pharmacy

summary:
Despite the documented benefits of breastfeeding and major governmental advocacy efforts, a paucity of data exists regarding the transfer of most drugs into breast milk. Passive diffusion governs the extent of accumulation for most drugs and the exposure risk can therefore be predicted using mathematical models. However, examples of xenobiotic accumulation into breast milk well above that predicted by passive diffusion have been documented and attributed to drug transport.  A thorough evaluation of the expression of xenobiotic transporters in mammary epithelial cells (MECs), the cells that form the anatomical barrier between maternal serum and breastmilk, during lactation is necessary to determine the drugs for which an active transport mechanism governs transfer into breast milk and to improve predictive models.
We used microarrays to evaluate gene expression in human mammary epithelial cells and identified xenobiotic trasnporter genes that were upregulated during lactation.

overall_design: Mammary epithelial cells were isolated from breast milk provided by nursing women (lactating; n=3) and from surgical breast specimens provided by women undergoing reduction mammoplasty (nonlactating controls; n=3) using fluorescence-activated cell sorting (FACS).   RNA was extracted from this highly purified (>99%) cell population and hybridized on Affymetrix microarrays.

first: Patrick

last: McNamara


title: Molecular subtyping of Triple negative Breast Cancer from Taiwanese

status: Public on Jun 13 2017

city: Taipei City

first: Yun-Lin

last: Wang

address: No.201, Sec. 2, Shipai Rd., Beitou District

country: Taiwan

institute: Taipei Veterans General Hospital

summary: 'Precision medicine' is a concept that by utilizing modern molecular diagnostics, an effective therapy is accurately applied for each cancer patient to improve their survival rates. The aim of this study was to compare the molecular subtypes of triple negative breast cancer (TNBC) between Taiwanese and other datasets.

overall_design:
The study is designed to include GEO Datasets for nonunion (12 groups, n=1450) and Taiwanese (3 groups, n=465) female breast cancer samples, including 617 triple negative breast cancer (TNBC) samples. Our 57 samples is included in Taiwanese dataset. The GE from these datasets were acquired, normalized and cluster analyzed. In total, 1915 human breast cancer samples were included and among these samples a total of 617 TNBCs were identified.

Please note that the GEO accession numbers for the data included in the overall study are provided in the 'dataset_accns_included_in_the_study.txt'.


title: Tissue and differentiation stage specific expression of CALM/AF10 is required for leukemogenesis

city: Munich

first: Tobias

last: Herold

address: Marchioninistr. 15

department: Department of Internal Medicine III

country: Germany

institute: University Hospital Grosshadern, Ludwig-Maximilians-University (LMU)

summary: The translocation t(10,11)(p13;q14) resulting in the formation of the CALM/AF10 fusion gene is involved in various hematological malignancies including acute myeloid leukemia, T-cell acute lymphoblastic leukemia, and malignant lymphoma and is usually associated with poor prognosis. We established a knock-in mouse model allowing tissue-specific CALM/AF10 expression from the Rosa26 locus using a loxP-STOP-loxP cassette to study leukemic transformation by the CALM/AF10 fusion protein during hematopoiesis. vav-Cre induced pan-hematopoietic expression of the CALM/AF10 fusion gene led to acute leukemia with a median latency of 12 months. Leukemias were either myeloid or had myeloid feature and showed expression of the B cell marker B220. Gene expression profiling of leukemic bone marrow cells revealed the overexpression of Hoxa cluster genes and the Hox co-factor Meis1. The long latency to leukemia development suggested that additional, collaborative genetic lesions are required. We identified an average of 2 to 3 additional mutations per leukemia using whole-exome sequencing. When CALM/AF10 was expressed in the B lymphoid compartment using mb1-Cre or CD19-Cre inducer lines no leukemia development was observed. Our results indicate that CALM/AF10 needs to be expressed from the stem or early progenitor cell stage onward to permit the acquisition of additional mutations required for leukemic transformation.

overall_design: Total RNA was extracted from BM cells of leukemic (n=8) and pre-leukemic CA+/vav-Cre+ mice (n=3) and of wild type C57Bl/6 mice (n=3) and from the B cells of CA+/mb1-Cre+ mice (n=3), pre-leukemic CA+/vav-Cre+ mice (n=3) and of wild type C57Bl/6 mice (n=3) using TRIzol reagent (Life Technologies, Darmstadt, Germany). Leukemic bone marrow cells were sorted using Gr1, Mac1 and B220 antibodies, purchased from BD Biosciences and cells were sorted using BD FACSVantage SE system. cDNA was prepared using the Ambion WT expression kit (Life Technologies) and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays (Affymetrix, Santa Clara, CA, USA) for whole transcriptome microarray analysis.

first: Sayantanee

last: Dutta

last: Krause

first: Sebastian

last: Vosberg

first: Bianka

last: Ksienzyk

first: Leticia

last: Quintanilla-Fend

first: Belay

last: Tizazu

first: Stefan

last: Krebs

first: Helmut

last: Blum

first: Philipp

last: Greif

first: Marlon

middle: R

last: Schneider

first: Maik

last: Dahlhoff

first: Ursula

last: Zimber-Strobl

first: Eckhard

last: Wolf

last: Bohlander


title: Expression data from early passage UACC melanoma cell lines

city: Rockville

first: Jiyeon

last: Choi

state: Maryland

address: 9615 Medical Center Drive, Rm 3116

institute: NCI

summary: eQTL is a powerful method to detect genotype-expression correlation. To be able to identify the genes whose expression levels are correlated with melanoma-associated common variants, eQTL analysis was performed in 59 early passage melanoma cell lines

overall_design: To perform eQTL analysis, 59 early passage melanoma cell line collected through University of Arizona Cancer Center (UACC) were grown in culture and harvested at log phase. RNA was extracted using method described below.

first: Kevin

last: Brown

first: Nicholas

last: Hayward

first: Michael

last: Gartside

first: Jeffery

last: Trent

first: Stuart

last: Macgregor

first: Matthew

middle: H

last: Law


title: Identification of endometrial cancer methylation features using combined methylation analysis methods

city: Columbus

first: Ralf

last: Bundschuh

address: 191 West Woodruff Avenue

department: Department of Physics

institute: The Ohio State University

summary: This study aimed at identifying a methylation signature for a hypermethylation phenotype in endometrial cancer.  Specifically, this data set consisting of 9 primary endometrial cancer tissue samples was investigated with a Illumina Infinium 450k Human Methylation Beadchip in order to technically validate the findings from the larger MethylCap-Seq study deposited in BioProject PRJNA360573.

overall_design: Bisulfite converted DNA from the 9 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip GPL13534

middle: P

last: Trimarchi

first: Pearlly

last: Yan

first: Joanna

last: Groden

first: Paul

last: Goodfellow


title: Microarray analyses of T-ALL (COG study)

city: Albuquerque

first: Ksenia

last: Matlawska

state: NM

address: 915 Camino de Salud

department: Pediatrics

institute: University of New Mexico

summary: The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure or relapse. We used the Affymetrix U133 Plus 2.0 chip to profile 100 newly diagnosed patients who were treated in the Children's Oncology Group (COG) T-ALL AALL0434.  We performed unsupervised hierarchical clustering of 25 HOXA probe sets within the cohort of 100 T-ALL cases.  We identified a cluster of 20 cases (20%) characterized by increased expression of HOXA3, 5, 7, 9, and 10.  In samples with HOXA9/10 deregulation, the presence of specific molecular lesions were confirmed through a systematic review of cytogenetic databases, FISH and PCR testing, and by RNA sequence analysis.  Because MLL and AF10 genes rearrangements (MLL-R, AF10-R) are hallmarks of HOXA-deregulated leukemias, we sought to identify specific genes that are enriched with these genomic abnormalities.

overall_design: We performed expression profiles on 100 patients with T-ALL treated on Children's Oncology Group studies AALL0434 (100 patients). Expression profiles were obtained from patients with newly diagnosed T-ALL. This approach allowed us to perform discovery experiments related to disease progression while being blinded to outcome.


title: Gene Expression Pattern in EP300 knocked-down MCF7 cells and corresponding paclitaxel resistant derivatives

city: Zaragoza

first: Patricia

last: Sancho

state: Aragón

address: P. Isabel la Católica 1-3

department: Traslational Research Unit

country: Spain

institute: Hospital Miguel Servet IIS Aragón

summary:
EP300, a transcriptional co-activator of E-cadherin, has been recently found by our group to regulate doxorubicin resistance via by-pass of senescence and paclitaxel resistance by overcoming apoptosis in a minimally transformed mammary epithelial cells (MTMEC). Moreover, EP300 deleted MTMEC cells exhibit an multi-drug resistant (MDR) phenotype independent of P-glycoprotein (ABCB1), an efflux pump or ABC drug transporter.
This whole transcriptome array study was undertaken in order to explore the downstream targets in the EP300-mediated drug resistance, epidermal-to-mesenchymal transition and cancer stem cell phenotypes in breast cancer cell line MCF7.

overall_design: MCF7 cells were stably knocked down for EP300 by RNA interferance using short hairpins cloned into pGIPZ. Two different lentiviral shEP300 constructs were used. Stable lines were selected with puromycin. The stable lines obtained were further used to generate their corresponding paclitaxel resistant derivatives, which were also included in the study.  MCF7 cells carrying empty pGIPZ vector was used as control.

first: Muhammad

last: Asaduzzaman

first: Selina

last: Raguz

first: Ernesto

last: Yague


title: Expression in E. coli of hyper- and hypo-amyloidogenic RepA-WH1 variants

city: Madrid

first: Rafael

last: Giraldo

state: Madrid

address: C/ Ramiro de Maeztu, 9

department: Cellular & Molecular Biology

institute: CIB-CSIC

summary:
RepA-WH1 is a synthetic bacterial prionoid, i.e., a protein that aggregates as amyloid in bacteria leading to cell death
The purpose of this approach was to outline the pathways of cytotoxicity linked to RepA-WH1 expression from the set of genes induced/repressed in an Escherichia coli strain with reduced genome (MDS42)

overall_design: Transcription profiles in cells expressing the mildly-citotoxic RepA-WH1(∆N37)-mCherry aggregates were subtracted from the profiles for cells expressing the acutely-cytotoxic A31V amyloid aggregates. This approach was intended to supress the contribution from genes related to the general, non-specific pathways of the stress response to aggregation (i.e., quality control of proteostasis), thus highlighting those specific for RepA-WH1 cytotoxicity.

first: Pedro

last: Botias


title: Comparative expression of bone metastasis clones and their parent cells Chinese lung adenocarcinoma cell lines CPA-Yang1, CPA-Yang2, CPA-Yang3, SPC-A-1 and human larger cell lung cancer cell line NCI-H460 by cRNA array

status: Public on Jun 28 2017

city: Shanghai

first: Shunfang

last: Yang

address: 241 Huaihai west Road

department: Nuclear Medicine

institute: Shanghai Chest Hospital

summary: Human lung adenocarcinoma cell lines (CPA-Yang1, CPA-Yang2, CPA-Yang3, SPC-A-1) and human larger cell lung cancer cell line NCI-H460 were injected into left cardiac ventricle of nude mice for bone metastases clone, respectively. Bone metastatic lesions were detected by bone scintigraphy with 99mTc-methylene diphophonate and X ray. Removed bone metastatic lesions for cell primary culture, chromosome analysis for determine the bone metastatic cells have a characterization of unchanged humanization, in the anesthesia death mice. Through in vivo ~ in vitro selections, the bone-seeking clones 1st, 3th, 4th, 8th, 8th passage cells of CPA-Yang1, CPA-Yang2, CPA-Yang3, SPC-A-1, NCI-H460 and their parent cells were used for microarray analysis, respectively.

overall_design: Bone-seeking clones 1st, 3th, 4th, 8th, 8th passage cells of CPA-Yang1, CPA-Yang2, CPA-Yang3, SPC-A-1, NCI-H460 by in vivo ~ in vitro selections and their parent cell lines respectively expression by cRNA array. Comparative expression of these biological replicates with osteolytic, osteoblestic, mixed bone metastases and their parent cells respectively.

first: Meiping

last: Shi

first: Jie

last: Cao

first: Lanxiang

last: Zhao

first: Jianzhong

last: Su


title: Changes in gene expression upon treatment of SH-SY5Y cells to cisplatin

status: Public on Jun 12 2017

city: Düsseldorf

first: Ana-Maria

last: Florea

state: NRW

address: Moorenstr. 5

department: Neuropathology

institute: University Düsseldorf

summary: In this study we investigated the changes in mRNA expression upon treatment of SH-SY5Y cells to 10µM cisplatin for 72h.

overall_design: Three samples of parental SH-SY5Y cells and four samples of 72h treated SH-SY5Y neuro-blastoma cell line with 10µM CDDP were subjected to Affymetrix chip analyses. RNA quality was determined using the Agilent Bioanalyzer and the Eukaryote Total RNA Nano Chip (Ag-ilent Technologies, Hayward, CA, USA). The RNA integrity number (RIN) was measured as 9.9-10. The Affymetrix HuGene 2.0 ST and WT plus reagent kit (Affymetrix, Santa Clara, California, United States) was used following the provider’s recommendation with a start ma-terial of 100ng of total RNA.

first: Steffen

last: Sass


title: DNA methylation profiling in lungs tissues of smokers and patients with COPD

city: Kansas City

first: Isaac Kirubakaran

last: Sundar

state: KS

address: 3901 Rainbow Blvd.

department: Internal Medicine

institute: University of Kansas Medical Center

summary: Epigenetics changes have been shown to be affected by cigarette smoking. It is possible that cigarette smoke (CS)-mediated DNA methylation would affect several cellular and pathophysiological processes, acute exacerbations, and comorbidity in lungs of patients with chronic obstructive pulmonary disease (COPD). We sought to determine whether genome-wide lung DNA methylation profiles of smokers and patients with COPD were significantly different from non-smokers. We isolated DNA from lung tissues of patients including 8 lifelong non-smokers, 8 current smokers, and 8 patients with COPD, and subsequently analyzed the samples using the Illumina’s Infinium HumanMethylation450 BeadChip.

overall_design: We performed Genome-Wide DNA methylation analysis using lung parenchyma tissue DNA samples from Non-smokers (NS), Smokers (S) and patients with COPD (C) in 2 separate batches. In the first batch of samples, we used Sample ID# 1-4 in each of the three groups: Non-smokers (NS.1, NS.2, NS.3, NS.4), Smokers (S.1, S.2, S.3, S.4) and COPD (C.1, C.2, C.3, C.4). The second batch of samples, we used additional samples in each of the three groups (Sample ID# 5-8): Non-smokers (NS.5, NS.6, NS.7, NS.8), Smokers (S.5, S.6, S.7, S.8) and patients with COPD (C.5, C.6, C.7, C.8).

first: Isaac

first: Irfan

last: Rahman


title: MYEOV as a novel biomarker for human non-small cell lung cancer

city: Los Angeles

first: Masafumi

last: Horie

address: 2011 Zonal Ave

institute: University of Southern California

summary: To investigate the roles of MYEOV in lung cancer cell proliferation, we compared the expression profiles of A549 lung adenocarcinoma cell lines transfected with control siRNA and siMYEOV.

overall_design: We collected RNA from A549 cell lines transfected with control siRNA and siMYEOV.

first: Akira

last: Saito


title: DNA methylation analysis during neutrophilic granulopoiesis under ELF-MF exposure

city: Basel

first: Primo

last: Schär

address: Mattenstrasse 28

institute: University of Basel

summary: To address whether ELF-MF influences the epigenetic landscape in differentiating haematopoietic cells, we performed an in vitro haematopoietic differentiation under powerline-simulating ELF-MF exposure (50 Hz, 1 mT, 5’ on/10’ off) in comparison to sham exposure (50 Hz, 7 µT, 5’ on/10’ off) or no exposure. We differentiated CD34+ cells (allcells, CB008F, lot: CBC121009M) isolated from human cord blood into the neutrophilic lineage, and performed genome-wide methylation analysis at single CpG sites of CD34+ cells and day 5 progenitors, using the Illumina Infinium HumanMethylation 450 platform. Exposure to ELF MF did not significantly impact the programming of DNA methylation pattern during granulopoiesis. However, ELF MF exposure has an influence on the robustness of the epigenetic landscape during global chromatin programming of granulopoiesis. Our data suggests that ELF MF has a stochastic effect on the epigenetic landscape of individual cells.

overall_design: Bisulphite converted DNA from CD34+ cells, sham and ELF-MF exposed neutrophilic progenitors in triplicates and not-exposed neutrophilic progenitors in duplicates were hybridised to the Illumina Infinium HumanMethylation 450 Beadchip.

first: Melissa

last: Manser

first: Mohamad

last: Sater

first: Christoph

last: Schmid

first: Faiza

last: Noreen

first: Manuel

last: Murbach

first: David

last: Schurmann

last: Schar


title: Identification of FOSL1 transcriptional targets in mutant KRAS lung adenocarcinoma cells

city: Pamplona

first: Silvestre

last: Vicent

state: Outside the US or Canada

address: 55 PIO XII Ave

department: Oncology

institute: Center for Applied Medical Research (CIMA)

summary: Mutant KRAS lung adenocarcinoma cells, H2009, were depleted of FOSL1 by a specific shRNA and its transcriptome was profiled

overall_design: H2009 cells were infected with lentivirus carrying a FOSL1 or a control (GFP) shRNA for 2 days. Then, cells were selected for 3 days using 5ug/ml puromycin. After that, cells were counted and plated at a density of 600,000 cells/well (6-well plate). RNA was harvested on the following day using Trizol.


title: Social defeat effect on mice prefrontal cortex

city: bethesda

first: abdel

last: elkahloun

state: MD

address: 50 south dr

institute: nih

summary: Behavioral analysis confirmed that the 14-day social defeat sessions resulted in induction of depressive-like states measured in social interaction and light/dark tests.  The combined data show that stress-induced depressive states are associated with molecular and structural changes that demyelinate the prefrontal cortex.

overall_design: CSD and HC male mice (6 per group) were tested in the social interaction test and light/dark test to gauge mood.  One behavioral test was run per day.

first: Abdel

middle: G

last: Elkahloun

first: Michael

last: Lehmann


title: CoGAPS matrix factorization algorithm identifies AP-2alpha as a feedback mechanism from therapeutic inhibition of the EGFR network

city: Baltimore

first: Elana

middle: Judith

last: Fertig

address: 670 W. Baltimore Street, 3rd floor

department: Institute for Genome Sciences

institute: University of Maryland, Baltimore

summary: Patients with oncogene driven tumors are currently treated with targeted therapeutics such as epidermal growth factor receptor (EGFR) inhibitors. The inhibited oncogenic pathway often interacts with other signaling pathways and alters predicted therapeutic response. Genomic data from The Cancer Genome Atlas (TCGA) demonstrates pervasive molecular alterations to EGFR, MAPK, and PI3K signaling in previously untreated tumors. Therefore, this study uses bioinformatics algorithms to infer the complex pathway interactions that result from EGFR inhibitor use in cancer cells that contain these these common EGFR network genetic alterations. To do this, we modified the HaCaT keratinocyte cell line model of premalignancy to simulate cancer cells with constitutive activation of EGFR, HRAS, and PI3K in a controlled genetic background. We then measured gene expression after treating modified HaCaT cells with three EGFR targeted agents (gefitinib, afatinib, and cetuximab) for 24 hours.

overall_design: The study has a total of 96 samples in 4 experimental batches. 89 of the samples are from HaCaT constructs with a control empty vector (HaCaT-Mock), overexpression of EGFR (HaCaT-Mock), of PIK3CA-HR (HaCaT-PIK3CA), and of HRASVal12D (HaCaT-HRAS) treated with siEGFR, afatinib, gefitinib, cetuximab, or appropriate controls. All experiments are run in triplicate unless otherwise specified. In addition, the design includes 1 FaDu cell line, 1 HaCaT parental cell line, 2 UMSCC1, and 2 UMSCC25 cell lines to facilitate normalization across batches.

middle: J

first: Christine

last: Chung


title: HNSCC cell lines for CoGAPS matrix factorization algorithm identifies AP-2alpha as a feedback mechanism from therapeutic inhibition of the EGFR network

summary: To determine the expression AP2-alpha target genes,  global gene expression of 7 HNSCC cell lines with and without cetuximab treatment (100 nM, 24 hrs) and the HaCaT keratinocyte cell line was performed.

overall_design: 42 total RNA collected from a panel of 7 HNSCC cell lines (control and cetuximab treated) and the HaCaT keratinocyte cell line.  Cell surival rates after 7 days with cetuximab treatment are assessed using matrigel colony formation assays.

first: C

first: E


title: Molecular signatures associated with cognitive deficits in schizophrenia: a study of biopsied olfactory neural epithelium

last: Sawa

address: 600 North Wolfe St.

department: Psychiatry and Behavioral Sciences

institute: Johns Hopkins University School of Medicine

summary:
Cognitive deficit is a key feature of schizophrenia (SZ) and determines functional outcome. Nonetheless, molecular signatures underlying the deficit in neuronal tissues are not well understood.
We performed microarray analysis of olfactory epithelium (OE) tissues from SZ and control subjects with their neuropsychological assessment data. Furthermore, we examined gene expression profiles of lymphoblasts for the molecular signatures identified in the OE tissues .

overall_design: We used the following 3 sample sets for the microarray analysis: A) microdisected samples enriched for neuronal layers of OE tissues, B) paired lymphoblast samples , and C) non-paired lymphoblast samples. The first and second sampe sets (A and B) were derived from the same participants, while the third sample set (C) was from participants from another independent cohort.

first: Yasue

last: Horiuchi

first: Mari

last: Kondo

first: Kinya

last: Okada

first: Yoichiro

last: Takayanagi

first: Teppei

last: Tanaka

first: Tiffany

last: Ho

first: Mark

last: Varvaris

first: Katsunori

last: Tajinda

first: Hideki

last: Hiyama

first: Keni

last: Ni

first: Carlo

last: Colantuoni

last: Schretlen

first: Nicola

last: Cascella

first: Jonathan

last: Pevsner

first: Koko

last: Ishizuka


title: Branched-chain amino acids prevent hepatic fibrosis and development of hepatocellular carcinoma in a non-alcoholic steatohepatitis mouse model

city: Kanazawa

first: Masao

last: Honda

address: Takara-Machi 13-1

department: Gastroenterology

institute: Kanazawa University

summary:
BCAA were administered to atherogenic and high-fat (Ath & HF) diet-induced nonalcoholic steatohepatitis (NASH) model mice and platelet-derived growth factor C transgenic mice (Pdgf-c Tg). Liver histology, tumor incidence, and gene expression profiles were evaluated.
BCAA supplementation improved hepatic steatosis, inflammation, fibrosis, and tumors in the NASH mouse model, possibly through the modification of mTORC1 signaling.

overall_design: Using the Ath & HF diet mouse model, we investigated the effects of BCAA on steatosis, inflammation, fibrosis, and hepatocarcinogenesis in NASH.

first: Kai

last: Takegoshi

first: Hikari

first: Naoto

last: Matsuzawa-Nagata

first: Jean

middle: S

last: Campbell

first: Riuta

last: Takabatake

first: Tetsuro

last: Shimakami

first: Takayoshi

last: Shirasaki

first: Yoshio

last: Sakai

first: Taro

last: Yamashita

first: Toshinari

last: Takamura

first: Takuji

first: Shuichi

last: Kaneko


title: Expression data from AML1-ETO9a mouse primary leukemia blast

status: Public on Jun 20 2017

city: Heidelberg

first: Christian

last: Rohde

address: Im Neuenheimer Feld 410

institute: Heidelberg University

summary:
Microarray gene profilling indentified snoRNAs are downstream target of Amino Enhancer of Split (AES) and are essential for AML1-ETO9a induced leukemia.
Amino Enhancer of Split (Aes) is strongly induced by leukemia oncogenes AML1-ETO, PML-RARα and PLZF-RARα. With a conditional AES knockout mouse model we showed that AES is essential for AML1-ETO9a indeced leukemia. We performed gene expression microarray using mouse primary AML1-ETO9a transformed AES wildtype and knockout and showed that snoRNAs were downregulated in AES knockout cells. We found that SnoRNA induction is a common mechanism shared by distinct oncogenes including AML1-ETO, MYC and MLL-AF9. Suppression of C/D box snoRNA complexes or deletion of several single C/D box snoRNAs inhibit clonogenic growth of leukemia cells. These findings suggest that enhancement of snoRNA levels is a critical mechanism of leukemic transformation.

overall_design: AES wildtype or knockout AML1-ETO9a transformed cells in triplicates

first: Fengbiao

last: Zhou

first: Carsten

last: Müller-Tidow


title: Breast cancer risk factors are associated with DNA methylation in non-diseased breast tissue independent of cell type

city: Hanover

first: Kevin

last: Johnson

state: NH

address: 72 College Street

department: Epidemiology

institute: Geisel School of Medicine at Dartmouth College

summary: The underlying biology through which established breast cancer risk factors contribute to disease risk is not well characterized. One key risk factor for breast cancer is age, and age-related DNA methylation alterations may contribute to increased risk of disease. Here we assessed normal breast tissues and tested the relation of DNA methylation with known breast cancer risk factors. Cancer-free women donated breast tissue biopsy specimens through the Susan G. Komen Foundation and provided detailed risk factor data (n=100). Bisulfite modified DNA was profiled for DNA methylation genome-wide using the Infinium 450K DNA methylation array. We tested the relation of known breast cancer risk factors such as age, BMI, parity, and family history of disease with DNA methylation adjusted for variation in cell type proportions using a novel cellular mixture deconvolution algorithm. We identified 787 CpGs that exhibited significant (FDR adjusted, q-value < 0.01) differential DNA methylation associated with subject age, but not with other breast cancer risk factors. We observed an enrichment among the risk factor-related CpGs for Polycomb group target genes (Fisher’s Exact test, P = 1.74E-06), and breast myoepithelial cell enhancer regions (H3K4me1; Fisher’s Exact test, P = 7.1E-20). We validated our risk factor-related findings in two independent populations of normal breast tissue (n=18 and n=97). In addition, age-related CpGs were further deregulated in both pre-invasive (DCIS, n=40) and invasive breast cancers (TCGA, n=731). Overall, our results suggest that the breast cancer risk factor age contributes to epigenetic dysregulation in normal breast tissue that exhibit progressive changes in cancer.

overall_design: Bisulfite converted DNA from 100 healthy breast biopsy samples that were hybridised to the Illumina Infinium 450K Human Methylation beadchip

middle: C


title: Endometrial methylome of healthy women during the transition from pre-receptive to receptive phase

city: Tartu

first: Triin

last: Laisk-Podar

address: Puusepa 8

department: Obstetrics and Gynecology

country: Estonia

institute: University of Tartu

summary: The inner uterine lining (endometrium) has been shown to have a distinct methylation pattern that changes throughout the menstrual cycle. However, not much is known about how the endometrial methylome affects endometrial receptivity to implanting embryo in the second half of the menstrual cycle. The aim of the present study was to use genome-wide technologies and a paired study design to characterize the endometrial methylome in pre-receptive and receptive endometrium sampled from 17 healthy women within the same menstrual cycle.

overall_design: Infinium HumanMethylation 450K BeadChip arrays were used to explore DNA methylation profiles of paired endometrial tissue from early- and midsecretory phase of 17 healthy women

first: Viktorija

last: Kukushkina

first: Vijayachitra

last: Modhukur

first: Marina

last: Suhorutshenko

first: Maire

last: Peters

first: Reedik

last: Mägi

first: Nilufer

last: Rahmioglu

first: Agne

last: Velthut-Meikas

first: Signe

last: Altmäe

first: Francisco

last: Esteban

first: Jaak

last: Vilo

first: Krina

last: Zondervan

first: Andres

last: Salumets


title: Development of complete personalized treatment plans for early stage colorectal cancer patients

status: Public on Jun 10 2017

city: WARREN

first: nien

last: wei

state: NJ

address: 9 northridge way

institute: Auspex Diagnostics

summary:
593 FFPE colorectal cancer samples were used to generate three prediction models: Recurrence prediction, 5FU efficacy prediction, and FOLFOX efficacy prediction
The recurrence prediction study has 235 samples , 5FU efficacy prediction study has 192 samples, FOLFOX had 166 samples

overall_design: Microarray used to study gene expression difference to generate prediciton models

first: Nien-chih

last: Wei