title: Newborn and young adult (2 months) mouse dorsal skin cell culture time-series RNA-Seq

status: Public on Sep 14 2017

first: Mingxing

last: Lei

state: California

address: 2011 Zonal Ave HMR 304A

institute: University of Southern California

summary: Organoid formation is critical to the progress of regenerative medicine. We use the formation of skin organoids from dissociated cells to study the self-organization process. Here we live-image the process which reveals an unexpectedly complex morphogenetic process: dissociated cells – aggregates – polarized cysts – fused cysts– planar skin – hair placodes. Transcriptome profiling and functional testing show orderly expression peaks of adhesion molecules, insulin-like growth factors, Wnts, extracellular matrix molecules, and matrix metalloproteinases are crucial to the sequential morphological transitions. We draw an analogy between these self-organizing morphogenetic behaviours and the self-assembly of molecules in biophysics, with different morphological stages connected by phase transition-like switches. Adult cells, normally stalled as aggregates, can be restored to reform hairy skin by reactivation of the self-organization process with timely supply of molecular cues. Physical processes and molecular events may work in tandem to achieve organoid self-formation in tissue engineering and in vivo.

overall_design: Comparison of mRNA profiles in newborn and young adult (about 2 months) mouse dorsal skin reconstitution cells at different culture time points

first: Cheng-Ming

last: Chuong


title: Determination of Lsd1 function in inguinal white adipose tissue (ingWAT) by global transcriptome analysis

status: Public on Aug 22 2017

city: ILLKIRCH

first: Delphine

last: Duteil

address: 1 rue Laurent Fries

country: France

institute: IGBMC

type: Expression profiling by high throughput sequencing

summary: To investigate the role of Lsd1 in ingWAT we crossed mice harboring conditional Lsd1 alleles (Zhu et al., 2014) with the Adipoq-Cre deleter strain (Eguchi et al., 2011), which results in Cre-mediated loss of Lsd1 selectively in adipocytes. Transciptome analysis of ingWAT obtained from control and knock-out mice revealed 727 genes differentially expressed between Lsd1 knock-out and control mice at 6 weeks of age (p-value<10-2).

overall_design: We selectively knocked-out Lsd1 in adipose tissue by crossing Lsd1 floxed mice to Adipoq-Cre mice. RNA from inWAT of 6 week.old control (Lsd1 floxed mice) and knock-out mice was extracted with trizol according to the manufacturer protocol. RNA samples were sequenced by the standard Illumina protocol to create raw sequence files (.fastq files). We annotated these reads to the mm10 build of the mouse genome using TopHat version 2. The aligned reads were counted with the homer software (analyze RNA) and DEG’s were identified using EdgeR and DESeq version 1.8.3.

first: Dominica

last: Willmann

first: Roland

last: Schüle


title: Activation of Heat Shock Response Augments Fibroblast Growth Factor-1 Expression in Wounded Lung Epithelium: A Possible Mechanism for Progressive Lung Fibrosis

status: Public on Sep 08 2017

city: Bethesda

first: Gabriela

middle: A

last: Ferreyra

state: MD

address: 9000 Rockville Pike - Building 10 room 4D03

department: CCMD

country: USA

institute: Clinical Center

summary: Human cells were resistant to apoptosis induced by TNFα and Heat Shock (HS). Wound healing in NHBE and A549 cells occurred 30-50% more rapidly when cells were exposed to HS immediately after wounding. Gene expression analysis showed that HS synergized with wounding to increase expression of FGF1 by 30-fold. Enhanced FGF1 expression was blocked by inhibitors of p38 MAP kinase (SB203580) and heat shock factor (HSF)-1 (KNK-437) and in HSF1 knockout BEAS2B cells. Accelerated wound closure was reduced by SB203580, KNK-437, and by SU-5402, an inhibitor of FGF receptors 1 and 3. FGF1 was expressed in A549 and BEAS2B from promoters C and D. Finally, we found that FGF1 and HSP70 mRNA levels were 7.5- and 5.9-fold higher in IPF than normal lung. Confocal immunofluorescent microscopy showed FGF1 and HSP70 to be co-localized in affected regions of IPF but not normal lung. Epithelial injury and HS synergize to activate expression of FGF1 in lung epithelium through mechanisms that include p38 MAP kinase and HSF1. FGF1 expression and heat shock pathway activation is increased and colocalizes to defined foci in IPF lung, suggesting this pathway may have an important impact on lung injury, healing, and fibrosis.

overall_design: A549 monolayers were grown on plastic and closure rate in the scratch wound assay measured. Differential gene expression was analyzed in untreated, heat shocked, multiply wounded, and wounded+heat shocked A549 monolayers by microarray and confirmed by qRT-PCR and Western blotting.

first: Rachel

middle: G

last: Scheraga

first: Jeffrey

middle: D

last: Hasday


title: Temporal Changes in MicroRNA Expression in Blood Leukocytes from Patients with the Acute Respiratory Distress Syndrome

summary: MicroRNA (miRNA) control gene transcription by binding to and repressing the translation of messenger RNA (mRNA). Their role in the acute respiratory distress syndrome (ARDS) is undefined. Blood leukocytes from 51 patients enrolled in a prior randomized trial of corticosteroids for ARDS were analyzed. After screening eight patients with microarrays for increased miRNA expression, 25 miRNAs were selected for further analysis using RT-PCR in all 51 patients on days 0, 3 and 7.

overall_design: Randomized, double blind, placebo-controlled trial compared placebo and standard supportive therapy (usual care) to standard therapy plus early low-dose methylprednisolone infusion (1 mg/kg/day for 14 days and then tapered over 2 wks) using a 1:2 randomization schedule in intubated patients enrolled within 72 hours of ARDS onset. Fifty-one patients (37 treated with corticosteroids and 14 with standard care alone) of the 91 patients enrolled in the original study had blood leukocyte samples available for analysis. Four patients samples from each group were used for microarray analysis at day 0 and day 3.

first: Purushottam

last: Narute

first: Nitin

last: Seam

first: Rongman

last: Cai

first: Junfeng

last: Sun

first: Anthony

middle: F

last: Suffredini


title: Z1031B Paired Gene Expression

status: Public on Jan 04 2017

city: st louis

first: Cynthia

last: Ma

state: Missouri

address: 4515 Mckinley, 4515 Mckinley

department: Medical Oncology

institute: Washington University

summary: Agilent gene expression arrays were used to compare proliferation signatures between pre-treatment and 2-4 weeks post treatment samples from Z1031B patients.

overall_design:
109 patients from clinical trial NCT00265759 with paired baseline (BL) and 2-4wk (2wk or M) post treatment arrays were analyzed.

This series contains re-analyzed samples from GSE29442, GSE35186, and GSE35191.

first: Jeremy

middle: W

last: Hoog


title: PD991 Gene Expression Arrays

status: Public on Apr 07 2017

summary: Agilent gene expression arrays were used for intrinsic subtyping and to measure changes after anastrozole (C1D1) and after combination of anastrazole and palbociclib (C1D15).

overall_design: 118 breast cancer patient samples (baseline, n=32; C1D1, n=33; C1D15, n=29; surgery, n=24) from clinical trial NCT01723774 were arrayed, subtyped, and used to detect changes with treatment.


title: Gene transcription analysis of Daphnia magna multigenerations exposed to carbendazim

status: Public on May 01 2017

city: Aveiro

first: Ana

last: Soares

address: Campus de Santiago

country: Portugal

institute: University of Aveiro

summary: Pesticides are continuously released into the environment, with possible long-term consequences on aquatic organisms. One of the pesticides still applied in several crops in some countries is the fungicide carbendazim, ending up in surface waters with concentrations reaching 5 µg/L. Daphnia magna (clone k6) was used in this study as a model organism and it was exposed to a sub-lethal concentration of carbendazim (5 µg/L) for twelve generations. Gene expression alterations induced by this compound were assessed in the F0 and F12 generations using D. magna custom microarrays. Results revealed that carbendazim caused changes at the gene expression level in both generations. Genes involved in response to stress, DNA replication/repair, neurotransmission, protein biosynthesis, ATP production, lipids and carbohydrates metabolism were the most affected in both F0 and F12, although a lower number of differentially expressed genes were observed in the F12 generation exposed to carbendazim. The exposure of daphnids to carbendazim did not cause a stable change in gene expression from F0 to F12 generations. Effects at the gene expression level were early detected at the F0 generation after a short-time exposure (10 days), highlighting the advantages of using high throughput tools as early warning analysis but also providing information on chemical mode of action, which can add value in risk assessment procedures.

overall_design: For the microarray experiment, neonates with less than 24h were picked from the F0 and F12 generations from both clean medium and carbendazim. Three replicates per each treatment were used and consisted of 5 daphnids aging 10 days old.    A total of three replicates per treatment were used and each biological replicate was individually hybridized on the array. A single-color design was used, using the Agilent one-color RNA Spike-In Kit (AgilentTechnologies, Santa Clara, CA, USA), following the manufacturers protocol.

middle: R

last: Silva

first: Patrícia

middle: V

last: Moura

first: Amadeu

middle: M

first: Susana

last: Loureiro


title: The impact of low molecular weight hyaluronan on the lipidomic profile and global gene expression of peripheral blood mononuclear cells in asthma

status: Public on Nov 14 2016

summary:
Hyaluronan (HA) is the major glycosaminoglycan in the extracellular matrix involved in the pathogenesis of asthma and other chronic inflammatory diseases. During inflammation there is an increased breakdown of HA, resulting in the local and systemic accumulation of low molecular weight (LMW) HA. Eicosanoids, derived from cytosolic phospholipase A2 group IVA activation, are potent lipid mediators also attributed to acute and chronic inflammation. We investigated the effect of LMW HA on lipidomic profile and global gene expression in PBMCs of patients with mild-to-moderate and severe asthma. We found that LMW HA increased production of 68 unique lipid species, among which PGE2, PGA2, PGD2, PGF2a, 15-HETE, TxB2, 11,12-EET,  14,15 EET, 13-HOTrE(y) and 16 (17) EpDPE were significantly upregulated in severe asthmatics. We also performed a systematic  genome-wide expression analysis of LMW HA signaling, confirming its highly immunostimulatory potential.  However, in severe asthmatics the LMW HA-induced global gene expression profile showed a comprehensive impairment in interferon signaling, cell apoptosis and cell movement, leading to diminished antiviral  responses. Likewise, LMW HA-induced production of IL12 p40, CXCL10, CXCL11 and CCL8was markedly reduced in severe asthmatics. Our findings suggest a previously unforeseen link between extracellular matrix, global lipid production and antiviral responses in the pathogenesis of severe asthma.
We used microarray to perform a systematic genome-wide expression analysis of LMW HA effect in peripheral blood mononuclear cells in control subjects, mild-to moderate asthma and severe asthma patients

overall_design: Blood specimens from patients with mild-to moderate asthma and severe asthma, and control subjects were drawn after obtaining informed consent. Blood samples were processed immediately using lymphocyte separation medium (LSM) (Lonza, Walkersville, MD), according to the manufacturer’s protocol to obtain peripheral blood monuclear cells (PBMCs). 4x106 PBMCs were resuspended in 1 ml of RPMI 1640 medium with 2 mM of L-glutamine, supplemented with 10% heat-inactivated FBS and treated with purified LMW HA (MP Biomedicals; Solon, OH) (stimulated samples) or vehicle (unstimulated samples) for 6 h. Each experiment was performed in duplicates. LMW HA used in this study was a purified mixture of fragments between 50 kDa to 600 kDa. Each experiment was performed in the presence of polymyxin B sulfate (Calbiochem) (10 ug/ml) to exclude an effect of LPS contamination. Supernatants were collected and kept frozen in -80oC before further analyses. Cell pellets were lysed in RLT buffer, homogenized using QIAshredder columns (Qiagen, Valencia, CA) and stored at -80C before total RNA extraction. Only one unstimulated and one stimulated sample was used for microarray per each study subject. There were 3 groups of subjects: control nonasthmatics (n=6), mild-to-moderate asthmatics (n=7), and severe asthmatics (n=6). In total we run 38 chips.

first: Milena

last: Sokolowska

first: James

middle: H

last: Shelhamer


title: Mineralocorticoid receptor (MR) trans-activation of inflammatory AP-1 signaling: dependence on DNA sequence, MR conformation, and AP-1 family member expression

status: Public on Sep 20 2016

summary:
Mineralocorticoid receptor (MR) primarily promote cardiovascular inflammation by incompletely understood mechanisms.
The differential effects of GR and MR on inflammatory signaling and their contextual dependencies are relevant to the design of next generation drugs with improved safety and efficacy
While MR has been shown to weakly repress NFκB, its role in modulating AP-1 has not been established

overall_design: HEK293 cells were transfected with MR treated with vehicle alone, DOC (100 nM), PMA (10 nM) or DOC plus PMA

first: Edward

middle: J

last: Dougherty

first: Robert

middle: L

last: Danner


title: Comprehensive mapping of 5-hmC epigenetic dynamics in axon regeneration

status: Public on Dec 09 2016

city: New York

first: Hongyan

last: Zou

state: NY

address: 1425 Madison Avenue

department: Neuroscience

institute: Icahn School of Medicine at Mount Sinai

type: Methylation profiling by high throughput sequencing

summary: In contrast to CNS neurons, dorsal root ganglia (DRG) neurons can switch to a regenerative state after peripheral axotomy. In a screen for chromatin regulators of the regenerative responses in this conditioning lesion paradigm, we identified Tet methylcytosine dioxygenase 3 (Tet3) as upregulated, along with increased 5-hydroxymethylcytosine (5-hmC) in DRG neurons. We generated genome-wide 5-hmC maps in adult DRG, which demonstrated that peripheral and central axotomy (no regenerative effect) triggered differential 5-hmC changes that are associated with distinct signaling pathways. 5-hmC was altered in half of regeneration-associated genes (RAGs), supporting its role for RAG regulation. Our analyses predicted transcription factors HIF-1, STAT and IRF that may collaborate with Tet3 for 5-hmC modifications. Intriguingly, central axotomy lead to widespread 5-hmC modifications with little overlap with peripheral axotomy, thus potentially constituting a roadblock for regeneration. Our study revealed 5-hmC as a previously unrecognized epigenetic mechanism underlying the divergent responses after axonal injury.

overall_design: 5-hmC profiles generated from DRGs at 3 conditions (PL, DCL, Ctrl) plus Input, performed in triplicate


title: Molecular classification of bladder cancer: global mRNA classification versus tumor cell phenotype classification.

status: Public on Mar 13 2017

city: Lund

first: Pontus

last: Eriksson

state: Select:

address: Scheelevägen 2

department: Department of Clinical Sciences

country: Sweden

institute: Lund University

summary: In this study gene expression profiles for 307 cases of advanced bladder cancers were compared to molecular phenotype at the tumor cell level. TUR-B tissue for RNA extraction was macrodissected from the close vicinity of the tissue sampled for immunohistochemistry to ensure high-quality sampling and to minimize the effects of intra-tumor heterogeneity. Despite excellent agreement between gene expression values and IHC-score at the single marker level, broad differences emerge when samples are clustered at the global mRNA versus tumor cell (IHC) levels. Classification at the different levels give different results in a systematic fashion, which implicates that analysis at both levels is required for optimal subtype-classification of bladder cancer.

overall_design: 307 FFPE embedded bladder cancers and 28 lymph node metastasis were analyzed using the GeneChip Human Gene 1.0 ST Arrays (Affymetrix). Total RNA was extracted using the High Pure FFPET RNA isolation kit (Roche), assessed for quality using Nanodrop ND-1000, and labeled using SensationPlus FFPE Amplification and WT labeling kit. The full dataset of 335 CEL files were normalized using RMA by labeling batches. Batches were combined and RMA normalized. The data was filtered for probes with signal intensity less than the median of negative control probes for >80% of the values. Gene symbols and EntrezID were appended using Bioconductor (hugene10stprobeset.db Version 8.3.1). Probes not mapping to a gene symbol were removed. The probes were median merged by gene symbol and log-transformed. Batch correction was performed using ComBat. 307/335 samples were used in this cohort. These samples were median centered. ConsensusClusterPlus was run on the data with 7031 genes (50% variance filter).

first: G

last: Sjödahl

first: P

first: F

last: Liedberg

first: M

last: Höglund


title: Effects of BMPR2 Loss in Human Pulmonary Artery Endothelial Cells

status: Public on Dec 04 2015

first: Gabriela

last: Ferreyra

summary:
Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a proliferative endothelial cell phenotype, inflammation and pulmonary vascular remodeling. BMPR2 loss-of-function has been linked to pathologic plexiform lesions with obliteration of distal pulmonary arteries distal pulmonary arteries
BMPR2 silencing inprimary human pulmonary artery ECs (HPAECs) recapitulate important aspects of cellular dysfunction and deregulated signaling associated with PAH.

overall_design: Primary HPAECs were transfected with gene-specific siRNA pools targeting BMPR2 or control siRNA followed PMA or control stimulation.

first: Keytam

last: Awad

first: Jason

last: Elinoff


status: Public on Apr 01 2016

city: St. John's

first: Jessica

last: Esseltine

state: NL

address: 300 Prince Philip Drive

department: Division of Biomedical Sciences

country: Canada

institute: Memorial University of Newfoundland

summary:
Genome-wide expression array  measurements for  9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI)
Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma.
Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma.

overall_design: Comparison of transcription profiles between OSCC tumors with a more invasive (WPOI 5) versus a less invasive (WPOI 3) pattern of invasion using two independent Illumina platforms.

first: Thomas

last: Belbin

first: Jeffrey

last: Segall

first: Geoffrey

last: Childs


title: Dual Specificity Phosphatase 1 and Tristetraprolin cooperate to regulate macrophage responses to LPS and dexamethasone

status: Public on May 15 2015

city: Birmingham

first: John

middle: Daniel

last: O'Neil

address: Queen Elizabeth Hospital

department: Immunity and Infection

country: United Kingdom

institute: University of Birmingham

summary:
The mitogen-activated protein kinase (MAPK) p38 pathway is reported to regulate macrophage responses to lipopolysaccharide (LPS) at least partly via the phosphorylation of the mRNA-destabilizing factor tristetraprolin (TTP). LPS-activated MAPK p38 phosphorylates and activates the downstream kinase MAPK-activated protein kinase 2 (MK2), which then phosphorylates serines 52 and 178 of TTP, resulting in loss of mRNA-destabilizing activity. As a consequence, mRNAs that contain binding sites for TTP are stabilized in a manner that is acutely sensitive to the activity of the MAPK p38 pathway. Dual specificity phosphatase 1 (DUSP1) dephosphorylates and inactivates MAPK p38. Dusp1-/- macrophages overexpress a number of pro-inflammatory mediators, but their genome-wide responses to LPS have not yet been described in detail. Dusp1-/- mice are exceptionally sensitive to a wide variety of inflammatory challenges, including experimental models of endotoxemia or sepsis. It has been suggested (but not yet proven) that DUSP1 controls the inflammatory response of macrophages in part via the regulation of MAPK p38 activity and TTP phosphorylation status.
We generated a mouse knock-in strain, in which codons 52 and 178 of the endogenous Zfp36 gene (which encodes TTP) were mutated to alanine codons. The mutation gives rise to a constitutively active form of TTP, which cannot be inactivated via the p38 MAPK pathway. The Zfp36aa/aa strain was back-crossed against C57/BL6 for > 10 generations. We also generated a double-targeted strain in which the Zfp36 mutation was combined with disruption of the Dusp1 gene. This expression array describes LPS responses of primary mouse bone marrow-derived macrophages of four genotypes, and closely matched genetic background: wild type (Dusp1+/+ : Zfp36+/+); TTP mutant (Zfp36aa/aa); DUSP1 knock out (Dusp1-/-); and double targeted (Dusp1-/- : Zfp36aa/aa). The data provide a comprehensive picture of the impact of Dusp1 deletion or TTP mutation on the responses of primary macrophages to LPS. They also demonstrate that the excessive inflammatory responses of Dusp1-/- macrophages are largely a consequence of the phosphorylation and inactivation of TTP.

overall_design: Genome wide expression profiles of wild type, Dusp1-/-, Zfp36aa/aa and Dusp1-/-/Zfp36aa/aa M-CSF derived macrophages, stimulated with LPS for 1 or 4 hours, or LPS plus dexamethasone for 4 hours.

first: Tim

last: Smallie

first: Ewan

last: Ross

first: Michael

last: Ridley

first: Andrew

last: Clark


title: Epigenome analysis of oropharygeal squamous cell carcinoma

status: Public on Jun 07 2014

summary: Genome wide DNA methylation profiling of normal and primary oropharyngeal squamous cell carcinoma tissue samples, some infected with the human papilloma virus (HPV). The Illumina Infinium 27k Human DNA methylation Beadchip  was used to obtain DNA methylation profiles across approximately 27,000 CpGs in tissue samples. Samples included 46 oropharyngeal SCC primary tumors and 46 normal adjacent mucosal samples. For each tumor sample, HPV status (positivity based on both DNA and E6/E7 RNA) and p16 immunohistochemistry status is included.

overall_design: Bisulphite converted DNA from the 46 primary tumors and 46 matched adjacent normal samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip.

first: Nicolas

last: Schlecht


title: Late Multiple Organ Surge in Interferon-regulated Target Genes Characterizes Staphylococcal Enterotoxin B Lethality

status: Public on Mar 01 2014

summary: Bacterial superantigens are virulence factors that cause toxic shock syndrome. Here, the genome-wide, temporal response of mice to lethal intranasal staphylococcal enterotoxin B (SEB) was investigated in six tissues (PBMC, lung, spleen, kidney, heart, Liver).The earliest responses and largest number of affected genes occurred in tissues (PBMCs, spleen and lung) with the highest content of both T-cells and monocyte/macrophages, the direct cellular targets of SEB.  In contrast, the response of liver, kidney and heart was delayed and involved fewer genes, but revealed a dominant genetic program that was seen in all 6 tissues.  Many of the 85 uniquely annotated transcripts participating in this shared genomic response have not been previously linked to SEB.  Global gene-expression changes measured serially across multiple organs identified new candidate mechanisms of SEB-induced death.

overall_design: Toxin or saline (control) was administered to male C3H/HeJ mice in 5 independent experiments. Toxin or saline was administered i.n. followed by an i.p dose two hours later. Lung, liver, heart, spleen and kidney were harvest and preserved for tRNA purification at each time point. Each PBMC sample corresponded to a pooled sample (10 mice per time point).  Samples from control animals were collected at time 0, 2.75 h, 5 h and 24 h.  Samples from SEB treatment were collected at 0h, 2.75h, 5 h and 24 h. Only 4 set of samples per tissue type were used for microarray.

first: Cumhur

middle: Y

last: Demirkale

first: Robert

last: Danner


title: Lysine-specific demethylase 1 controls beige adipogenesis

status: Public on Jun 10 2014

first: Delphine

last: Duteil

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The aim of this study is to identify the LSD1 genome binding profile in adipocytes.

overall_design: LSD1 binding profile in fat cells - samples and experiments will continue to be added to this study over the course of the project.

first: Eric

last: Metzger

first: Dominica

last: Willmann

first: Roland

last: Schüle


title: Transcriptional profiling comparing MiaPaCa2 pancreatic cancer cells transfected with S100PBP siRNA to MiaPaCa2 cells transfected with non-targeting control siRNA

status: Public on Jan 01 2014

city: London

first: Claude

last: Chelala

state: London

address: Charterhouse square

department: Institute of Cancer

institute: Barts & The London School of Medicine (QMUL)

summary: S100PBP is significantly down-regulated in pancreatic cancer compared to normal samples. The functional roles of S100PBP are unknown, and therefore, profiling cells after silencing of this gene may lead to further understanding of its functional mechanisms.

overall_design: We have performed microarray gene expression analysis of MiaPaCa2 cells treated with S100PBP siRNA compared to the same cells transfected with non-targeting control siRNA.

first: Kate

last: Lines

first: Tatjana

last: Crnogorac-Jurcevic


title: Expression data from chronic lymphocytic leukemia (CLL) cells

status: Public on Jun 01 2015

city: Boston

first: Jennifer

middle: R.

last: Brown

state: MA

address: 450 Brookline Avenue

department: Department of Medical Oncology

institute: Dana-Farber Cancer Institute

summary: We compared gene expression profiles of CLL patients with and without MYD88 L265P mutations, taking into consideration IGHV mutation status.

overall_design: Total RNA was isolated from lymphocytes of CLL patients and gene expression was measured using Affymetrix U133 Plus 2.0 microarrays.

first: B

last: Tesar

first: M

last: Improgo

first: J

last: Klitgaard

first: R

last: Magori-Cohen

first: L

last: Yu

first: H

last: Kim


title: Transcriptional profiling comparing S100PBP over-expressing FA6 pancreatic cancer cells to vector-only control FA6 cells

summary: S100PBP is significantly down-regulated in pancreatic cancer compared to normal samples. The functional roles of S100PBP are unknown, and therefore, profiling cells over-expressing this gene may lead to further understanding of its functional mechanisms.

overall_design: We have performed microarray gene expression analysis of FA6 cells over-expressing S100PBP to vector-only control cells to gain clues on the cellular functions of S100PBP.


title: WHIM Gene Expression Data_Update Through WHIM 26

status: Public on Oct 10 2013

first: Cynthia

last: Ma

summary: The objective of this microarray study was to obtain whole genome gene expression data from breast cancer, human to mouse xenograft models and from the primary cancer used for the xenograft, when possible.  We also profiled these xenograft breast cancer tumors as they were passaged into additional mice.  Whole Genome expression data allows us to monitor gene expression conservation and/or changes that occur from human to mouse, and from the initial mouse graft through subsequent passages.  PAM50 molecular subtypes are also processed using the expression data.  The xenografts provide in-vivo models for  functional and therapeutic studies.

sample_organism:
Homo sapiens
Mus musculus

overall_design: 62 mRNA microarray experiments were completed for 19 different WU-BC (Washington University-Breast Cancer) lines which also had data from a patient biospy as well as multiple passages from a mouse xenograft.  2 tumors had data from mouse xenograft passages but no data from the patient biopsy.  Each representative patient tumor sample and mouse xenograft passage was amplified, labeled, and co-hybridized with a reference sample.

first: Jeremy

last: Hoog


title: Transcriptional profiling of pancreatic cancer cell lines not expressing or over-expressing S100BP

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

overall_design: Refer to individual Series


title: Retinoic acid determines the in vivo fate-commitment of splenic pre-dendritic cells

status: Public on Aug 16 2013

first: Gabriela

last: Ferreyra

summary: Comparison of gene expression changes of FACS sorted splenic CD11b+CD8a- and CD11b-CD8a+ cDC subsets reconstituted in vivo following total body irradiation in combination with exogenous retinoic acid or vehicle control.

overall_design: Mice maintained on a control diet were subjected to 6 Gy total body irradiation and then provided exogenous retinoic acid or vehicle control beginning on D(+)3 after irradiation. All treated mice also received adoptive T cell transfer of either Trp-1 CD4+ or Pmel-1 CD8+ T cells, rVV, and IL-2.  Splenic cDCs were isolated on D(+)10 after total body irradiation by FACS sorting.

first: Christopher

last: Klebanoff


title: WU-BC 3, 4, and 5 PAM50 Subtypes with Passage and Gene Expression Comparison Between Xenografts and Primary Tumors

status: Public on Oct 10 2012

summary: Whole genome expression studies were performed on Xenograft panels with multiple passages from 3 different patient tumors.  We assessed the global gene expression concordance from passages to passage and from passage to primary tumor when available and performed PAM50 subtype classification.  These results were examined within the context of 40  PAM50 prototype experiments.

overall_design: Thirteen experiments representing different tumor passages from WU-BC 3, 4, and 5 were compared using unsupervised hierarchical clustering and PAM50 Subtype Classification.  These experiments were analyzed within the context of previously published PAM50 Prototypes (GSE26082).

first: C

middle: X

first: S

last: Cai

last: Li

middle: E

last: Ryan

first: Z

last: Guo

last: Lin

last: Goiffon

first: A

last: Prat

last: Aft

last: Ellis

last: Piwnica-Worms


title: Paradigm Test Set aCGH Array

status: Public on Jun 21 2012

type: Genome variation profiling by genome tiling array

summary: aCGH data was used in Paradigm analysis for exploration of networks affected by copy number and gene expression changes based on mutation spectra of recurrently mutated genes in breast cancer.

overall_design: 124 patients including 3 Pre-Operative Letrozole and 43 Z1031 patients were arrayed and analyzed


title: Paradigm Test Set


title: Changes of genes in time-dependent photoaged mouse model

status: Public on Jul 14 2014

city: Seoul

first: SP

last: JIN

address: 101 Daehak-ro

country: South Korea

institute: Seoul National University Hospital

summary:
Photoaging results from the damaging effects of long-term exposure to UV. It is characterized by deep wrinkle, but the mechanism is still lack. To better understand molecular events contributing to photoaging,
We used microarray analysis using an optimized in time-dependent wrinkle model in mice.

overall_design: We used non UV-irradiated 1 and 8 weeks as a control group and compared expression patterns with UV-irradiated 1, 2, 4, 6 and 8 weeks mouse skin. Three animals were used per each group.

first: Eun

last: Seo

first: Jin

last: Chung


title: BRC77 Agilent Gene Expression Arrays

last: Ma

summary: Agilent 44K whole genome studies were used to correlate gene expression values with mutations found in massively parallel sequencing experiments.

overall_design: 77 patients were profiled using Agilent's two-color microarray platform.  Tumor(cy5) was co-hybridized to a reference(cy3).


title: Paradigm Test Set Expression Array

summary: Expression data was used in Paradigm analysis for exploration of networks affected by copy number and gene expression changes based on mutation spectra of recurrently mutated genes in breast cancer.

overall_design: cohort of 124 total patients arrayed and analyzed.

last: Hoog


title: Oxygen induced complication of prematurity: from experimental data to prevention strategy

status: Public on Nov 01 2011

city: Oslo

first: Ståle

last: Nygård

address: Institute for Experimental Medical Research, Oslo University Hospital - Ulleval

country: Norway

institute: University of Oslo

summary: A prospective study was conducted in the Neonatal Intensive Care Unit of the University Children's hospital between September 1, 2008 and November 30, 2010. The entry criteria were (1) preterm birth below 32 weeks gestational age, (2) birthweight<1500g (VLBW). During the follow-up period, bronchopulmonary dysplasia (BPD) was diagnosed in 68 (61%) infants, including 40 (36%) children with mild disease, 13 (12%) with moderate and 15 (13%) with severe BPD. Forty-three babies served as a control group (no BPD).

overall_design: One hundred twenty newborns were included at the start of the study. Three blood samples (0.3 ml) were drawn from all the study participants for microarray assessment of gene expression profiles around the 5th, 14th  and  28th days of life. Note that microarrays were not taken for all patients at all time points (A,B,C).

first: Przemko

last: Kwinta


title: A global map of RNA binding protein occupancy guides functional dissection of post-transcriptional regulation of the T cell transcriptome [Mm]

status: Public on Jul 01 2017

city: San Francisco

first: Adam

middle: Jacob

last: Litterman

state: CA

address: 513 Parnassus Avenue, UCSF Box 0414, HSE-201

department: Microbiology and Immunology

institute: UCSF

summary: RBP binding sites were globally mapped by a biochemical technique in mouse and human T cells

overall_design: Protein bound segments of mammalian mRNAs were sequenced by capture of crosslinked, biotinylated RBPs and compared to RNAseq

first: K

last: Ansel


title: Scf-GFP+ cells from the bone marrow and whole bone marrow microarray

status: Public on Feb 01 2012

first: Lei

last: Ding

institute: Columbia University Medical Center

summary:
The HSC niche factor SCF is required for HSC maintenance. Using an Scf-GFP knockin mouse, we have identified a perivascular cell type in the bone marrow expressing high level of Scf.
To characterize the novel Scf-GFP+ cells from the bone marrow, we performed microarray analysis on these cells.

overall_design: Total RNA were isolated from 3 independent, freshly aliquots of FACS sorted 5,000 SCF-GFP+ cells or whole bone marrow cells isolated from young adult mice. Purified RNA was amplified using the WT-Ovation™ Pico RNA Amplification system (NuGEN Technologies). Sense strand cDNA was generated using WT-Ovation™ Exon Module (NuGEN), then fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.

first: Sean

last: Morrison


title: Prototypes for 4x44K PAM50 Subtyping

status: Public on May 10 2011

first: Cynthia

summary: PAM50 intrinsic subtype classification (Parker JS, Mullins M, Cheang MCU, et al: Supervised Risk Predictor of Breast Cancer Based on Intrinsic Subtypes. J Clin Oncol 27:1160-1167, 2009) was used for the Z1031 patient cohort.  However, to account for potential technical biases such as differences in platforms and laboratory protocols between the Z1031 data set and the PAM50 training set2, we normalized the Z1301 data set before applying the PAM50 algorithm. This is a critical step that must be taken into consideration for appropriate subtype predictions as our group and others have previously shown3,4. To appropriately normalize the Z1301 microarray data, which is entirely composed of ER-positive tumors, we needed to estimate technical bias from a cohort with equivalent subtype representation as the PAM50 training set. A set including ER-negative, HER2-positive and true normal breast samples were profiled under the same platform, protocol and laboratory (i.e. WashU) as the Z1301 data set. A total of 40 prototypic samples of the various molecular subtypes were selected to match the distribution in the PAM50 training set. The mean expression of each PAM50 gene was calculated in this set of 40. These values obtained from the prototypical sample set were used for calibration purposes and were included as a new WashU_4X44K_Calibration column in the CalibrationParameter file, which has been already provided in the PAM50 algorithm2. This adjustment step assures that each sample is placed in the appropriate ‘prototypic space’ by subtracting the calibration value of each PAM50 gene from the expression value of the corresponding gene in each tested sample. Finally, single sample predictions were performed in every Z1301 sample using the WashU_4X44K_Calibration parameter.  The complete data set for the 40 prototypic arrays is submitted under GSE26082.

overall_design: 40 experiments were used as prototypical cases for subtype calibration purposes.

first: M

first: V

last: Suman

first: J

first: L

last: Lin

last: Snider

last: Parker

last: Luo

last: Deshryver

last: Esserman

first: G

last: Unzeitig

last: Margenthaler

last: Barbiera

first: P

middle: K

last: Marcom

last: Guenther

last: Watson

last: Leitch

last: Hunt

last: Olson


title: PIK3CB aCGH Cell Line Results

status: Public on Mar 06 2009

last: Ma

summary: The purpose of this study was to screen breast cancer cell lines for genomic amplification of the PIK3CB gene.

overall_design: 13 cell lines were analyzed for PIK3CB amplification.

first: Robert

last: Crowder

first: Chanpheng

last: Phommaly

first: Yu

last: Tao

first: Jeremy

last: Hoog

first: Jingqin

first: Charles

last: Perou

first: Joel

first: Melinda

middle: A

last: Miller

first: David

middle: G

last: Huntsman

first: Li

first: Jacqueline

first: Sherri

last: Davies

first: John

first: Mark

first: Anthony

last: Saporita

first: Jason

last: Weber

first: Matthew

last: Ellis


title: PIK3CB aCGH Patient Results

first: Cynthia

summary:
The purpose of this study was to screen pre-treatment breast cancer patients for genomic amplification of the PIK3CB gene.

Keywords: comparative genomic hybridization

overall_design: This experiment design includes 35 patient hybridizations using Agilent's 244k whole genome cgh array.  DNA from both the patient's tumor tissue and the patient's blood (germline) were processed and competitively hybridized to the same microarray.

first: Robert

last: Luo

last: Parker

last: Lin

last: Snider

middle: D


title: PI3K inhibition in ER+ breast cancer microarray data


title: Prognostic significance of copy-number alterations in multiple myeloma

status: Public on Aug 20 2009

city: Saint Herblain

first: Wilfried

last: Gouraud

address: bd Jacques Monod

department: Integrated Center of Oncology René Gauducheau

institute: ICO (Integrated Center of Oncology Nantes)

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

summary:
Purpose
Chromosomal aberrations are a hallmark of multiple myeloma but their global prognostic impact is largely unknown.

Methods
We performed a genome-wide analysis of malignant plasma cells from 192 newly myeloma patients using high-density, single-nucleotide polymorphism (SNP) arrays to identify genetic lesions associated with prognosis.

Results
Our analyses revealed deletions and amplifications in 98% of cases. Amplifications in 1q and deletions in 1p, 12p, 14q, 16q, and 22q were the most frequent lesions associated with adverse prognosis while recurrent amplifications of chromosomes 5, 9, 11, 15 and 19 conferred a favorable prognosis.
Multivariate analysis retained three independent lesions: amp(1q23.3), amp(5q31.3) and del(12p13.31).  When adjusted to the established prognostic variables ie t(4;14), and serum beta2-microglobulin (Sb2M), del(12p13.31) remained the most powerful independent marker (P <.0001; hazard ratio = 3.17) followed by Sb2M (P <.0001; hazard ratio = 2.78) and amp(5q31.3) (P =.0005; hazard ratio = 0.37). Cases with amp(5q31.3) alone and low Sb2M had an excellent prognosis  (5-year overall survival = 87%) conversely cases with del(12p13.31) alone or amp(5q31.3) and del(12p13.31) and high Sb2M had a very poor outcome (5-year overall survival = 20%). Moreover, integration of SNP mapping and gene expression identified CD27 as potential critical gene responsible for poor prognosis of del(12p) myeloma patients.

Conclusion
These findings demonstrate the power and accessibility of molecular karyotyping to identify novel strong independent prognostic markers:  amp(5q31.3) and del(12p13.31) and to provide insights into putative pathways deregulated in sub classes of cancer patients.

Keywords: Human chromosome copy-number alterations study

overall_design: 192 myeloma patients at diagnosis examined with 500K Set Affymetrix chips

first: Hervé

last: Avet-Loiseau

first: Cheng

last: Li

first: Florence

last: Magrangeas

first: Catherine

last: Charbonnel

first: Jean-Luc

last: Harousseau

first: Michel

last: Attal

first: Gerald

last: Marit

first: Claire

last: Mathiot

first: Thierry

last: Facon

first: Philippe

last: Moreau

first: Kenneth

middle: C

last: Anderson

first: Loïc

last: Campion

first: Nikhil

last: Munshi

first: Stéphane

last: Minvielle


title: PIK3C A/B/D expression distinctions between LumA/LumB, and between PIK3CA mut/wt, breast cancer patients

first: Cynthia

last: Ma

summary:
This ER+ patient dataset was used to retrieve gene expression values for the PIK3CA, PIK3CB, and PIK3CD genes.  Patient data was separated into two groups for two separate analyses to determine statistical differences between means of the PIK3 genes between 1) LumA and LumB patients, and 2) PIK3CA mutant and wildtype patients.

Keywords: Gene expression profiling

overall_design: Patient tumors were profiled on Agilent's 1x44k Whole Human Genome array.  Patient tumor RNA was amplified and labeled in the cy5 channel and competitively hybridized with a reference control sample that was amplified and labeled in the cy3 channel. 75 patient experiments were included: 31 LumA and 44 LumB, 27 PIK3CA mutant and 47 PIK3CA wild-type.

last: Crowder

first: Chanpheng

last: Phommaly

first: Yu

last: Tao

first: Jeremy

middle: W

last: Hoog

first: Jingqin

last: Luo

first: Charles

last: Perou

first: Joel

last: Parker

first: Melinda

last: Miller

first: David

last: Huntsman

first: Li

last: Lin

first: Jacqueline

first: Sherri

middle: R

last: Davies

first: John

last: Olson

first: Mark

last: Watson

first: Anthony

last: Saporita

first: Jason

last: Weber

first: Matthew

last: Ellis


title: FGFR1 Signature

status: Public on Dec 31 2016

first: Cynthia

last: Ma

type:
Expression profiling by array
Third-party reanalysis

summary: The gene encoding fibroblast growth factor receptor 1 (FGFR1) amplification is associated with poor prognosis in estrogen receptor positive (ER+) breast cancer, and thus represents a potential therapeutic target. Fluorescent in situ hybridization (FISH) has been used as the gold standard methodology for detection of FGFR1 amplification, but it is a relatively long labor-intensive procedure and not efficient to process a large number of patient samples, especially formalin fixed paraffin embedded (FFPE) samples. This study sought to identify genes discriminative at the mRNA level for FGFR1 amplification and to construct a multi-gene test to facilitate efficient screening for FGFR1 amplified ER+ breast tumors.

overall_design: 64 Pre-Operative Letrozole and Z1031 patients found to be FGFR1 amplified by aCGH were analyzed for their gene expression patterns. This study involves one new sample and 63 previously submitted samples. After applying a quality control filter, the new and reprocessed data are linked to the Series record.