title: In silico characterization of miRNA and long non-coding RNA interplay in multiple myeloma (95 MM miRNA data sets)

overall_design: We searched for putative significant correlation between lncRNAs and miRNAs expression level in paired samples, with the support of target prediction analysis. Wilcoxon rank-sum test was applied using standard functions in R base package. The Benjamini-Hochberg method was applied for multiple testing correction. miRNA targets custom predictions were obtained for lncRNA sequences by merging the results of two different algorithms: RNA-22 version 2.0 prediction algorithm and miRanda , which both allow customizing input sequences and parameters. The RNA-22 perl script was run on the combination of the 459 miRNA and 1546 (number of different transcripts corresponding to 235 lncRNAs) lncRNA FASTA sequences selected as relevant among all the miRNAs and lncRNAs respectively detected by the arrays. Default sensitivity/specificity ratio of 1.032 was chosen, provided a minimum seed size of 7 bases with only one mismatch exception, a minimum number of 12 paired-up bases in heteroduplex with -12 Kcal/mol maximum folding energy, and no more than one G-U wobble in the seed region. The miRanda algorithm has been run under default conditions, without any a-priori restrictions on score, energy and trimming parameters.


title: In silico characterization of miRNA and long non-coding RNA interplay in multiple myeloma

status: Public on Feb 10 2017

city: MILAN

first: Luca

last: Agnelli

address: Venezian 1

department: Department of Advanced Diagnostics

country: Italy

institute: IRCCS Istituto Nazionale dei Tumori

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

platform_organism:
Homo sapiens
synthetic construct

overall_design: Refer to individual Series


title: microRNA data from high-fat diet fed mice with and without exercise

status: Public on Feb 09 2017

city: Shanghai

first: Yihua

last: Bei

address: 133 Nanchen Road

department: School of Life Science

country: China

institute: Shanghai University

summary:
Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle. Exercise is known to be beneficial for NAFLD treatment. Recent studies have shown the critical involvement of microRNA in NAFLD. However, it is unclear whether exercise could prevent NAFLD via miRNA targeting.
We used microarrays to examine microRNA profiles in high-fat diet fed mice with and without exercise in comparison to normal diet fed mice.

overall_design: Mouse livers from normal diet fed mice (group C, n=5), high-fat diet fed mice without exercise (group HF, n=5), and high-fat diet fed mice with exercise (groupe HE, n=5) were used for RNA extraction and hybridization on Affymetrix miRNA 3.0.

first: Junjie

last: Xiao


title: pp71-stimulated genes in U87 stable cells

city: Newark

first: Saleena

last: Ghanny

address: 185 South Orange Ave

country: USA

institute: Rutgers University

summary:
Glioblastoma multiforme (GBM) is a highly malignant primary central nervous neoplasm characterized by tumor cell invasion, robust angiogenesis, and a mean survival of 15 months.  Human cytomegalovirus (HCMV) infection is present in > 90% of GBMs, although the role the virus plays in GBM pathogenesis is unclear.   We report here that a majority of human GBM tumors express HCMV pp71, which has previously been found to promote cell cycle progression and viral replication, and that pp71 is expressed preferentially within the CD133+ cancer stem cell-like subpopulation. Overexpression of pp71 in adult neural precursor cells (NPCs) resulted in a dramatic induction of stem cell factor (SCF) gene expression, which has been identified as an important pro-angiogenic factor in GBM.
We further demonstrate that pp71 induces a pro-inflammatory response via NFΚB activation, which drives SCF upregulation.  In summary, we show for the first time that HCMV pp71 is expressed in a majority of human GBMs and that pp71 activates NFΚB signaling, resulting in increased expression and secretion of SCF, an important paracrine modulator of GBM angiogenesis.

overall_design: U87 GBM cells were transduced with either pLXSN-pp71 or pLXSN empty vector retroviruses and selected with G418 for selection of stable cells.  Total RNA was isolated from both cell lines and hybridized to Affymetric microarrays. The fold change in expression for all cellular genes in pp71 stable cell lines versus the empty vector control was then calculated.

first: Lisa

middle: A

last: Matlaf

first: Liliana

last: Soroceanu


title: Impact of laminin α1 chain on colorectal cancer cells in culture

status: Public on Feb 08 2017

city: Strasbourg

first: Olivier

last: Lefebvre

address: 3 Avenue Molière

country: France

institute: Inserm

summary: Expression analysis of control HT29 or Laminin α1 expressing HT29 cells in culture.

overall_design: RNA from 3 independents cell culture passages per group were analyzed.


title: Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [4 weeks]

city: Torrance

first: Robert

last: Gelfand

state: CA

address: 1124 W. Carson St

department: surgery

institute: LABiomed at Harbor UCLA,  and Charles Drew Univ

summary:
Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are  unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells.
MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for either 1 week or 4 weeks. Total RNA samples were assayed for gene expression and for microRNA expression.

overall_design: Cells were cultured in DMEM/F12 in the presence of horse serum and growth factors. RNA was extracted using either the RNeasy Micro Plus kit for DNA microarray assays, or with the miRVana kit for microRNA analysis. Gene expression values were collected for control, ethanol treated, and acetaldehyde treated cells. In addition, MCF12A cells subjected to 4 week exposure with 2.5 mM ethanol were grown in soft agar to test for anchorage independence. A cellular clone of anchorage independent cells was isolated and grown as a monolayer culture, and DNA microarray analysis and microRNA analysis were carried out.

first: Dolores

last: Vernet

first: Kevin

middle: K

last: Bruhn

first: Jaydutt

last: Vadgama

first: Nestor

middle: F

last: Gonzalez-Cadavid


title: Gene expression analysis of MCF12A human breast cultures exposed to ethanol or acetaldehyde [1 week]


title: Gene expression of prostate tumor tissues treated with leuprolide acetate plus ipilimumab

city: Houston

first: Hao

last: Zhao

state: TX

address: 7455 Fannin St

institute: The University of Texas MD Anderson Cancer Center

summary: To study the immune response of the prostate tumor tissues after the leuprolide acetate plus ipilimumab, we compared the gene expression of 6 post-therapy with 3 pre-therapy samples. We identified 690 differential expressed genes (DEGs).  Pathway analysis showed that these genes are associated with critical immune pathways such as CTLA4 signaling, antigen presenting etc.

overall_design: We compared 6 post-therapy prostate tumor with 3 pre-therapy samples.

first: Padmanee

last: Sharma

first: Jianjun

last: Gao

first: Hong

last: Chen


title: Total blood monocyte gene expression from neovascular age-related macular degeneration patients and age-matched controls

city: Jerusalem

first: Michelle

last: Grunin

address: Hadassah Ein Kerem Medical Center

department: Ophthalmology

country: Israel

institute: Hadassah-Hebrew University Medical Center

summary: Mononuclear phagocytes (MPs), including monocytes and macrophages, play complex roles in the pathogenesis of age-related macular degeneration (AMD). We aimed to perform global transcriptome analysis on monocytes from AMD patients to obtain additional insight to the role of MPs in AMD. Peripheral blood was taken from treatment-naïve neovascular AMD (nvAMD) patients (n=14), and age-matched controls (n=15). Peripheral blood mononuclear cells (PBMCs) were separated and monocytes were isolated via negative selection. Gene expression was evaluated with Affymetrix Gene1.0 ST microarrays. Statistical/bioinformatics analysis was performed using open sourceware programs.

overall_design: 14 neovascular age-related macular degeneration patients, 15 age-matched controls, peripheral blood monocytes were extracted via histopaque separation and negative selection using magnetic beads. Total monocyte RNA was extracted using tri-reagent, and cleaned using columns. RIN was evaluated using Agilent Bioanalyzer

first: Itay

last: Chowers


title: Affymetrix Cytoscan HD 2,600K SNP array data for 9 GISTs

status: Public on Feb 03 2017

city: Boston

first: Jonathan

last: Fletcher

state: MA

address: 75 Francis Street

department: Pathology

institute: Brigham and Women's Hospital and Harvard Medical School

summary: KIT, PDGFRA, NF1, and SDH mutations are alternate initiating events, fostering hyperplasia in gastrointestinal stromal tumors (GISTs), and additional genetic alterations are required for progression to malignancy. The most frequent secondary alteration, demonstrated in ~70% of GISTs, is chromosome 14q deletion. Here we report hemizygous or homozygous inactivating mutations of the chromosome 14q MAX gene in 16 of 76 GISTs (21%). We find MAX mutations in 17% and 50% of sporadic and NF1-syndromic GISTs, respectively, and we find loss of MAX protein expression in 48% and 90% of sporadic and NF1-syndromic GISTs, and in 3 of 8 micro GISTs, which are early GISTs. MAX genomic inactivation is associated with p16 silencing in the absence of p16 coding sequence deletion, and MAX induction restores p16 expression and inhibits GIST proliferation. Hence, MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early GISTs.

overall_design: High molecular weight genomic DNA was isolated from 9 GISTs using QIAamp DNA Mini Kit (Qiagen, Valencia, CA, USA) and analyzed by Affymetrix Cytoscan HD 2,600K-SNP array (Affymetrix, Santa Clara, CA, USA) with Affymetrix Chromosome Analysis Suite 2.0.

first: Inga-Marie

last: Schaefer

first: Adrian

last: Marino-Enriquez


title: MicroRNA data in the mouse liver at 48 hrs versus 0 hr post 70% partial hepatectomy

first: Yihua

last: Bei

summary:
MicroRNAs have been reported to control liver regeneration though the underlying mechanisms remain largely unclear.
We used microarrays to examine microRNA profiles in the mouse liver at 48 hrs versus 0 hr post 70% partial hepatectomy.

overall_design: Mice livers at 48 hrs post partial hepatectomy (group PH-48h, n=4) and mice livers at 0 hr post partial hepatectomy (group PH-0h, n=4) were used for RNA extraction and hybridization on Affymetrix miRNA 3.0.

first: Yang

last: Song

first: Junjie

last: Xiao

first: Changqing

last: Yang


title: Gene expression array of neuroblastoma human tumors in NSG upon treatment with CXCR4 inhibitor BL8040

city: Modiin

first: Shiri

last: Klein

address: Migdal Halevanon 7

department: Gene Therapy

institute: Hebrew University

summary: Purpose: CXCR4 plays a role in neuroblastoma development. The goal of this study is to search for pathways controlled by CXCR4 which contribute to neuroblastoma tumor development. Methods: Human SK-N-BE(2) cells were orthotopically injected into the left adrenal gland of 6-8 weeks old mice. During treatment protocol mice were monitored for 21 days. As of day 7, mice were treated with a daily injection of  the CXCR4 inhibitor BL-8040 (400µg) for 14 consecutive days. Tumor RNA was generated from 3 mice in each group using Trizol. Amplified and biotinylated sense-strand DNA were prepared according to the standard Affymetrix protocol from 200ng total RNA (Expression Analysis Technical Manual, 2005, Affymetrix). Following fragmentation, 5.5µg of Biotinylated ssDNA were hybridized for 17 hr at 45ºC on GeneChip Human Gene 1.0 ST Array. GeneChip were washed and stained in the Affymetrix Fluidic Station 450. GeneChips were scanned using Affymetrix GeneChip Scanner 3000. Results: 98 genes were differentially expressed in the treated tumors. Conclusions: Inhibition of CXCR4 prevented tumor growth and reduced survival of tumor cells by significantly altering several apoptotic and cell cycle signaling pathways.

overall_design: NSG mice injected with SK-N-BE(2) cells to the adrenal gland. One week following cell injection mice were treated with BL-8040 for 14 consecutive days. Tumors were harvested and RNA purified from 3 control and treated mice were analyzed using the GeneChip Human Gene 1.0 ST Array and scanned with the  Affymetrix GeneChip scanner 3000.

first: Amnon

last: Peled


title: Intra and inter-tumoral heterogeneity in syndromic neuroendocrine tumors

status: Public on Feb 02 2017

city: Melbourne

first: Aidan

middle: John

last: Flynn

state: Victoria

address: 305 Grattan St

department: Research

country: Australia

institute: Peter MacCallum Cancer Center

type: Genome binding/occupancy profiling by SNP array

summary: Hereditary endocrine neoplasias, including phaeochromocytoma/paraganglioma (PPGL) and medullary thyroid cancer (MTC), are caused by autosomal dominant mutations in a multitude of familial cancer genes. A common feature of these diseases is the presentation of multiple primary tumours or multifocal disease representing independent tumour clones that have arisen from the same initiating genetic lesion but have undergone independent clonal evolution. Such tumours provide a unique opportunity to discover common co-operative changes required for tumorigenesis while controlling for the genetic background of the individual. We performed an in-depth genomic analysis of synchronous and  metachronous  tumours from  five patients harbouring germline mutations in the genes SDHB, RET and MAX. Using whole exome sequencing and high-density SNP-arrays we analyzed between two and four primary tumours from each patient. Furthermore, we applied multi-regional sampling to assess intra-tumoral heterogeneity and clonal evolution in two cases involving PPGL and MTC, respectively. Heterogeneous patterns of genomic change existed between synchronous or metachronous tumours with evidence of branching evolution. We observed striking examples of evolutionary convergence involving the same rare somatic copy-number events in synchronous primary PPGL. Convergent events also occurred during clonal evolution of metastatic MTC. These observations suggest that genetic or epigenetic changes acquired early within precursor cells, or pre-existing within the genetic background of the individual, create contingencies that determine the evolutionary trajectory of the tumour.

overall_design: The Affymetrix CytoscanHD platform was used to perform copy number profiling on four synchronous paragangliomas from a patient (C1) with a germline SDHB mutation. The Affymetrix CytoscanHD platform was also used to analyse a primary tumour and metastasis from a medullary thyroid carcinoma from a patient (C5) with a germline RET mutation. In addition, the Affymetrix OncoScan platform was used to analyse high interest regions from within the first primary, as well as two additional primary tumours from patient C5.

middle: J

first: Richard

middle: W

last: Tothill


title: MicroRNA expression in medulloepitheliomas

city: Baltimore

first: Deepak

last: Edward

state: MD

address: SOM Oph Ophthalmology Chairmans Office

department: School of Medicine

institute: The Johns Hopkins University

summary:
Purpose: To study the differential expression of microRNA (miRNA) profiles between  intraocular medulloepithelioma (ME) and normal control tissue.
Material and methods: Total RNA was extracted from formalin fixed paraffin-embedded intraocular  ME (n=7) and from age matched ciliary body controls (n=8).  The clinical history and phenotype was recorded.  MiRNA profiles were determined using the Affymetrix® GeneChip® miRNA Arrays analyzed using expression console 1.3 software. Validation of significantly dysregulated miRNA was confimed by quantitaive real-time PCR. The web-based DNA Intelligent Analysis (DIANA)-miRPath v2.0 was used to perform enrichment analysis of differentially expressed (DE) miRNA gene targets in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway.
Results: The pathologic evaluation revealed one benign and six malignant tumors (malignant teratoid, n=2; malignant non-teratoid, n= 4; benign non-teratoid, n=1).  A total of 88 miRNAs were upregulated and 43 miRNAs were down regulated significantly in the tumor specimens (P<0.05).  Many of these significantly dysregulated miRNAs were known to play various roles in carcinogenesis and tumor behavior.  RT-PCR validated three significantly upregulated miRNAs and three significantly down regulated miRNAs namely miR-217,miR-216a,miR-216b,miR-146a.miR-509-3p and miR-211. 56 miRNAs were significantly dysregulated in teratoid versus non-teratoid malignant tumors.  Many DE miRNAs that were significant in ME tumors showed dysregulation in retinoblastoma, and glioblastoma.   Several miRNAs in teratoid tumors were significantly up-regulated  as in precursor, normal and reactive human cartilage.  Enriched pathway analysis suggested a significant association of upregulated miRNAs with 15 pathways involved in prion disease and several types of cancer.  The pathways involving significantly down-regulated miRNAs included the toll-like receptor  (p<4.36E-16) and NF-kappa B signaling pathways (p<9.00E-06).
Conclusions:  We report significantly dysregulated miRNAs in intraocular ME tumors, which exhibited abnormal profiles in other cancers as well such as retinoblastoma and glioblastoma.  Pathway analysis of all dysregulated miRNAs shared commonalities with other cancer pathways.

overall_design: Compared expression profiles of 7 tumor and 8 control samples. The 7 tumor smaples were charcaterized as bening_teratoid (n=1), malignant_teratoid (n = 2) and malignant_non-teratoid (n=4). Malignant_teratoid and malignant_non-teratoid were compared against each other for further analysis.

middle: P

first: Hind

last: AlKatan

first: Qundeel

last: Rafiq

first: Charles

last: Eberhart

first: Altaf

last: Kondekar

first: Nicola

last: Ghazi

first: Khaled

last: Abu-Amero


title: Microarray of primary human breast cells with or without Hippo kinases LATS1/2

status: Public on Jan 27 2017

city: Basel

first: Tim

last: Roloff

address: Maulbeerstrasse 66

department: Functional Genomics

country: Switzerland

institute: FMI

summary:
Perturbation of the tightly regulated dynamic process of cell fate underlies many human diseases. The molecular mechanisms regulating breast cell fate in the hierarchically organized luminal and basal lineages of breast epithelium remain largely elusive. We performed a high-content confocal image-based shRNA screen for regulators of primary human breast cell fate. Inhibition of the Hippo kinases LATS was found to promote luminal fate and increase the number of progenitors, which is a paradox given that Hippo effectors YAP/TAZ have been associated with basal fate. Mechanistically, LATS loss increases the activities of YAP/TAZ and ERα, which in concert control breast cell fate via intrinsic and paracrine effects. Reduced LATS expression is found in breast cancers with a poor prognosis; this diminishes the sensitivity of ERα-positive- and increases the sensitivity of ERα-negative cancers to endocrine therapy. Thus, in this study we have unraveled crosstalk between Hippo and estrogen signaling and shown that LATS loss triggers expansion of luminal progenitors, the highly suspected cell-of-origin in most breast cancers.
In this dataset, we provide microarray gene expression analysis of normal breast epithelial cells, freshly dissociated from reduction mammoplasties, in which LATS1/2 were knocked down comparing it to non-targeting control expressing breast cells.

overall_design: 11 samples were analyzed, 4 different donors (cells from reduction mammoplasties MP16, MP20, MP28 and MP33) in which LATS1/2 were knocked down by two different shRNAs (shLATS1_3 = LATS1 knockdown, shLATS2_3 = LATS1 and LATS2 double knockdown). Cells expressing a non-targeting shRNA were used as controls

last: Britschgi

first: Stephan

last: Duss

first: Mohamed

last: Bentires-Alj

last: Thiry


title: Expression data regarding the effect of NPM1 knockdown on TNF-a induced gene expression in HeLa

status: Public on Feb 01 2017

city: Pheladelphia

first: Jianhuang

last: Lin

state: PA

address: 3601 Spruce St

institute: Wistar Institute

summary:
NPM1 was reported to regulate the SOD2 gene expression through regulation of NF-kB. However, the effect of NPM1 on the NF-kB-dependent transcriptome has not been exmained.
To examine the effect of NPM1 on NF-kB-dependent transcriptome. We used microarray to examine the effect of knockdown of NPM1 on the gene expression induced by TNF-a treatment which activates NF-kB pathway.

overall_design: HeLa cells were transfected with siNPM1 or non-specific siRNA for 72 h, followed by without or with treatment of TNF-a. The cells were used for RNA extraction and hybridization on Affymetrix microarrays. Through comparing the samples, we aimed to identify the TNF-a induced genes that were regulated by knockdown of NPM1.

first: Mitsuru

last: Okuwaki


title: Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse

status: Public on Jan 31 2017

city: Salamanca

first: Norma C.

last: Gutiérrez

state: Salamanca

address: Campus Miguel de Unamuno

department: Hematologia

country: Spain

institute: Centro de Investigación del Cáncer de Salamanca

type: Methylation profiling by genome tiling array


title: Expression of p27 target  genes in WT HCT116 cells vs shPCAF knock down cells

status: Public on Jan 18 2017

city: Barcelona

first: Oriol

last: bachs

address: Casanova 143

department: Biomedical Sciences

institute: University of Barcelona

summary:
We analyzed the transcriptional programs regulated by PCAF and p27 in the colon cancer cell line HCT116 by ChIP-seq. PCAF or p27 knock down revealed that both regulated the expression of common genes.
In this dataset, we include the expression data of 852 genes regulated by PCAF, obtained from the comparison between  WT HCT116 cells and shPCAF knock down cells

overall_design: 4 samples were analyzed in total. 2 control samples: asynchronously growing HCT116 cells transfected with shRNA control. 2 reference samples: asynchronously growing HCT116 cells transfected with shRNAPCAF.

last: Bachs

first: Serena

last: Orlando


title: A short-term intervention with selenium affects expression of genes implicated in the epithelial-to-mesenchymal transition in the prostate

status: Public on Jan 19 2017

city: Wageningen

first: Guido

last: Hooiveld

address: HELIX, Stippeneng 4

department: Div. Human Nutrition & Health

country: Netherlands

institute: Wageningen University

summary: In parallel with the inconsistency in observational studies and chemoprevention trials, the molecular mechanisms by which selenium may affect prostate cancer risk have not been elucidated. We conducted a randomized, placebo-controlled intervention trial to examine the effects of a short-term intervention with selenized yeast on whole-genome expression profiles in non-malignant prostate tissue. Twenty-three men receiving prostate biopsies were randomly assigned to take 300 µg selenized yeast per day (n=12) or placebo (non-selenized yeast, n=11) during a median intervention period of 35 (interquartile range: 31-35) days. Prostate specimens, collected from the transition zone before and after intervention, of 15 participants (n=8 selenium, n=7 placebo) were available for analysis using Affymetrix GeneChip Human 1.0 ST Arrays. Pathway and gene set enrichment analyses revealed that the intervention with selenium resulted in a down-regulated expression of genes involved in signaling pathways related to cellular adhesion, migration, invasion, remodeling and immune responses. Specifically, expression of the well-established epithelial marker E-cadherin was up-regulated, while mesenchymal markers, such as vimentin and fibronectin, were down-regulated after the intervention with selenium. This implies an effect of selenium on the epithelial-to-mesenchymal transition (EMT). Moreover, selenium affected expression of genes involved in wound healing and inflammation, processes which are both related to EMT. In conclusion, our data showed that selenium affected expression of genes implicated in EMT, mainly represented by a change in the direction of the epithelial rather than the mesenchymal phenotype.

overall_design:
For this randomized, placebo-controlled intervention trial, 23 men were randomly assigned to take 300 µg selenized yeast per day (n=12) or placebo (non-selenized yeast, n=11) during a median intervention period of 35 (interquartile range: 31-35) days. Prostate specimens, collected from the transition zone before and after intervention, of 15 participants (n=8 selenium, n=7 placebo) were available for analyses using Affymetrix GeneChip Human 1.0 ST Arrays.

This study is registered at clinicaltrials.gov with identifier NCT00446901.

first: Dieuwertje

last: Kok

first: Lambertus

last: Kiemeney

first: Gerald

last: Verhaegh

first: Jack

last: Schalken

first: Emile

last: van Lin

first: Michiel

last: Sedelaar

first: Alfred

last: Witjes

first: Christina

last: Hulsbergen

first: Pieter

last: van 't Veer

first: Ellen

last: Kampman

first: Lydia

last: Afman


title: JunB overexpression effect on microvascular endothelial cell culture

city: Kahoku-gun

first: Yasuo

last: Yoshitomi

state: Ishikawa

address: 1-1 Daigaku, Uchinada-machi

department: Biochemistry

country: Japan

institute: Kanazawa Medical University

summary: Analysis of gene expression in immortalized human microvascular endothelial cells (TIME cells) following forced expression of the JunB. Results provide insight into a role for the JunB signaling pathway in endothelial cell.

overall_design: Gene expression profiling of Tert-immortalized human microvascular endothelial cells (TIME cells) with or without JunB overexpression.


title: Identification of Circulating Fibrocytes and Dendritic Derivatives in Corneal Endothelium of Patients with Fuchs' Dystrophy

status: Public on Jan 24 2017

city: Leuven

first: Joost

last: van den Oord

address: Minderbroedersstraat 12, block q, box 1032

department: Department of Imaging & Pathology

country: Belgium

institute: KU Leuven

type:
Expression profiling by array
Expression profiling by RT-PCR

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

overall_design: Refer to individual Series


title: Identification of Circulating Fibrocytes and Dendritic Derivatives in Corneal Endothelium of Patients with Fuchs' Dystrophy [microarray expression analysis]

summary:
PURPOSE: Fuchs’ endothelial corneal dystrophy (FECD) is a degenerative eye disorder affecting 4% of Americans older than 40. It is the leading indication for corneal endothelial (CE) transplantation for which there is a global donor shortage. This study aimed to gain further insight into the pathophysiology of FECD and identify targets for nonsurgical therapy.

METHODS: CE from patients with late-onset FECD was compared with that of normal controls using microarray expression analysis (n = 4 FECD, n = 4 normal), reverse transcriptase quantitative PCR (n = 9 FECD, n = 8 normal), and immunohistology (n = 55 FECD, n = 15 normal).

RESULTS: This led to the identification of circulating fibrocytes and their dendritic derivatives in all examined CE samples with FECD (in all clinical stages of symptomatic FECD and independent of prior cataract surgery). These cells were not present in normal CE. In this study we characterize their morphology, protein expression profile, number, and localization within the CE layer of patients with FECD.

CONCLUSIONS: Circulating fibrocytes and their dendritic derivatives are a new aspect of FECD that deserves further investigation. Because they are known to cause fibrosis in a variety of organs, they may play a similar role in FECD and might be a valuable target for nonsurgical therapy.

overall_design: This study was performed on CE monolayers with Descemet membrane from patients with late-onset FECD. Microarray expression analysis was performed on 8 samples (n = 4 FECD, n = 4 normal). RT-qPCR was done for 179 genes of interest and at least three reference genes (n = 9 FECD, n = 8 normal). Molecules of interest were validated with immunohistochemical and immunofluorescent staining on fresh corneal endothelial whole-mounts (n = 55 FECD, n = 15 normal). All stainings were optimized on external control tissues, which were included as batch controls. Dye swaps ensured specificity of double staining.

first: An-Katrien

last: De Roo

first: Jasper

last: Wouters

first: Olivier

last: Govaere

first: Beatrijs

last: Foets


title: The significance of different algorithms in transcriptome analysis of leukemic cells with rearranged MLL (gene expression)

city: Rehovot

first: Dena

last: Leshkowitz

department: Bioinformatics Unit, Life Sciences Core Facilities

institute: Weizmann Institute of Science

summary: This study shows how the way by which the RNA-Seq data is analyzed affects the resulting gene expression profile. Three parameters were explored: the RNA-Seq analysis algorithm pipeline (cufflinks – Cuffdiff 2 or HTSeq & DESeq), sequencing depth and sequencing protocol: single or paired end, 100 or 50 bases. For comparison, the same samples were processed by gene microarrays.

overall_design: RNA-Seq and gene microarray were conducted on total RNA from four acute lymphoblastic leukemia (ALL) precursor B cell lines, two lines carrying the chromosome translocation t(4;11) in which the human MLL gene is rearranged, and two lines lacking this abnormality.

first: Eli

last: Canaani


title: Molecular Evidence of Chronic Cellular Rejection in C4d and Microvascular Inflammation Negative Transplant Glomerulopathy

status: Public on Jan 17 2017

city: Galway

first: Pilib

last: Ó Broin

address: University Rd

country: Ireland

institute: NUI Galway

summary:
Transplant glomerulopathy (TGP) is frequently found in the setting of chronic antibody mediated rejection along with microvascular inflammation (MVI) (peritubular capillaritis+glomerulitis score > 1) and/or positive c4d staining. We assessed the molecular profiles of TGP in the absence of microvascular inflammation and C4d staining as compared to TGP with positive MVI and/or C4d.
Gene expression profiles of TGP in the absence of microvascular inflammation and C4d lack molecular features of antibody-mediated rejection but suggest chronic cellular rejection.

overall_design: 44 for-cause renal allograft biopsies were studied using Affymetrix HuGene 1.0 ST expression arrays; 12 with normal biopsy findings (G1), 17 with a diagnosis of TGP, C4d positive and/or a MVI score >1 (G2), and 10 with a diagnosis of TGP and C4d negative and MVI score <=1 which were DSA negative (G3A) and 5 TGP and C4d negative and MVI score <=1 (G3B).

first: Enver

last: Akalin


title: Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse [gene expression]

first: Norma C.

last: Gutiérrez

summary:
Multiple myeloma (MM) remains incurable despite the introduction of novel agents and a relapsing course is observed in the majority of patients. Although the development of genomic technologies has greatly improved our understanding of MM pathogenesis, the mechanisms underlying relapse have been less investigated. In this study, an integrative analysis of DNA copy number, DNA methylation and gene expression was conducted in matched diagnosis and relapse samples from 17 MM patients. Overall, the acquisition of abnormalities at relapse was much more frequent than the lost of lesions present at diagnosis, and DNA losses were significantly more frequent at relapse than in diagnosis samples. Interestingly, copy number abnormalities involving more than 100 Mb of DNA at relapse significantly impact the gene expression of these samples, provoking a particular deregulation of IL-8 pathway. On the contrary, no relevant modifications of gene expression were observed in those samples with less than 100 Mb affected by chromosomal changes. Although different statistical approaches were used to uncover genes whose abnormal expression at relapse was regulated by DNA methylation, only two genes significantly deregulated in relapse samples (SORL1 and GLT1D1) showed a negative methylation-expression correlation. A deeper analysis demonstrated that DNA methylation was involved in regulation of SORL1 expression in MM. Finally, relevant changes in gene expression observed in relapse samples, such us downregulation of CD27 and P2RY8, were not apparently preceded by alterations in corresponding DNA. Taken together, these results showed that genomic heterogeneity, both at the DNA and RNA level, is a hallmark of MM transition from diagnosis to relapse.
Please note that an a first step all analyses were carried out independently in each series, being the number of samples of 40 in methylation, 38 in SNP and 34 in expression series. In the next step, association studies were performed only in the overlapping samples, being 34 matching samples between expression and methylation and 32 samples between expression and SNP data.

overall_design: Seventeen paired bone marrow samples were obtained at diagnosis and relapse (n = 34). A CD138 positive PC isolation using the AutoMACs automated separation system was carried out in all the BM samples. Total RNA was extracted using Allprep Kit (Qiagen, Valencia, CA, USA) following manufacturer’s protocol and hybridized following manufacturer’s protocol.

first: Patryk

last: Krzeminski

first: Luis

last: Corchete

first: Juan

middle: L

last: García

first: Lucía

last: López-Corral

first: Encarna

last: Fermiñán

first: Eva

middle: M

first: Ana

last: Martín

first: Jesús

last: Hernández-Rivas

first: Ramón

last: García-Sanz

last: San Miguel

first: Norma

middle: C


title: Genomics of Chronic Rejection

summary:
We hypothesized that T cell-mediated immune mechanisms play a role in two conditions; 1: donor-specific antibody (DSA) negative transplant glomerulopathy (TGP) and 2: interstitial fibrosis and tubular atrophy (IFTA) with inflammation (i>0). We investigated gene expression profiles of those biopsies compared to biopsies with antibody-mediated rejection(ABMR) and to biopsies with non-specific IFTA and no inflammation.
DSA negative TGP and IFTA with inflammation biopsies have a unique molecular signature distinct to that seen in biopsies with ABMR and IFTA without inflammation with significant expression of cytotoxic and regulatory T cells.

overall_design: 101 biopsies were studied using Affymetrix HuGene 1.0 ST expression arrays; 16 with normal biopsy findings (G1), 33 with a diagnosis of chronic antibody-mediated rejection (cAMR), 17 with chronic T-Cell mediated rejection and IFTA (TCMR_IFTA), 10 with T-Cell mediated rejection without DSA (TCMR_DSA-), 12 with pure IFTA (IFTA), and 13 with DSA and IFTA (DSA_IFTA).


title: Expression data from human stem cell memory (TSCM) CD8+ T cells induced by Notch signaling

status: Public on Jan 06 2017

city: Tokyo

first: Taisuke

last: Kondo

department: Medicine

institute: Keio University

summary:
Adoptive T-cell immunotherapy provides a promising approach to cancer therapy. Stem cell memory T (TSCM) cells have been proposed as a new class of memory T cells that possess longevity and a high proliferative potential. It has been shown that CD8+ TSCM cells can be generated in vitro from naïve CD8+ T cells via Wnt signaling; however, the methods for inducing TSCM cells from activated or memory T cells remain to be developed.
Here, we established a new strategy for generating TSCM-like cells in vitro (designated as “iTSCM” cells) from activated CD4+ and CD8+ T cells in mice and humans by coculturing with stromal cells expressing a Notch ligand. These iTSCM cells lost PD-1 and CTLA-4 expression and produced a large number of tumor-specific effector cells after restimulation. The present study illustrates a novel approach to generating a large number of antigen-specific effector T cells for adoptive immunotherapy.

overall_design: For all samples, total RNA was isolated using a ReliaPrep RNA Cell Miniprep System (Promega, Madison, WI, USA).  Microarray analysis was performed using fragmented and labeled with a Low Input Quick Amp Labeling Kit, one-color and hybridized to SurePrint G3 Mouse Gene Expression 8x60K (Agilent), all according to the respective manufacturer's instructions.

first: Rimpei

last: Morita

first: Yuumi

last: Okuzono

first: Takashi

last: Sekiya

first: Shunsuke

last: Chikuma

last: Shichita

first: Mitsuhiro

last: Kanamori

first: Masato

last: Kubo

first: Keiko

last: Kog

first: Takahiro

last: Miyazaki

first: Yoshiaki

last: Kassai

first: Akihiko

last: Yoshimura


title: Expression analysis of single and double knockdown of UBE4B and LSD1 in HEK293T cells.

first: Jiou

last: Wang

address: 615 N. Wolfe St.

institute: Johns Hopkins University

summary: Ubiquitin Ligase (UBE4B) and Lysine-Specific Demethylase (LSD1) are post-translational modifying enzymes affecting lysine ubiquitination and methylation of several important regulatory proteins, and are synergisticaly important for protein quality control. To inwestigate their role in cell signaling, we analyzed global mRNA levels in HEK293T cells that were knocked down with shRNAs against UBE4B, LSD1, both UBE4B and LSD1, and non-targeting control (CTRL).

overall_design: HEK293T cells were transfected with knockdown shRNA plasmids to reduce protein levels of UBE4B, LSD1, both UBE4B and LSD1, or none (control  knockdown with non-targeting shRNA plasmid). After 78h of knockdown, we isolated total RNA. We pairwise compared mRNA levels from control samples to single UBE4B, LSD1, and double UBE4B+LSD1 knockdown samples.

first: Goran

last: Periz


title: Investigation of the role of PRL-3 in leukemogenesis

status: Public on Jan 11 2017

city: Singapore

first: Chong-Lei

last: Bi

address: #12-02, Centre for Translational Medicine, Yong Loo Lin School of Medicine, National University of Singapore, 14 Medical Drive

country: Singapore

institute: Cancer Science Institute Singapore

summary: In order to investigate the role of PRL-3 in the leukemogenesis, we transfected a control vector (pEGFP) and (human) PRL-3 gene into an acute myeloid leukemia (AML) cell line TF-1, respectively. After drug selection and FACS sorting, we established TF1-pEGFP and TF1-hPRL-3 isogenic cell lines. In vitro and in vivo experiments were conducted to characterized this pair of isogenic cell lines. Results provided insight into the molecular basis of PRL-3 in contributing the development of AML.

overall_design: Whole genome microarray comparsion of TF1-pEGFP vs TF1-hPRL-3 cell line

first: Jianbiao

last: Zhou

first: Chonglei

first: Wee

last: Chng


title: OBESITY ALTERS MOLECULAR AND FUNCTIONAL CARDIAC RESPONSES TO ISCHEMIA-REPERFUSION AND GLUCAGON-LIKE PEPTIDE-1 RECEPTOR AGONISM

city: Indianapolis

first: Kieren

middle: James

last: Mather

state: IN

address: 1120 West Michigan St, CL365

institute: Indiana University

summary:
Diet induced obesity in swine was associated with altered cardiovascular functional, miR transcriptome, and proteomic response to ischemia-reperfusion. Furthermore, the GLP-1 mimetic exendin-4 altered functional, miR and protein responses differently in obese versus lean swine, demonstrating the pervasive effect of obesity on modulating cardiac response to pathophysiologies and therapeutics.
This study tested the hypothesis that obesity alters the left ventricular microRNA (miR) transcriptome, proteome and functional cardiac response to ischemia-reperfusion (I/R) injury and to glucagon like peptide-1 (GLP-1) receptor activation. Ossabaw swine were fed normal chow or obesogenic diet for 6 months followed by IV infusion of either saline (vehicle) or the GLP-1 mimetic exendin-4 (Ex-4).  Left ventricular pressure volume relationships were assessed under baseline conditions, during a 30-minute occlusion of the circumflex artery and during a 2 hour reperfusion period. Cardiac biopsies were obtained from normally-perfused and ischemia-reperfusion territories, and analyzed using Affymetrix 3.0 miR microarray and protein mass spectrometry. I/R was found to depress global cardiac function in lean swine (systolic pressure, end-diastolic volume). In contrast, Ex-4 therapies did not affect blood pressure in obese animals, but significantly reduced end-diastolic volume following the reperfusion period. These divergent physiologic response to regional I/R in obese vs lean hearts were associated with significantly different protein and miRNA changes. Obesity was associated with altered abundance of proteins associated with calcium handling and contractility, and with changes in miRs relating to metabolism, hypertrophy, and cell death, including the miR-15 and miR-30 families, miR-199a, and miR-214. These effects were modified differently by EX-4 treatment in lean vs obese swine. These findings suggest specific miR and proteomic differences contribute to differences in functional cardiac responses to ischemia-reperfusion injury and pharmacologic activation of GLP-1 signaling in the setting of obesity, volume, stroke volume and ejection fraction) with partial amelioration seen in Ex-4 treated animals.

overall_design: Comparing miRNA profiles in lean myocardium of lean and obese swine, with and without ischmia and plus and minus exendin-4.

first: Jonathan

middle: D

last: Tune

first: Daniel

last: Sassoon

first: Adam

middle: G

last: Goodwill

first: Jeanette

middle: N

last: McClintick

first: Jillian

last: Noblet

first: Brain

last: Herring


title: Microarray of MCF10A cells with/without LATS1/2, expressing YAP/TAZ or ESR1 cDNA

first: Tim

last: Roloff

summary:
Cell fate perturbations underlie many human diseases, including breast cancer. However, the regulation of breast cell fate remains largely elusive. The mammary gland epithelium consists of differentiated luminal epithelial and basal myoepithelial cells, as well as undifferentiated stem cells and more restricted progenitors. Breast cancer originates from this epithelium but the molecular mechanisms underlying breast epithelial hierarchy remain ill-defined. Mouse and human luminal cells express keratins (K)18, 8, 19 and/or estrogen receptor α (ERα) and progesterone receptor (PR), their basal counterparts express K5, 14 and/or p63 and/or α-smooth-muscle actin (α-SMA)4-6. In this study, using a high-content confocal image-based shRNA screen for tumor suppressors regulating human breast cell fate, we discovered that ablation of the Hippo kinases large tumor suppressor (LATS) 1 and 2, promoted luminal fate and increased the number of bipotent and luminal progenitors, the proposed cell-of-origin of most human breast cancers. Mechanistically, we discovered a crosstalk between Hippo and ERα signaling. In the presence of LATS, ERα was targeted for ubiquitination and proteasomal degradation. Loss of LATS stabilized ERα and Hippo effectors YAP/TAZ, which in concert control breast cell fate via intrinsic and paracrine mechanisms. Our findings uncover a novel non-canonical (i.e., YAP/TAZ-independent) effect of LATS in the regulation of human breast cell fate.
In this dataset, we provide microarray gene expression analysis of normal breast epithelial cells, freshly dissociated from reduction mammoplasties, in which LATS1/2 were knocked down comparing it to non-targeting control expressing breast cells.

overall_design: 18 samples were analyzed, 3 replicates. MCF10A cells in which LATS1/2 were knocked down by two different shRNAs (shLATS1B = LATS1 knockdown, shLATS1+2 = LATS1 and LATS2 double knockdown), cells expressing a non-targeting shRNA were used as controls (shNT). Each of these three cell lines was transfected with either a ctrl, YAP/TAZ and/or ESR1 cDNA expressing vector.

first: Adrian

last: Britschgi

first: Mohamed

last: Bentires-Alj

first: Stephan

last: Thiry


title: cDNA microarray analysis of human keratinocytes cells of patients submitted to chemoradiotherapy and oral low level laser therapy. Pilot study

status: Public on Feb 14 2017

city: Rio de Janeiro

first: Fabio

last: Passetti

address: Av. Brasil, 4365

department: Pav. Leonidas Deane

country: Brazil

institute: FIOCRUZ

summary: This study investigated possible molecular changes in the oral mucosa of head and neck squamous cell carcinoma  patients submitted to chemoradiotherapy with and without low-level laser therapy  by cDNA microarray analysis.

overall_design: Patients were randomized in the laser group (LG) and placebo (PG), with 4 patients in LG and 3 patients in PG with 2 techical replicates each in a non-stratified manner and underwent the same protocol of chemotherapy and radiotherapy. Samples were collected after the 10th day of CRT and laser treatment or placebo and were analyzed using Affymetrix Gene 1.0 ST array.

first: Heliton

middle: S

last: Antunes

first: Gabriel

last: Wajnberg

first: Marcos

middle: B

last: Pinho

first: Natasha

last: Jorge

first: Joyce

last: Luanna

first: Claudio

last: Stafanoff

last: Herchenhorn

first: Carlos

last: Araújo

first: Mariana

last: Rampini

first: Celia

last: Viégas

first: Fernando

last: Dias

first: Patricia

last: de Araujo-Souza

last: Ferreira


title: miRNA data in human placentas from normal pregnancies and from pregnancies complicated by SGA and IUGR

city: Los Angeles

first: Alison

last: Chu

address: 10833 LeConte Avenue

institute: UCLA

summary:
Placental insufficiency leading to intrauterine growth restriction demonstrates perturbed gene expression affecting placental angiogenesis and nutrient transfer from mother to fetus. To understand the post-transcriptional mechanisms underlying such placental gene expression changes, our objective was to identify key non-coding microRNAs that express biological function. To this end, we undertook microarray targeting microRNAs in placentas of appropriate (AGA, n=3) versus small for gestational age (SGA, n=3) weight infants and observed upregulation of 97 miRs in SGA versus AGA. In a larger cohort of samples, we validated by qRT-PCR, differential expression of three specific microRNAs that target genes mediating angiogenesis and nutrient transfer.
We performed microarray on a small cohort of samples in order to identify differential expression in pathways involved with angiogenesis and nutrient transfer, essential processes for placental function that when perturbed, may result in intrauterine growth restriction.

overall_design: Human placental samples were obtained immediately post-parturient. There were three samples from the AGA group (Bw>10% and <90%) and three samples from the SGA/IUGR (Birthweight <10%) group. All placental samples were from term, singleton pregnancies.

first: Sherin

middle: U

last: Devaskar


title: Differences in transcriptomic profiles between glioblastoma-initiating cells (GICs) and non-GICs upon radiation treatment

status: Public on Jan 01 2017

first: Miguel Angel

last: Pujana

address: Gran Via 199

institute: Institut Catala d'Oncologia IDIBELL

summary: GICs are considered a major determinant in glioblastoma treatment failure, as they exhibit a marked resistance to radiotherapy. However, the exact mechanisms that confer this radioresistance to GICs are still not fully understood. We have performed a microarray analysis after radiation treatment of GICs and non-GICs cultures with the aim of identifying genes, pathways and transcription factors differentially expressed between these two cellular compartments.

overall_design: GICs and non-GICs cultures derived from a glioblastoma patient named as PG35s and PG35, respectively, were irradiated with fractionated radiotherapy at a dose of 2Gy/day up to 8Gy. After recovery, GICs once irradiated were exposed to a second cycle of radiation. Then, total RNA was extracted from both, controls and irradiated conditions. Three independent experiments were performed using different batches for each sample.

first: Avelina

last: Tortosa

first: Elisabetta

last: Stanzani

first: Josefina

last: Martinez


title: Comparison of Glomerular Transcriptome Profiles of Adult-Onset Steroid Sensitive Focal Segmental Glomerulosclerosis and Minimal Change Disease

status: Public on Jan 04 2017

city: Shanghai

first: Jun

last: Tong

state: Shanghai

address: 197,Ruijin Er Road

department: Nephrology

institute: Shanghai Jiaotong University

summary: To search for biomarkers to differentiate Adult-Onset Steroid Sensitive  focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD).

overall_design: Compared the profiles of glomerular transcriptomes between patients with FSGS and patients with MCD using microarray analysis.

first: Jingyuan

last: Xie

last: Chen


title: MKL1/2 dependent target genes

city: Munich

first: Constanze

last: Mittermeier

address: Goethestr. 33

department: Walther Straub Institute of Pharmacology and Toxicology

country: Germany

institute: LMU Munich

summary: Megakaryoblastic Leukemia 1 and 2 (MKL1 and 2) are coactivators of the transcription factor Serum Response Factor (SRF). We recently showed that depletion of MKL1 and 2 abolished HCC xenograft growth, associated with oncogene-induced senescence. To identify suitable MKL target genes mediating these effects, we performed microarray analyses using HuH7 hepatocellular carcinoma cells stably expressing shRNA against MKL1/2 (HuH7 MKL1/2 KD). We therefore used a Affymetrix oligonucleotide array and filtered for genes whose expression in HuH7 MKL1/2 KD cells was reduced by a factor of at least 2.5 as compared to control HuH7 cells.

overall_design: We analyzed duplicates of HuH7 cells stably expressing a control shRNA and duplicates of HuH7 cells stably expressing MKL1/2 shRNA, overall we used 4 samples.

last: Hermanns

first: Susanne

last: Muehlich

first: Veronika

last: Hampl

first: Dietmar

middle: E

last: Martin

first: Kerstin

last: Maier


title: Differential expression of miRNAs in the GW627368X and PGE2 induced exosomes

status: Public on Dec 31 2016

city: Miaoli

first: HUAJUNG

last: LI

address: 35 Keyan Road,

country: Taiwan

institute: National Health Research Institutes

summary: Exosomes are small membrane bound cell-derived vesicles that are present in biological fluids include blood and cell culture medium. Exosomes contain various functional proteins, mRNAs and microRNAs (miRNAs). We used miRNA microarrays to detail the miRNA content in the GW627368-induced and PGE2-induced exosomes from non-adherent mammary epithelial cells (NAMECs).

overall_design: GW627368X and PGE2 induced-exosomes were collected from NAMECs culture medium for miRNA extraction and hybridization on Affymetrix GeneChip® miRNA 3.0 array.

first: Hua-Jung

last: Li

first: Meng-chieh

last: Lin


title: Esophageal adenocarcinoma gene expression profiling

status: Public on Dec 15 2016

city: Nashville

first: Yan

last: Guo

state: TN

address: 639 Preston Research Bld

institute: Vanderbilt Cancer Center

summary: Gene expression analysis was conducted to determine changes in gene expression and predict signaling networks in esophageal adenocarcinomas. For this analysis we used 12 EAC samples and 9 normal esophageal tissue samples. The analysis indicated deregulation of a large number of genes. Pathway analysis demonstrated the presence of KRAS signature and predicted activation of multiple transcription networks.

overall_design: Expression profile were obtained on 21 Samples (9 normals, and 12 tumors, 9 were tumor-normal pairs) using Affymetrix Human Gene Set St 1.0 arrays.

first: Wael

last: El-Rifai

first: Dunfa

last: Peng


title: Differential gene expression in neuroblastoma cells after treatment with JQ1, nanaomycin, or combination of JQ1 and nanaomycin

city: Sydney

first: Tao

last: Liu

state: NSW

address: C25 Lowy Cancer Research Center Gate 9 High St UNSW

department: Histone Modifications

institute: Children's Cancer Institute

summary:
BET bromodomain inhibitors are emerging as very promising novel anticancer agents. Combination of BET bromodomain inhibitor JQ1 and quinone-containing compound nanaomycin exerts synergistic anticancer effect in neuroblastoma
We analysed whether a treatment with BET bromodomain inhibitor JQ1, and quinone-containing compound Nanaomycin synergistically modulate gene expression

overall_design: Neuroblastoma BE(2)-C cells were treated with vehicle control, 500nM JQ1, 125nM nanaomycin, or combination of JQ1 and nanaomycin. RNA was extracted from the cells 6 hours after treatment, and subjected to differential gene expression studies with Affymetrix microarrays.

first: Liu

last: Tao


title: Microarray gene-expression profiles of 50 pancreatic tumors tissue from patients with pancreatic ductal adenocarcinoma

city: Bethesda

first: Perwez

last: Hussain

address: 37 Convent Drive, Building 37, Room3044B

institute: National Cancer Institute

summary: In order to identify biologically relevant tumor markers, and novel therapeutic target we have compared the tumor gene expression profiles of long (OS>=24 months,n=14) and short (OS <=7months, n=11) survival patients. Then we conducted Kaplan-Meier survival analysis using all the 50 samples listed here. The Affymetrix gene-expression data of these 50 samples were also included in the earlier submission by us as GEO accession number GSE62452.

overall_design: We compared the gene expression profiles of long and short survival patients, significantly differentially expressed genes were subjected to Ingenuity Pathway Analysis (IPA). Significantly differentially expressed genes with 1.5 fold change were further analyzed by Coxregression Proportional harzard ratio.

first: S


title: miRNA expression data from primary human tissue (gastric mucosa)

status: Public on Dec 12 2016

city: Kiel

first: Robert

last: Haesler

address: Schittenhelmstr. 12

department: IKMB / 1st Dept. of Medicine

institute: University Clinic of Schleswig Holstein

summary:
The experiment aims to identify mRNAs that are regulated in response to RYGB surgery
The overall aim of the study was to identify mechanisms by which RYGB surgery promotes improvement of clinical paramters on a molecular level

overall_design: Comparison of mRNA profiles from primary tissue before, during and after RYGB surgery

first: R

last: Häsler


title: Gene expression profile of the NF-κB subunit p52 in Hodgkin’s lymphoma

status: Public on Dec 21 2016

city: Berlin

first: Claus

last: Scheidereit

address: Robert Roessle Str. 10

department: Signal Transduction in Tumor Cells

institute: Max Delbrueck Center for Molecular Medicine

summary: Malignant cells of Hodgkin's lymphoma (HL) cells are characterized by constitutive activation of the canonical as well as the non-canonical NF-κB signaling cascades. Knockdown of a subunit combination corresponding to the non-canonical NF-κB dimer (p52/RelB) in the HL cell line L-1236 caused up-regulation of a set of genes that are associated with hematopoietic and lymphoid organ development. As p52 can form homodimeric complexes, which can repress transcription either alone or in association with transcriptional repressors such as HDAC1, we knocked down p52 alone to analyze its role in gene repression in HL cells. We found that the single knockdown of p52 is indeed sufficient to up-regulate an interesting set of genes that may play a role in B-cell and/or HL development.

overall_design: The knockdown of the NF-κB subunit p52 was carried out in L-1236 cells. Two distinct siRNA sequences against NFKB2 and two non-targeting siRNA sequences (control) were used.  Experiments were performed in biological triplicates.

first: Kivia

middle: A

last: de Oliveira

first: Matthias

last: Heinig

first: Norbert

last: Huebner


title: Affymetrix SNP array data of 35 multiple myeloma patients from UZ Leuven (Belgium)

status: Public on Dec 01 2016

first: Isabel

middle: Juliana Frans

last: Hofman

address: Herestraat 49

department: Oncology

institute: KU Leuven

type: Genome variation profiling by genome tiling array

summary: Chromosomal region 1p22 is deleted in ~20% of multiple myeloma (MM) patients, suggesting the presence of an unidentified tumor suppressor gene. Using high-resolution genomic profiling, we delimit a 58 kb minimal deleted region (MDR) on 1p22.1 encompassing only two genes: ectopic viral integration site 5 (EVI5) and ribosomal protein L5 (RPL5). Although mutations in 1p22 genes are rare in MM, the tumor suppressor role of EVI5 and RPL5 may be supported by the fact that these genes show the highest frequency of mutations predicted to impair protein function on 1p22.

overall_design: Samples were selected among patients that were diagnosed with MM in UZ Leuven (Belgium) based on plasma cell infiltration of the bone marrow. Only bone marrow samples with at least 70% plasma cells were used in this study to achieve an optimal signal to noise ratio. In total, 36 samples of 35 patients were hybridised to the arrays; for one patient (MM10), also a remission sample was analysed.

first: Kim

last: De Keersmaecker


title: Expression data from the neuron model of Alzheimer's disease (AD) with or without treatment of recombinant human mitochondrial transcriptional factor A (rhTFAM) protein

city: Fukuoka

first: Yusaku

last: Nakabeppu

state: Fukuoka

address: 3-1-1 Maidashi Higashi-ku

department: Department of Immunobiology and Neuroscience

institute: Medical Institute of Bioregulation, Kyushu University

summary:
To delineate the mechanism by which hTFAM suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment.
One-way ANOVA was performed with the transcript clusters altered in PS1P117L cells with rhTFAM treatment compared with those without the treatment. Comparative analyses of PS1P117L cells with or without rhTFAM treatment showed that the expression of genes involved in protein synthesis, gene expression, and cancer were significantly altered. From these microarray analyses, we found that the expression levels of the genes associated with neuritogenesis were decreased in PS1P117L neurons compared with those in the wild type, and that hTFAM significantly increased these gene expression.

overall_design: Cholinergic neurons derived from human iPSCs established from normal subjects, in which a mutant (PS1P117L) copy of the PSEN1 gene was introduced were used in this study, (n=3 for each group). PS1P117L neurons with or without recombinant hTFAM protein treatment. RNA samples prepared from the cells were subjected to microarray analysis using the Affymetrix human Gene 1.0 ST platform (GPL6244).

first: Sugako

last: Oka


title: Leukotriene E4 is a full functional agonist for human cysteinyl leukotriene type 1 receptor

city: London

first: Grzegorz

last: Woszczek

state: London

address: 5th Floor, Tower Wing, Guy's Hospital

department: Division of Asthma, Allergy and Lung Biology

country: United Kingdom

institute: King's College London

summary: Leukotriene E4 (LTE4) the most stable of the cysteinyl leukotrienes (cysLTs) binds poorly to classical type 1 (CysLT1) and 2 (CysLT2) receptors although it induces potent responses in human airways in vivo, such as bronchoconstriction, airway hyperresponsiveness and inflammatory cell influx suggesting the presence of a novel receptor that preferentially responds to LTE4. To identify such a receptor two human mast cell lines, LAD2 and LUVA, were selected that differentially responded to LTE4 when analysed by intracellular signalling and gene expression.  Comparative transcriptome analysis and recombinant gene overexpression experiments revealed CysLT1 as a receptor responsible for potent LTE4-induced response in LAD2 but not in LUVA cells, an observation confirmed further by gene knockdown and selective inhibitors. Lentiviral overexpression of CysLT1 in LUVA cells augmented intracellular calcium signalling induced by LTE4 but did not restore full agonist responses at the gene expression level. Our data support a model where both an increased expression of Gαq-coupled CysLT1, and sustained intracellular calcium mobilisation and extracellular signal-regulated kinase (Erk) activation, are required for LTE4-mediated regulation of gene expression in human cells. Our study shows for the first time that CysLT1 expression is critically important for responsiveness to LTE4 within a human cell system.

overall_design: LAD2 cells were cultured and stimulated for 2 h with LTD4 (100nM), LTE4 (100nM) or medium (vehicle) control. LUVA cell were cultured. Total RNA was extracted and analysed using Affymetrix Human Gene 1.0 ST Arrays.

first: Holly

middle: R

last: Foster

first: Elisabeth

last: Fuerst

first: William

first: Tak

middle: H

last: Lee

first: David

last: Cousins


title: Tumor infiltrating HLA-matched CD4+ T cells retargeted against Hodgkin and Reed-Sternberg cells

status: Public on Nov 29 2016

city: Frankfurt

first: Claudia

last: Döring

address: Theodor Stern Kai 7

department: Medical School, Institite of Pathology

institute: Johann Wolfgang-Goethe University Frankfurt a.M.

summary: Hodgkin's lymphoma (HL) is one of the most frequent hematological malignancies. Due to its extraordinary composition, few tumor cells surrounded by a reactive infiltrate, HL can be seen as an ideal model system for research focusing on tumor immunology. In fact, the tumor cells of HL, so called Hodgkin/Reed-Sternberg (HRS) cells attract CD4+ T cells, which then build rosettes with the HRS cells. HRS cells further modulate the tumor microenvironment with the help of CD4+ T cells to avoid tumor rejection. Here, we mimicked this scenario using compatible CD4+ T cells receiveing data of profound interactions for the first time, as former studies were performed with allogeneic donors. Finally, we genetically retargeted compatible CD4+ T cells to kill HRS cells.

overall_design: 19 samples of 7 day-old co-cultures of L428 cells and primary T cells were MACS-depleted of T cells. When indicated addition of 0.75µM dexamethasone.

first: Bejamin

last: Rengstl


title: mRNA exrpession from human gdT-cells

status: Public on Dec 10 2016

first: Robert

last: Haesler

summary:
The experiment aims to identify mRNAs illustrating the unique nature of the gd T-cell subtype
The overall aim of the study was to elucidate gdT-cells as a producer of specific cytokines

overall_design: comparing differently stimulated gdT-cells

first: R


title: Uncovering obsessive-compulsive disorder risk genes in a pediatric cohort by high-resolution analysis of copy number variation.

status: Public on Dec 11 2016

city: Toronto

first: Stephen

middle: W

last: Scherer

state: Ontario

address: 686 Bay Street

department: Genetics and Genomic Biology

country: Canada

institute: The Hospital for Sick Children

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

overall_design: Refer to individual Series


title: Effects of POTEF-AS1 knockdown in prostate cancer cells

status: Public on Dec 14 2016

city: Itabashi-ku

first: Ken-ichi

last: Takayama

address: Sakaecho

institute: Tokyo Metropolitan Institute of Gerontology

summary:
Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified POTEF-AS1 is an androgen-regulated non-coding RNA gene.
In order to investigate the POTEF-AS1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines after siPOTEF-AS1 treatment. We also treated cells with vehicle or androgen to analyzed the effects of POTEF-AS1 on AR function.

overall_design: Observation of androgen dependent gene expression changes after treatment with siRNAs targeting POTEF-AS1 wiith microarray.

first: K

first: S

last: Inoue


title: Expression data of LncRNA from the rat knee articular cartilage at different developmental stages

status: Public on Dec 06 2016

city: Shanghai,

first: Feng

middle: jun

last: lin

state: xvhuiqv

address: 2Institute of Health Sciences

department: Department of Pathophysiology

country: China

institute: 1Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education

summary: We performed microarray analysis to compare the gene expression profile of sunitinib-treated primary xenograft tumors (sensitive or resistant status) with that of vehicle-treated.

overall_design: Total RNA was extracted from KURC1,2 xenograft tumors treated with sunitinib or vehicle. Forty mg/day of sunitinib was orally administered once a day, and KURC3 developed resistance to sunitinib.

first: XiaJi

last: Ba

first: GaoShi

last: Gao


title: Expression data from breast cancer tumors treated with a single window of the antiangiogenic agent Sunitinib

city: Oeiras

first: Joana

last: Cardoso

address: Instituto Gulbenkian de Ciência, 6

country: Portugal

institute: Instituto Gulbenkian de Ciência

summary:
We have witnessed the rise and fall of antiangiogenic therapy in breast cancer (BC). Nevertheless, clinical remissions were observed in patients and we were interested in studying the activity of antiangiogenic drugs in BC. Inefficacy of sunitinib was observed in mouse models of metastatic BC, where evidence of enhanced metastasis was reported, and lack of efficacy of sunitinib-docetaxel combination was recently reported in a phase III clinical trial. Our aim was  to understand the mechanisms and predictors of response to sunitinib in BC in a cohort of patients with untreated locally advanced or operable BC treated with an upfront window of single agent sunitinib, followed by the combination of sunitinib and docetaxel.
We have used microarray profiing to monitor the transcriptional changes associated with three distinct stages of treatment: at diagnosis and prior to any treatment (t1), after an upfront window of single agent sunitinib (t2) and after the combined treatment of sunitinib and docetaxel (t3). In addtion, this microarray data also allowed us to observe the  transcriptional changes associated with primary resistance to angiogenic therapy in 4 of 12 patients likely mediated by an adaptive transcriptional response to hypoxia in these resistant tumors. In BC patients this is the first demonstration of primary resistance to antiangiogenic therapy.

overall_design: Breast cancer samples were colected from human patients (n=8) for RNA extraction and hybridization on Affymetrix microarrays. Expression profiling on tumor material collected at the three timepoints, diagnosis and prior to any treatment (t1), after an upfront window of single agent Sunitinib (t2) and after the combined treatment of sunitinib and docetaxel (t3), was used to obtain an unbiased view of sunitinib response. Several tumor biopsies and specimens had no frozen sample available or RNA with insufficient quality for expression analysis. Were include in the analysis, at diagnosis (t1), replicated material from patients 4, 5, 6, 7 and 11 (patient 10 had no replica), at day 15 (t2) replicated material from patients 5, 7, 11 and 12 (patient 4 had no replica) and at surgery (t3) replicated material from patients 7, 9, 10, 11 and 12 (patient 6 had no replica)

first: Sofia

last: Braga

first: Saudade

last: André

first: Margarida

last: Brito

first: Predro

last: Sánchez

first: Lurdes

last: Orvalho

first: Lucília

last: Salgado

first: Sérgio

last: Dias

first: José

last: Pereira-Leal

middle: L

last: Passos-Coelho


title: Expression data from the neuron model of Alzheimer's disease (AD)

first: Yusaku

last: Nakabeppu

summary:
To delineate the mechanism by which human mitochondrial transcriptional factor A (hTFAM) suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment.
One-way ANOVA was performed with the transcript clusters altered in PS1P117L cells compared with wild-type cells. Comparative analyses of PS1P117L cells and wild-type cells showed that the expression of genes involved in cellular assembly and organization, cellular function and maintenance, and tissue development were significantly altered.

overall_design: Cholinergic neurons derived from human iPSCs established from normal subjects, in which a wild-type or mutant (PS1P117L) copy of the PSEN1 gene was introduced were used in this study, (n=3 for each group). RNA samples prepared from the cells were subjected to microarray analysis using the Affymetrix human Gene 1.0 ST platform (GPL6244).

first: Sugako

last: Oka


title: Gene expression analysis of human permanent dental pulp

status: Public on Nov 22 2016

city: Seoul

first: Seong-Oh

last: Kim

address: 250 Seongsanno, Seodaemun-gu

department: Pediatric dentistry

country: South Korea

institute: Yonsei University College of Dentistry

summary: Gene expression analysis data of human permanent dental pulp tissues

overall_design: human permanent dental pulp tissues was collected from healthy permanent premolars (n=25; from 5 males and 6 females, aged 11-25 yeas) extracted for orthodontic reasons. Gene expression profiles were conducted using cDNA microarray analysis.


title: Trichloroethylene-induced miRNA expression changes in B6C3F1 mouse liver

city: SuZhou

first: Tao

last: Chen

state: JiangSu

address: 199 Ren-Ai-rd

institute: Soochow University

summary: To know if Trichloroethylene (TCE) can induce miRNA expression changes in mouse liver, we use microarray to screen for differentially expressed miRNAs in the liver of mice exposed to TCE at a dose of 1000 mg/kg b.w. for 5days . In our results, nine miRNAs were selected by volcano plot filtering (fold change ≥ 2 and P-value ≤ 0.05), out of which eight were up-regulated and one was down-regulated. The differential expression of miR-182-5p, miR-34a-5p and miR-451a were validated by qPCR.

overall_design: Six B6C3F1 male mice were oral administrated with either corn oil or TCE (dissolved in corn oil, 1000mg/kg b.w per day) for 5 days. The expression changes of miRNAs in TCE exposured mouse liver were screened by microarray and were validated by qPCR.

first: Yan

last: Jiang


first: Stephen

last: Scherer

type: Genome binding/occupancy profiling by genome tiling array

summary: The Affymetrix CytoScan HD 2.5M and Illumina HumanOmni2.5  arrays are high resolution SNP platform for studying copy number variations in the human genome.  Both platforms have widely being used in both clinical and research settings for identifying causative variants as well as interrogating the genome for benign variants. We employed both platforms to investigate the risk factor CNVs in trios diagnosed with OCD. We genotyped 307 unrelated probands (including 174 complete parent-child trios; mean age of probands 7.9±3.5 years) and compared their genotypes to those of 3,861 population controls, in order to identify rare CNVs (<0.5% frequency) of at least 15 kb in size that might contribute to OCD. We uncovered de novo CNVs and Decipher Syndromes in probands. We have identified additional potentially risk factor CNVs impacting the coding sequencing of genes involved in brain functions.

overall_design: We employed Affymetrix Chromsome Analysis Suite (ChAS), iPattern, Nexus, and Partek algorithms to call CNVs from the CytoScan HD array data. Similarly, we detected CNVs from OMNI2.5M microarray data using iPattern, PennCNV, CNVPartition, and QuantiSNP. We defined a stringent set of variants when each variant was called by at least by two algorithms. We defined the ancestry and relatedness of the samples using PLINK

first: Paul

last: Arnold

first: Matthew

middle: J

last: Gazzellone

first: Mehdi

last: Zarrei


title: Expression data from Human CD4 T cells subpopulations of HIV+ patients and HIV- controls

status: Public on Nov 25 2016

city: Mexico

first: Gustavo

last: Olvera-García

address: Calzada de Tlalpan 4502

department: Research in Immunology

country: Mexico

institute: National Institute of Respiratory Diseases

summary:
Central memory CD4 T cells (TCM) have a critical homeostatic role in chronic HIV infection. We asked if TCM cells from HIV+ patients have a gene expression profile related with less proliferation and less survival capacities.
To determine the gene expression profile of CD4+ T cells subpopulations we performed microarrays (Human Gene 1.0 ST, Affymetrix) to identify differentially expressed genes between CD4+ T cells subpopulations from HIV+ patients and controls.

overall_design: We analyzed mRNA expression patterns of naive CD4+ T cells (TN), central memory CD4+ T cells (TCM), and effector memory CD4 T cells (TEM) from healthy controls, and TN and TCM cells from HIV+ patients for a total of 15 microarrays.

middle: O

last: García

first: Tania

last: Aguilar-García

first: Fany

last: Gutiérrez-Jasso

first: Ivan

last: Imaz-Rosshandler

first: Claudia

last: Rangel-Escareño

first: Lorena

last: Orozco

first: Irma

last: Aguilar-Delfín

first: Joel

last: Vázquez-Pérez

first: Joaquín

last: Zúñiga

first: Santiago

last: Pérez-Patrigeon

first: Enrique

last: Espinosa


title: Clonal variation in drug and radiation response among glioma-initiating cells is linked to  proneural-mesenchymal transition (CytoScanHD)

status: Public on Dec 13 2016

city: Uppsala

first: Bo

last: Segerman

address: Dag Hammarskjolds v 20

country: Sweden

institute: Uppsala University

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

summary: Intra-tumor heterogeneity is a hallmark of glioblastoma multiforme, and thought to negatively affect treatment efficacy. Here we establish libraries of glioma-initiating cell (GIC) clones from patient samples and find extensive molecular and phenotypic variability between clones, including a wide range of responses to radiation and drugs. This widespread variability was observed as a continuum of multitherapy resistance phenotypes linked to a proneural-to-mesenchymal shift in the transcriptome.

overall_design: Affymetrix CytoScan HD array analyses were performed according to the manufacturer's directions on DNA extracted from 30 clonal malignant glioma cultures and 6 bulk cultures representing the parental material used to derive clones.

first: Bengt

last: Westermark


title: Gene expression profiling of MRC-5 cells treated with 100 ug/mL regular-length pristine SWCNTs for 72 h

status: Public on Nov 23 2016

city: Bukit Jalil

first: Chee-Onn

last: Leong

country: Malaysia

institute: International Medical University

summary: A total of 30 genes were up-regulated and 19 genes were down-regulated > 1.5-fold following 100 ug/mL regular-length pristine SWCNTs treatment

overall_design: Microarray experiments were performed in duplicate as follows: MRC-5 cells were treated with 100 ug/mL regular-length pristine SWCNTs or control vehicle for 72 h. Total RNA from cells was extracted using Qiagen RNA isolation kit (Qiagen, Valencia, CA, USA) according to the manufacturers’ protocol. RNA purity was examined by spectrophotometric determination at 260/280 nm. The microarray hybridizations were carried out using the Affymetrix Human Gene 1.0 ST arrays.


title: Gene expression analysis of umbilical cord

first: Seong-Oh

last: Kim

summary: There were no studies about gene expression of umbilical cord tissue before. We performed this study to identify the gene expression of umbilical cord tissue.

overall_design: Umbilical cord  were obtained from three newborns. Gene expression profiles were conducted using cDNA microarray analysis.


title: Loss of the Histone Methyltransferase EZH2 induces Resistance to Multiple Drugs in Acute Myeloid Leukemia

city: Heidelberg

first: Christian

last: Rohde

address: Im Neuenheimer Feld 410

institute: Heidelberg University

summary: Here, we analyzed global gene expression changes that were associated with drug resistance in Acute Myeloid Leukemia using the Affymetrix microarray platform.

overall_design: Changes in global gene expression were determined with Affymetrix microarrays in the AML cell lines MV4-11 (drug-sensitive) and MV4-11R (drug-resistant). We generated the resistant cell line by continous cultivation of parental MV4-11 for 3 months with increasing concentrations of the Tyrosine Kinase Inhibitor PKC412.

first: Stefanie

last: Göllner

first: Carsten

last: Müller-Tidow


title: Kruppel like factors family expression in cervical cancer cells

status: Public on Nov 09 2016

city: México

first: MAURICIO

middle: SALCEDO

last: VARGAS

address: Cuauhtemoc 300

department: UIMEO

institute: Mexican Institute for Social Security

summary: Analysis of cervical carcinomas and cervical cell lines privides insight into gene expression profiling in mexican women

overall_design: The invasive carcinomas samples were squamous cell carcinomas. Normal cervix tissues were from women who underwent hysterectomy for non-malignant condition or for non-cervical cancer were included. All samples were taken after informed consent from the patients and were confirmed by phatology. The cervical cell lines included in this study were: Casky, SiHa, Hela, Inbl, CaLo, Rova, MS-751, Vipa, C-4 I, C-33A and keratinocyte cell line Hacat. These cell line were cultured in Dulbecco´s Modified Eagle Medium (DMEM) (Gibco Life Technologies Carlsbad, CA USA), suplemented with 10% Fetal bovine serum (Gibco) and 1% Penicillin-Streptomycin (Gibco) at 37°C and 5% CO2. All cells were cultured at 70-80% of confluence.

first: M

last: Salcedo

first: H

last: Arreola

first: O

last: Perez-Gozalez

first: D

last: Marrero

first: K

last: Taniguchi


title: Vulnerability of Purkinje cells induced from spinocerebellar ataxia type 6 patient-derived iPS cells

status: Public on Nov 08 2016

city: Hirakata

first: Keiko

last: Muguruma

address: 2-5-1 Shinmachi

department: Graduate School of Medicine

institute: Kansai Medical University


title: Microarray Samples for shACTL6A in HNSCC Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

status: Public on Nov 18 2016

city: Boston

first: Kenneth

last: Ross

address: 450 Brookline Ave., Rm M640

department: Pediatric Oncology

country: USA

institute: Dana-Farber Cancer Institute

summary:
Loss-of-function mutations in SWI/SNF chromatin remodeling subunit genes are observed in many cancers, but an oncogenic role for SWI/SNF is not well established. Here we reveal that ACTL6A, encoding a SWI/SNF subunit linked to stem and progenitor cell function, is frequently co-amplified and highly expressed together with the p53 family member p63 in head and neck squamous cell carcinoma (HNSCC). ACTL6A and p63 physically interact and cooperatively control a transcriptional program that promotes proliferation and suppresses differentiation, in part through activation of the Hippo-YAP pathway via regulators including WWC1.  Consequently, loss of ACTL6A or p63 in tumor cells induces YAP phosphorylation and inactivation, associated with growth arrest and terminal differentiation, all phenocopied by WWC1 overexpression. In vivo, ectopic ACTLC6A/p63 expression promotes tumorigenesis, while ACTL6A expression and YAP activation are highly correlated in primary HNSCC and predict poor patient survival. Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC.
Gene expression profiling of HNSCC cells with and without ablated endogenous ACTL6A via lentiviral shRNA.

overall_design: Examination of mRNA levels in head and neck squamous cell carcinoma (HNSCC) cell line FaDU after treatment with shRNA for a vector control or ACTL6A (2 hairpins) with 3 replicates for each treatment.

first: Srinivas

middle: V

last: Saladi

first: Leif

last: Ellisen


title: Expression data from glucosamine-treated human synovial MH7A cells

status: Public on Nov 07 2016

city: Bunkyo-ku

first: AKIMASA

last: SOMEYA

state: Tokyo

address: 2-1-1 Hongo

department: Department of Host Defense and Biochemical Research

institute: Juntendo University

summary:
Osteoarthritis (OA) is one of the major joint diseases. Glucosamine (GlcN) is widely used as a dietary supplement for OA. However, its precise mechanisms are not well understood. GlcN is utilized for the O-linked-N-acetylglucosamine (O-GlcNAc) modification of proteins, which participates in the regulation of cellular functions. In this study, we comprehensively analyzed the effect of GlcN and alloxan (O-GlcNAc transferase inhibitor, which prevented O-GlcNAc modification) on the gene expression using DNA microarray.
GlcN downregulated or upregulated genes. Furthermore, among the GlcN-downregulated or upregulated genes, the expression of 62.7% of the genes was restored by alloxan.. Thus, it is suggested that GlcN regulates the gene expression by an O-GlcNAc modification-dependent or -independent mechanism.

overall_design: Human synovial MH7A cells in 6-well plates were incubated in the presence or absence of GlcN (5mM), and then stimulated with 15 pg/ml IL-1β for 13h. In some experiments, cells were preincubated with 5 mM alloxan, and then incubated with 2 mM alloxan and 5mM GlcN, followed by stimulation with IL-1β. We prepared 5 kinds of cell samples. 1; Non-treated cells. 2; IL-1β-stimulated cells. 3; GlcN-treated  IL-1β-stimulated cells. 4; GlcN and alloxan-treated  IL-1β-stimulated cells. 5;  alloxan-treated  IL-1β-stimulated cells. All expreriments were repeated three times.

first: Akimasa

last: Someya

first: Isao

last: Nagaoka

first: Takako

last: Ikegami

first: Koji

last: Sakamoto


title: Microarray Samples for shTP63 in HNSCC Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

summary:
Loss-of-function mutations in SWI/SNF chromatin remodeling subunit genes are observed in many cancers, but an oncogenic role for SWI/SNF is not well established. Here we reveal that ACTL6A, encoding a SWI/SNF subunit linked to stem and progenitor cell function, is frequently co-amplified and highly expressed together with the p53 family member p63 in head and neck squamous cell carcinoma (HNSCC). ACTL6A and p63 physically interact and cooperatively control a transcriptional program that promotes proliferation and suppresses differentiation, in part through activation of the Hippo-YAP pathway via regulators including WWC1.  Consequently, loss of ACTL6A or p63 in tumor cells induces YAP phosphorylation and inactivation, associated with growth arrest and terminal differentiation, all phenocopied by WWC1 overexpression. In vivo, ectopic ACTLC6A/p63 expression promotes tumorigenesis, while ACTL6A expression and YAP activation are highly correlated in primary HNSCC and predict poor patient survival. Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC.
Gene expression profiling of HNSCC cells with and without ablated endogenous p63 via lentiviral shRNA

overall_design: Examination of mRNA levels in head and neck squamous cell carcinoma (HNSCC) cell lines JHU-029 and FaDU after treatment with shRNA for a vector control or TP63 with 3 replicates for each cell line and treatment


title: Microarray Samples for shTP63 in Immortalized HFK to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

summary:
Loss-of-function mutations in SWI/SNF chromatin remodeling subunit genes are observed in many cancers, but an oncogenic role for SWI/SNF is not well established. Here we reveal that ACTL6A, encoding a SWI/SNF subunit linked to stem and progenitor cell function, is frequently co-amplified and highly expressed together with the p53 family member p63 in head and neck squamous cell carcinoma (HNSCC). ACTL6A and p63 physically interact and cooperatively control a transcriptional program that promotes proliferation and suppresses differentiation, in part through activation of the Hippo-YAP pathway via regulators including WWC1.  Consequently, loss of ACTL6A or p63 in tumor cells induces YAP phosphorylation and inactivation, associated with growth arrest and terminal differentiation, all phenocopied by WWC1 overexpression. In vivo, ectopic ACTLC6A/p63 expression promotes tumorigenesis, while ACTL6A expression and YAP activation are highly correlated in primary HNSCC and predict poor patient survival. Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC.
Gene expression profiling of untransformed keratinocytes (HaCaT) with and without ablated endogenous p63 via lentiviral shRNA.

overall_design: Examination of mRNA levels in the immortalized human keratinocyte (HFK) cell line HaCaT after treatment with shRNA for a control vector or TP63 with 3 replicates for each treatment.


title: Vulnerability of Purkinje cells induced from spinocerebellar ataxia type 6 patient-derived iPS cells [1]

summary: Spinocerebellar ataxia type 6 (SCA6) is a dominantly inherited neurodegenerative disease characterized by loss of Purkinje cells in the cerebellum. SCA6 is caused by CAG trinucleotide repeat expansion in CACNA1A, which encodes Cav2.1, α1A subunit of P/Q-type calcium channel. However, the pathogenic mechanism and effective therapeutic treatments are still unknown. Here we have succeeded in generation of differentiated Purkinje cells that carry the patient genes by combining disease-specific iPS cells and self-organizing culture technologies. SCA6-iPS cells derived Purkinje cells exhibited increased level of whole Cav2.1 protein while decreased level of its C-terminal fragment and downregulation of the transcriptional targets TAF1 and BTG1. We further demonstrate that SCA6-Purkinje cells exhibit thyroid hormone depletion-dependent degeneration, which can be suppressed by two compounds, thyroid releasing hormone and Riluzole. Thus we have constructed an in vitro disease model recapitulating both ontogenesis and pathogenesis. This model would be useful for pathogenic investigation and drug screening.

overall_design: Examination of mRNA profile in 1 ES cell line, two healthy donnor-derived iPS cell lines, three case-derived iPS cell lines and 1 normal dermal fibroblasts.

first: Yoshihito

last: Ishida

first: Hideshi

last: Kawakami

first: Hiroyuki

last: Kitajima

first: Ayaka

last: Nishiyama

first: Yoshiki

last: Sasai

first: Haruhisa

last: Inoue


title: Comparative gene expression analysis of the human periodontal ligament and dental pulp in the human permanent teeth

first: Seong-Oh

last: Kim

summary: The periodontal ligament(PDL) and dental pulp tissues of human permanent teeth have a number of differences in their developmental processes, histological characteristics and functions. It can be figured out that these differences are attributable to genetic backgrounds of their cells organized tissues. The purpose of this study was to identify the gene-expression profiles and their molecular biological differences of periodontal ligament and dental pulp tissues from the human permanent teeth.

overall_design: PDL and pulp samples were obtained from healthy persons. Total RNA from the PDL and the pulp tissues were used to cDNA microarray analysis.


title: Differentially expression profiling in a brain metastasis of a papillary thyroid carcinoma and its technical replicate vs. non-brain metastatic papillary thyroid carcinomas,  and primary brain tumors

status: Public on Nov 01 2016

city: Jeddah

first: Hans-Juergen

last: Schulten

department: Center of Excellence in Genomic Medicine Research

country: Saudi Arabia

institute: King Abdulaziz University

summary: Experiment: Establishment of expression profiles in a brain metastasis from a PTC (RNA processing and hybridization to Affymetrix microarray done twice to yield a technical replicate), in non-brain metastatic, stage III and IV PTCs, and primary brain tumors. Biostatistics analysis identified genes and biofunctions related to the brain metastatic PTC.

overall_design: We extracted RNA from tumor specimens and RNA with an RIN > 5 was processed using the recommended processing kits and hybridized to Affymetrix Human Gene 1.0 ST arrays. The CEL files were quantile-normalized and ANOVA was applied to generate differentially expressed probe sets. Probe sets that were significantly associated with the brain metastasis were subjected to biofunctional analysis.

first: Sajjad

last: Karim


title: Gene expression data of micro RNA from skeletal muscle sample of pig breed Duroc and Pietrain with malignant hyperthermia syndrome homozygous negative

status: Public on Oct 21 2016

city: Dummerstorf

first: Siriluck

last: Ponsuksili

address: Wilhelm-stahl-allee 2

institute: FBN

summary: Gene expression data of micro RNA from skeletal muscle sample of pig breed Duroc and Pietrain at adult stage.

overall_design: miRNAs of skeletal muscle from Duroc and Pietrain at adult stage were hybridized to Affymetrix miRNA-3 Array.

first: Klaus

last: Wimmers


title: LncrRNA and mRNA expression profiling in human esophageal squamous cancer

status: Public on Oct 25 2016

city: Chongqing

first: Yuanyuan

last: Wu

address: Sha ping ba

institute: Third Military Medical University

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

summary: LncRNAs are characterized by transcripts more than 200 nucleotides in length with no or limited protein coding potential, emerging as a novel class of vital regulators in recent years. Aberrant lncRNA and mRNA expression has been linked to various human tumors. This study was aimed to identify new aberrant expression  lncRNA and mRNA in esophageal squamous cell carcinoma (ESCC) and invested the potential functions in this tumor.

overall_design: lncRNA and mRNA microarray analysis with 5 ESCC and adjacent non-tumor tissues was performed.

first: Yun

last: Bai

first: Kang

last: Yang

first: Liwen

last: Hoo


title: Gene expression in HCQ-S and HCQ-R cells

status: Public on Oct 29 2016

city: Philadelphia

first: Ravi

last: Amaravadi

address: BRB II/III 8th floor 465 Curie Blvd

department: Medicine

institute: University of Pennsylvania

overall_design: mRNA expression profiling of 4 cancer cell lines


title: Differential gene expression in human valve interstitial cells of normal aortic valves and calcified aortic valves

status: Public on Oct 23 2016

city: AURORA

first: fei

last: li

state: CO

institute: university of colorado

summary:
Valve interstial cells(VICs) are the major cellular compents in the aortic valve. Under pathological circumstances, normal VICs differentiate into myofibroblasts or osteoblast-like phentotypes, which play important roles in the pathogenesis of calcified aortic valve disease.
We used micrroarrary analysis to compare the global programme of gene expression in normal and calcified human aortic valve intersitial cells (VICs), in order to find out some key factors that mediate the phenotype change of VICs.

overall_design: Calcified aortic valve leaflets (n=5) were obtained intraoperatively from patients undergoing aortic valve replacement due to severe aortic stenosis at University of Colorado Hospital. Patients with a history of infective endocarditis, rheumatic heart disease, or a genetic syndrome were excluded. The normal aortic valve leaflets (n=5) were collected from the explanted hearts of patients with cardiomyopathy and undergoing heart trans¬plantation. Valve leaflets were digested by collagenase 1 to procure P0 VICs. Then P0 VICs were sub-cultured to get P1 VICs.A fraction of P1 VICs subject to RNA extraction and microarray analysis.

first: rui

last: song

first: xianzhong

last: meng


title: Gene expression analysis of cells undegoing oncogene induced senescence upon knockdown or ARID1B

status: Public on Nov 12 2016

city: London

first: Gopuraja

last: Dharmalingam

address: Faculty of Medicine, Imperial College, Hammersmith Hospital Campus

department: Epigenetics section

institute: MRC London Institute of Medical Sciences

summary: We used IMR90 ER:RAS cells infected with an empty vector or an shRNA for ARID1B and induced senescence by addition of 4OHT. 6 days later RNA was collected for gene expression analysis. With a functional screen we previously identified ARID1B as a new regulator of cellular senescence. By performing gene expression analysis we confirmed this finding and showed that knockdown of ARID1B prevents the expression of genes induced during senescence.

overall_design: 3 samples examined: Non-senescent cells (vector - 4OHT), Senescent cells (vector + 4OHT), Senescent cells expressing shRNA for ARID1B (shARID1B + 4OHT)

first: Sadaf

last: Khan

first: Jesus

last: Gil


title: Gene expression data from A2780 cells with BMI1 and lncRNA FAL-1 knockdown

status: Public on Nov 05 2016

first: Lin

last: Zhang

address: 3400 CIVIC CENTER BLVD BUILDING 421

summary: Human ovarian cancer cell line A2780 cells were infected with shRNA targeting  lncRNA FAL-1 and proteincoding gene BMI1. We used microarray to identify genes which were co-regulated by lncRNA FAL-1 and BMI1.

overall_design: A2780 -BMI1 knockdown and A2780-FAL-1 knockdown cells were generated by lentivirus infection. Cells were transducted with BMI1 ctrl, BMI1 shRNA1, BMI1 shRNA2, FAL-1 ctrl, FAL-1 shRNA1 and FAL-1 shRNA2.  Medium containing lentivirus was replaced 24 hours post-infection. 96 hours after infection, cells were harvested for RNA extraction.

first: Xiaowen

last: Hu


title: Affymetrix CytoScan HD array data for del(17p) Chronic Lymphocytic Leukemia samples

first: Sunita

last: Setlur

address: 221 Longwood Avenue

institute: Brigham and Women's Hospital

summary: We performed whole genome profiling in order to determine the landscape of genetic alterations assoicated with a subset of CLL that is characterized by deletions in 17p The number of copy number alterations predicted shorter time to treatment among patients untreated at sampling. Chromosome 3p, 4p, and 9p were frequently deleted in del(17p) CLL and strongly associated with shorter OS. We conclude that del(17p) has a unique genomic profile characterized typically by TP53 mutation with novel CNAs and novel drivers, with increasing genomic complexity of any type associated with worse overall survival.

overall_design: Affymetrix CytoScan array analysis was performed on DNA extracted from peripheral blood samples (tumor) and saliva (normal) in order to determine genome-wide copy number alterations. Tumor DNA of 40 CLL patients with 17p deletion were included in the analysis along with DNA from one patient that did not harbor del(17p), but had a copy neutral LOH in 17p.

first: Jennifer

last: Brown


title: miRNA experiment of fresh frozen colonic biopsy samples

status: Public on Oct 19 2016

city: Budapest

first: Wichmann

last: Barna

address: Szentkirály

country: Hungary

institute: SOTE

summary: The aim of the present study was to perform an additional global miRNA microarray analysis of tubular and tubulovillous adenoma biopsy specimen completed with colorectal adenocarcinomas using fresh frozen tisse

overall_design: Total RNA was extracted from fresh frozen tissue samples from tubular and tubulovillous adenoma and colorectal adenocarcinoma samples were hybridized on Affymetrix Genechip miRNA 3.0 microarrays

first: Zsofia

last: Nagy

first: Barna

last: Wichmann

first: Béla

last: Molnár


title: The effect of vedolizumab (anti-α4β7-integrin) therapy on colonic mucosal gene expression in patients with ulcerative colitis (UC)

status: Public on Oct 11 2016

city: Leuven

first: Ingrid

last: Arijs

address: Herestraat 49

department: Clinical and Experimental Medicine

country: Belgium

institute: KULeuven

summary: Microarrays were used to investigate the the effect of vedolizumab (VDZ) therapy on colonic mucosal gene expression in UC patients and compared the changes to those observed with infliximab (IFX) therapy.

overall_design: 120 colonic biopsies from 44 UC patients were collected at protocol-specified time points [week (W) 0, W6, W12 and W52] during two phase 3 trials of VDZ (GEMINI I and LTS). Biopsies were compared with 12 non-IBD colonic biopsies and colonic biopsies from 23 UC patients before and W4-6 after first IFX. Response was defined as endoscopic mucosal healing (Mayo endoscoipc subscore 0 or 1) and was assessed for VDZ at W6/12/52, and for IFX at W4-6. Total RNA extracted from mucosal biopsies was used to analyze mRNA expression via Affymetrix Human Gene 1.0 ST arrays

first: Gert

last: De Hertogh

first: Leentje

last: Van Lommel

first: Frans

last: Schuit

last: Van Assche

first: Paul

last: Rutgeerts

first: Severine

last: Vermeire