status: Public on Jan 27 2010

city: Beijing

first: Bin

last: Wan

address: 18 shuangqing road, Haidian District

institute: Research centre for eco-environmental sciences, CAS

summary: Single-walled carbon nanotubes (SWCNTs) are being explored and used for a wide range of applications in industrial and medical sectors, and the increasing exposure of SWCNTs necessitate the studies of their potential environmental and health effects. Considerable efforts have been made to improve the dispersion of SWCNTs by chemical modifications. The present study was designed to determine if the acid functionalization of SWCNTs enhanced the toxicity and more efforts were made to understand the molecular mechanisms. RAW264.7 cells were exposed to 0-100μg/mL of SWCNTs and AF-SWCNTs for 24 hours and cell proliferation, viability, and gene expression profiles were assessed and compared. Results showed that the magnitude of AF-SWCNT-induced cell proliferation inhibition was higher than that of SWCNTs. 10μg/mL of AF-SWCNTs was determined as non-toxic to cells by viability analysis. AF-SWCNTs could enter and aggregate in cell cytoplasm and nuclear areas. Microarray, real-time reverse-transcriptase polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assays (ELISA) demonstrated that AF-SWCNTs (1, 10, and 50μg/mL) altered gene and protein expression patterns. The most differentially expressed genes were related to pro-inflammatory cytokines and chemokines (such as CCL-3 and CCL-4), apoptosis (e.g., Caspase-1, -4, and Dffa), protective response (such as Hmox-1and GSTM3), and cell surface molecules such as ICAM-1, Itgb2, indicating a possible involvement of SWCNT in inflammation, anti-apoptotic and DNA fragmentation, carcinogenesis and biased T cell polarization. Furthermore, a substantial amount of down-regulated genes were found related to ribosomal assembly and mitochondrial respiration chain, implicating a possible mechanism of SWCNT-induced oxidative stress and gene expression inhibition.

overall_design: RAW264.7 gene expression after exposure to 1-50ug/ml AF-SWCNT-24 hours. 0ug/ml of AF-SWCNT was used as control sample. The data were obtained from three biological replicates.


title: Affymetrix SNP array data for non-small cell lung cancer cell line samples, PC-9

status: Public on Dec 09 2009

city: Boston

first: Pasi

last: Janne

state: MA

address: 44 Binney Street Dana 820

department: Medical Oncology

country: USA

institute: Dana-Farber Cancer Institute

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

summary: PC-9 cells were exposed in vitro to the reversible EGFR inhibitor ZD1839 (gefitinib) and resistant clones were isolated. One of these resistant clones (PC-9 GR4) was then exposed to the irreversible EGFR inhibitor PF00299804 and dual-resistant clones (PC-9 DRs), or those resistant to both ZD1839 and PF00299804, were isolated.  In order to compare global genomic changes between PC-9, PC-9 GR, and PC-9 DR cells, we performed a genome-wide SNP analysis.

overall_design: Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from non-small cell lung cancer cell lines.  Each sample analyzed in single, with PC-9 serving as the reference sample.

middle: A

first: Ercan

last: Dalia


title: Gene expression of pancreatic cancer cells

status: Public on Jul 16 2009

city: Houston

first: Woonyoung

last: Choi

state: TX

address: 1515 Holcombe

institute: Md Anderson Cancer center

summary:
Global gene expression profiling on replicates of 9 pancreatic cancer cell lines (L3.6pl, BxPC3, CFPAC, SU8686, Panc-1, Hs766T, AsPC1, MIAPaca-2, MPanc 96) and normal HPDE cells was performed to elucidate multi-drug sensitivity/ resistance.

Keywords: D microarray (Illumina human 2)

overall_design: Duplicates of 9 pancreatic cancer cell lines and 1 normal HPDE cell line were used. Microarray experiment and data analysis were done at Dept. of Urology, MDACC (Houston, USA).

first: David

middle: J

last: McConkey


title: Transcriptional profiling of growth perturbations of the human malaria parasite Plasmodium falciparum

status: Public on Dec 16 2009

city: Singapore

first: Guangan

last: Hu

address: 60 Nanyang Drive

department: School of biological sciences

country: Singapore

institute: Nanyang Technological Unversity

summary: The microarray experiments were carried out using a long oligonucleotide DNA microarray that represent all 5363 P. falciparum genes with one oligonucleotide per 1.9kb of coding sequence on average (Hu et al. 2007). Total 247 microarray experiments were carried out including 29-drug treatment time courses with 20 compounds and corresponding untreated controls from different drug or inhibitor treatment. Data of each drug/inhibitor experiment were normalized using a linear normalization and background filtering as implemented by the NOMAD database (http://derisilab.ucsf.edu).

overall_design: Time-series sampling and experiments with synchronized ex vivo culturing parasites. Each experiment has treatment and controls, and starts at a specific time of post invasion. For an example of quinine treatment, the treatments start from late ring stage through trophozoite stage of the parasites. First, IC50 is determined by drug assay with synchronized parasites (5% parasiteomia and 2% RBC). Second, synchronized parasite cultures are splitted into 12 flasks (75ml culture/flask) for a 6 time-point time-series experiment. 6 flasks are treated with quinine (final concentration is IC50) and 6 flasks are negative controls. 1,2,4,6,8 and 10 hrs after the treatment, parasites in each flask were harvested for total RNA isolation and microarray hybridizaiton.

first: Sachel

last: Mok

first: Balbir

middle: K

last: Chaal

first: Zbynek

last: Bozdech


title: WT1 mutations in T-ALL

status: Public on Aug 10 2009

city: New York

first: Adolfo

last: Ferrando

state: NY

address: 1130 St Nicholas Ave Irving Cancer Research Center 5-505A

department: Institute for Cancer Genetics

institute: Columbia University

summary: The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood. We used single nucleotide polymorphism (SNP) array analysis to analyze paired diagnostic and relapsed T-ALL samples to identify recurrent genetic alterations in T-ALL. This analysis showed a notorious absence of acquired chromosomal changes at relapse. In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2/9 samples. Subsequent analysis showed WT1 mutations in 28/211 (13.2%) of pediatric and 10/85 (11.7%) of adult T-ALL cases. WT1 mutations present in T-ALL are predominantly heterozygous frameshift mutations resulting in truncation of the C-terminal zinc finger domains of this transcription factor. WT1 mutations are most prominently found in T-ALL cases with aberrant rearrangements of the oncogenic TLX1, TLX3 and HOXA transcription factor oncogenes. Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL. Overall these results show that overt chromosomal instability does not seem to be a major mutagenic mechanism contributing to disease progression in T-ALL and the presence of WT1 mutations as a recurrent genetic alteration in T-ALL.

overall_design: DNA samples from pediatric T-ALL patients (n=9) obtained at diagnosis, remission and relapse were analyzed with the GeneChip Human Mapping 250K Sty Array (Affymetrix, Santa Clara, California), which contains 238,000 SNPs. Copy number and LOH analysis was performed with dCHIP. Probe intensity data for each array was normalized to a baseline array with median signal intensity using the “invariant set” model, as previously described 11. We used matched remission samples as a reference for copy number estimation and loss of heterozygosity (LOH) analysis. LOH was analyzed using a Hidden Markov Model in dChip and an inferred LOH call threshold of 0.5.

first: Valeria

last: Tosello


title: Affymetrix SNP array data for non-small cell lung cancer cell line samples

status: Public on Oct 30 2009

summary: HCC827 cells were exposed in vitro to the irreversible EGFR inhibitor PF00299804 and resistant clones were isolated. These resistant clones (HCC827 PFR) contained an amplification of the MET gene and the growth of the HCC827 PFR cells was inhibited with the combination of PF00299804 and a MET kinase inhibitor.  Phenotypically, these HCC827 PFR cells were similar to our previously identified gefitinib resistant HCC827 (HCC827 GR) cells (Engelman et al. Science 2007). In order to compare global genomic changes between HCC827 GR and HCC827 PFR cells and to determine whether the MET amplicon was similar in both drug resistant cells we performed a genome wide SNP analysis.

overall_design: Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from non-small cell lung cancer cell lines.  Each sample analyzed in single, with HCC827 serving as the reference sample.

first: Jeffrey

last: Engelman


title: Affymetrix SNP array data for pediatric acute myeloid leukemia (AML) samples at diagnosis: Sty2 SNP array

status: Public on Jan 04 2010

city: Memphis

first: Jeffery

last: Klco

state: TN

address: 262 Danny Thomas Place

department: Pathology

institute: St Jude Children's Research Hospital

summary:
Genome-wide profiling of Copy Number Alterations (CNA) and Loss of Heterozygosity (LOH), gene expression and resequencing of pediatric AML.
This study characterizes the CNA and LOH in a representative cross-section through subtypes of pediatric AML. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved diagnostic bone marrow or peripheral blood samples.

overall_design:
111 pediatric AML samples were studied using either Affymetrix 100K + 500K 5.0 SNP arrays, 65 of the samples had paired germ line material.

The supplemental files 'GSE15731_AML_175_SNP_Sty_signal.txt' and 'GSE15731_AML_176_SNP_Sty_signal.txt' contain the raw signals generated by dChip without normalization.

The CNA and LOH data can be found in the Supplemental Information of the associated manuscript.

first: Ina

last: Radtke

first: James

middle: R

last: Downing


title: SNP array genomic profiling of PTCL NOS

status: Public on Mar 17 2010

city: Frankfurt am Main

first: Sylvia

last: Hartmann

country: Germany

institute: University Frankfurt

summary: DNA extracted from frozen tissue of 47 peripheral T-cell lymphomas–not otherwise specified [PTCL-NOS] was hybridized to 250k StyI SNP arrays

overall_design: 47 PTCL NOS compared to healthy reference DNA. DNA of PTCL NOS was extracted from frozen tissue blocks, DNA of healthy individual was extracted from peripheral blood mononuclear cells. Array hybridization was performed according to manufacturer´s protocol.


title: Affymetrix SNP array data for 30 NSCLC samples

status: Public on Sep 15 2009

city: Cambridge

first: Alexis

last: Ramos

address: 7 Cambridge Center

institute: Broad Institute

summary: In cancer, proto-oncogenes are often altered by genomic amplification.  Recent studies have highlighted a role for PDGFRA as an oncogene in non-small cell lung cancer.  To characterize 4q12 copy number status in NSCLC, both previously published (Weir et al. PMID 17982442) and unpublished Affymetrix 250K SNP array data for 733 NSCLC samples (628 primary samples, 105 cell lines) were evaluated for copy number aberrations.  4q12 amplifications overlapping the PDGFRA/KIT locus were observed in 31 (4.2%) NSCLC samples.  SNP array and FISH analysis indicate that 4q12 is amplified in 3-7% of lung adenocarcinomas and 8-10% of lung squamous cell carcinomas.  In addition, the NSCLC cell line NCI-H1703 exhibits focal amplification of PDGFRA and is dependent on PDGFRα activity for cell growth.  Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRα/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition. However, these observations do not extend to NSCLC cell lines with lower-amplitude and broader gains of chromosome 4q.  Together these observations implicate PDGFRA and KIT as potential oncogenes in NSCLC, but further study is needed to define the specific characteristics of those tumors that could respond to PDGFRα/KIT inhibitors.

overall_design: SNP array experiments were performed on 733 NSCLC tumor and cell line samples as described in Weir et al. (PMID: 17982442).  Experimental data for 30 of the 733 samples analyzed has not been previously published and is provided here.

first: Alex

middle: H

first: Amit

last: Dutt


title: Affymetrix SNP array data for 47 lung squamous cell carcinoma  and 40 esophageal squamous cell carcinoma samples.

status: Public on Oct 04 2009

first: Adam

middle: Joel

last: Bass

address: 44 Binney Street

summary: Lineage-survival oncogenes are targeted by gene amplification in cancers arising from the tissues where these genes play a role in normal development.  Here we show that the transcription factor SOX2—previously known to be mutated in hereditary human esophageal malformations, to be necessary for normal esophageal squamous development, to promote proliferation of basal tracheal cells and to co-operate in induction of pluripotent stem cells -- acts as an amplified oncogene in squamous cell carcinomas (SCC) of the lung and esophagus.  We identified SOX2 at a peak of genomic amplification on chromosome 3q26.33 in SCCs of both the lung and esophagus but did not find it to be significantly amplified in adenocarcinomas from these tissues.  Tumors with SOX2 amplification showed higher SOX2 mRNA expression, and suppression of SOX2 by RNAi in lung and esophageal SCC cell lines revealed that SOX2 expression is required for proliferation and anchorage-independent growth.  Furthermore, ectopic expression of SOX2 cooperated with FOXE1 or FGFR2 to transform immortalized tracheobronchial epithelial cells. SOX2-driven tumors showed expression of markers of both squamous differentiation and pluripotency.  These observations identify SOX2 as a novel lineage survival oncogene in lung and esophageal SCC and suggest novel connections between development, pluripotency and carcinogenesis.

overall_design: SNP array experiments were performed on 87  tumor samples and cell lines.  Tumor Samples were normalized against a reference panel of 1140 normal samples using tangent normalization.


title: ChIP-chip of H3K27Ac in Drosophila at different time points of development

status: Public on Mar 28 2009

city: Chicago

first: Kevin

middle: P.

last: White

state: IL

address: 900 E. 57th STR. 10th FL.

department: Institute for Genomics and Systems Biology

institute: University of Chicago

type: Genome binding/occupancy profiling by genome tiling array

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: H3K27Ac at 12 different time-points of Drosophila development.

Current Dataset:

[GSM386179..GSM386187]: ChIP-chip of H3K27AC in Drosophila embryos at 0-4 hours of development
[GSM386216..GSM386224]: ChIP-chip of H3K27AC in Drosophila embryos at 4-8 hours of development
[GSM386334..GSM386342]: ChIP-chip of H3K27AC in Drosophila embryos at 0-4 hours of development (second dataset)
[GSM418501..GSM418509]: ChIP-chip of H3K27AC in Adult male
[GSM441405..GSM441410]: ChIP-chip of H3K27AC in Drosophila embryos at 8-12 hours of development
[GSM441411..GSM441419]: ChIP-chip of H3K27AC in Drosophila embryos at 12-16 hours of development
[GSM441420..GSM441436]: ChIP-chip of H3K27AC in Drosophila embryos at 16-20 hours of development
[GSM441437..GSM441445]: ChIP-chip of H3K27AC in Drosophila embryos at 20-24 hours of development
[GSM441446..GSM441931]: ChIP-chip of H3K27AC in L1
[GSM441933..GSM441941]: ChIP-chip of H3K27AC in L2
[GSM441943..GSM441951]: ChIP-chip of H3K27AC in L3
[GSM441984..GSM441992]: ChIP-chip of H3K27AC in Adult male
[GSM441995..GSM442003]: ChIP-chip of H3K27AC in Pupae

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: For each combination of time-point and antibody, triplicate ChIP experiments have been performed and hybridized on Agilent 244K arrays. 3 arrays per genome have been used so that each time-point is a set of 9 tiling arrays.


title: ChIP-chip of H3K4me1 in Drosophila at different time points of development

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays H3K4me1 at 12 different time-points of Drosophila development.

Current Dataset:

[GSM386042..GSM386050]: ChIP-chip of H3K4Me1 in Drosophila embryos at 4-8 hours of development
[GSM386051..GSM386059]: ChIP-chip of H3K4me1 in Drosophila embryos at 12-16 hours of development
[GSM386060..GSM386068]: ChIP-chip of H3K4me1 in Drosophila embryos at 16-20 hours of development
[GSM386069..GSM386077]: ChIP-chip of H3K4me1 in Drosophila embryos at 20-24 hours of development
[GSM418275..GSM418283]: ChIP-chip of H3K4me1 in Drosophila embryos at 8-12 hours of development
[GSM442224..GSM442232]: ChIP-chip of H3K4me1 in Drosophila embryos at 0-4 hours of development
[GSM442233..GSM442241]: ChIP-chip of H3K4me1 in Drosophila Pupae
[GSM442242..GSM442250]: ChIP-chip of H3K4me1 in Drosophila L3
[GSM442251..GSM442259]: ChIP-chip of H3K4me1 in Drosophila L2
[GSM442260..GSM442268]: ChIP-chip of H3K4me1 in Drosophila L1
[GSM442269..GSM442277]: ChIP-chip of H3K4me1 in Drosophila Adult male
[GSM442278..GSM442286]: ChIP-chip of H3K4me1 in Drosophila Adulat female

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: ChIP-chip of CBP/p300 in Drosophila at different time points of development

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: CBP/p300 at 12 different time-points of Drosophila development.

Current Dataset:

[GSM386269..GSM386277]: ChIP-chip of CBP in Drosophila embryos at 4-8 hours of development
[GSM386279..GSM386287]: ChIP-chip of CBP in Drosophila embryos at 20-24 hours of development
[GSM418309..GSM418317]: ChIP-chip of CBP in adult female Drosophila
[GSM418318..GSM418326]: ChIP-chip of CBP in adult male Drosophila
[GSM418335..GSM418343]: ChIP-chip of CBP in Drosophila embryos at 16-20 hours of development
[GSM418454..GSM418462]: ChIP-chip of CBP in Drosophila L3 larvae
[GSM418463..GSM418471]: ChIP-chip of CBP in Drosophila pupae
[GSM442425..GSM442433]: ChIP-chip of CBP in Drosophila embryos at 0-4 hours of development
[GSM443119..GSM443127]: ChIP-chip of CBP in Drosophila L1 larvae

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: ChIP-chip of PolII in Drosophila at different time points of development

status: Public on Jun 24 2009

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. This Series contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: PolII at 12 different time-points of Drosophila development.

Note: 8wg16 is the name of PolII antibody for set2 datasets.

Current Dataset:

[GSM418514..GSM418522]: ChIP-chip of PolII in Drosophila pupae
[GSM418549..GSM418557]: ChIP-chip of 8wg16 in Drosophila adult female
[GSM418567..GSM418575]: ChIP-chip of 8wg16 in Drosophila embryos at 0-4 hours of development
[GSM418580..GSM418588]: ChIP-chip of 8wg16 in Drosophila embryos at 4-8 hours of development
[GSM418593..GSM418601]: ChIP-chip of 8wg16 in Drosophila L3 larvae
[GSM442398..GSM442406]: ChIP-chip of PolII in L2
[GSM442407..GSM442415]: ChIP-chip of PolII in L3
[GSM442416..GSM442424]: ChIP-chip of 8wg16 in Drosophila embryos at 4-8 hours of development - Set2
[GSM443110..GSM443118]: ChIP-chip of 8wg16 in Drosophila embryos at 16-20 hours of development

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: Nasopharyngeal carcinoma cell lines (copy number analysis)

status: Public on Mar 05 2009

city: Guangzhou

first: Zhong-Xi

last: Huang

address: Tonghe

department: Cancer Institute

country: China

institute: Southern Medical University

summary: Five NPC cell lines (HONE1, CNE1, CNE2, 5-8F, and 6-10B) and an immortalized nasopharyngeal epithelial cell line NP69 were evaluated with 250K SNP arrays (Affymetrix) to detect the genome-wide DNA copy number alterations.

overall_design: The same type of data of 45 Chinese samples from the HapMap project  was used as normal control. Data was analyzed using GCOS (GeneChip operating software, Ver.1.4), GTYPE (GeneChip Genotyping Analysis Software, Ver.4.1), and CNAT (chromosome copy number analysis tool, Ver.4.0, BRLMM algorithm).

first: Jin

last: Zhao

first: Jing

first: Yun

last: Liu

first: Kai-Tai

last: Yao


title: Imatinib targeting of KIT-mutant oncoprotein in melanoma

status: Public on Dec 24 2008

first: Stephen

last: Hodi

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

summary:
Metastatic melanoma is an aggressive treatment-refractory malignancy. Recently, c-Kit mutations were discovered in certain mucosal melanomas. A clinical trial was initiated with the c-Kit inhibitor imatinib mesylate.  The first treated patient experienced dramatic clinical improvement within days, followed by major responses by PET/CT four weeks later at all sites of metastatic disease. Several established mucosal melanoma cell lines exhibited imatinib sensitivity in a fashion correlating with c-Kit mutational status. Although c-Kit mutations are uncommon in cutaneous melanoma, they may arise in geographically distinct subsets for whom use of c-Kit targeted kinase inhibition should be considered in a rational therapeutic approach.
Keywords: Whole genome copy number analysis

overall_design:
Copy number analysis using high-density SNP arrays to investigate genetic gains and losses involved in the genesis of mucosal and cutaneous melanoma.

GSE8164_raw_copy_number_calls.xls contains raw copy number calls generated by dChip (build 5/2007) for GIST, K008, K029, M34, MEL1, MEL40, M6, and 5 Affymetrix controls (copy number identity 2 i.e. normal), which are available on the HapMAP site.

middle: F

first: Jun

last: Zhou

first: Noah

last: Yuen

first: Philip

last: Friedlander

first: Christopher

last: Corless

first: Michael

middle: C

last: Heinrich

first: Xiaofeng

last: Jiang

first: Suzanne

last: Mac Rae

first: Andrea

last: Kruse

first: Jyothi

last: Jagannathan

first: Annick

last: van den Abbeele

first: Elsa

last: Velazquez

first: Jonathan

last: Fletcher

first: Hans

last: Widlund

first: George

last: Demetri

first: David

middle: E

last: Fisher


title: ChIP-chip of H3K9me3 in Drosophila at different time points of development

first: Kevin

last: White

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. This Series contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: H3K9me3 at 12 different time-points of Drosophila development.

Current Dataset:

[GSM382158..GSM382166]: ChIP-chip of H3K9me3 in Drosophila embryos at 12-16 hours of development
[GSM384690..GSM384698]: ChIP-chip of H3K9me3 in Drosophila embryos at 0-4 hours of development
[GSM384723..GSM384731]: ChIP-chip of H3K9me3 in Drosophila embryos at 4-8 hours of development
[GSM384732..GSM384740]: ChIP-chip of H3K9me3 in Drosophila embryos at 16-20 hours of development
[GSM384741..GSM384749]: ChIP-chip of H3K9me3 in Drosophila embryos at 20-24 hours of development
[GSM384750..GSM384758]: ChIP-chip of H3K9me3 in Drosophila L1 larvae
[GSM384760..GSM384768]: ChIP-chip of H3K9me3 in Drosophila L2 larvae
[GSM418207..GSM418215]: ChIP-chip of H3K9me3 in Drosophila Adult male
[GSM418216..GSM418224]: ChIP-chip of H3K9me3 in Drosophila embryos at 8-12 hours of development
[GSM442371..GSM442379]: ChIP-chip of H3K9me3 in Drosophila Adult male - Set2
[GSM442380..GSM442388]: ChIP-chip of H3K9me3 in Drosophila Pupae
[GSM442389..GSM442397]: ChIP-chip of H3K9me3 in Drosophila L3 larvae

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: Fine-scale mapping of copy-number alterations with massively parallel sequencing

status: Public on Nov 14 2008

city: Chapel Hill

first: Derek

last: Chiang

state: NC

address: UNC Lineberger Cancer Center, 450 West Drive, CB #7295

department: Department of Genetics

institute: University of North Carolina

summary:
In order to benchmark the reproducibility of Affymetrix 238K Sty arrays for detecting copy-number alterations.  We performed replicate hybridizations of 3 tumor cell lines and 2 paired normal cell lines obtained from the American Type Culture Collection (ATCC).
We calculated copy numbers at each SNP probeset by array pre-processing with the GISTIC algorithm (PMID: 18077431). For each SNP probeset, we calculated the median copy number across replicate arrays.  The median copy number profile for each tumor cell line was segmented with the GLAD algorithm (PMID: 15381628) to partition the genome into regions of constant copy number.
We compared the copy-number alterations detected by GLAD segmentation of these arrays with statistical analyses of short sequence reads obtained from the Illumina/Solexa 1G GenomeAnalyzer.  Shotgun sequencing results can be found in the NCBI Short Read Archive, accession number SRP000246.

Keywords: disease state analysis

overall_design: 77 replicates of HCC1143 (breast ductal carcinoma), 69 replicates of HCC1143BL (matched normal), 42 replicates of HCC1954 (breast ductal carcinoma), 36 replicates of HCC1954BL (matched normal), 1 replicate of NCI-H2347 (lung adenocarcinoma)

middle: Y

first: Gad

last: Getz

last: Jaffe

first: Xiaojun

last: Zhao

first: Scott

middle: L

last: Carter

first: Carsten

last: Russ

first: Chad

last: Nusbaum

first: Matthew

last: Meyerson

first: Eric

middle: S

last: Lander


title: Optimizations of DNA isolation and copy number analysis identifies regions of genomic gain/loss in early breast cancer

status: Public on Sep 18 2008

first: Ralf

last: Krahe

address: 1515 Holcombe Blvd., Unit #1010

department: Cancer Genetics

institute: University of Texas M.D. Anderson Cancer Center

summary:
DNA copy number changes with or without accompanying copy neutral changes such as unparental disomy (UPD) is a feature of the cancer genome that is linked to cancer development.  However, technical problems with archived formalin-fixed, paraffin-embedded (FFPE) tissue samples have limited their general use in genomic profiling studies done using high-density single nucleotide polymorphism (SNP) microarray.  To overcome the current problems with the use of this material in the detection of DNA copy number and copy neutral changes, we have devised two new protocols for extracting DNA from FFPE tissue.  Genotyping efficiency and accuracy were improved using our novel protocols.  After censoring the larger fragments, we obtained call rates for FFPE DNA equivalent to those for FF tissue DNA, with concordance rates between FFPE and FF tumor exceeding 99%.  Identical DNA copy number changes were obtained for FFPE and FF; and between two new extraction protocols in tumor samples by using Affymetrix® high-density oligo-based SNP microarray platform.  We observed UPD and recurrent gains and losses in tumor samples.  Interestingly, we also identified UPD in the 5q and 13q regions in matching normal blood, FF adjacent breast tissue and tumor tissue in two samples.  In conclusion, our new two DNA extraction protocols should substantially improve the ability to use archived material to help elucidate the complexity of early-stage breast cancer genomes.
Keywords: SNP based array

overall_design:
Using the Affymetrix GeneChipR Mapping 250K Assay we studied primary breast tumor and normal samples with different DNA extraction protocols

Abbreviations: Tumor (T), Normal (N)_sample number_tissue type (FFPE formalin fixed parafin embedded), FF (fresh frozen), peripheral blood (PBL)_DNA extraction protocol (01, DNA extraction protocol 1; 02, DNA extraction protocol 2; 03, DNA extraction protocol 3)

first: Musaffe

last: Tuna

first: Patricia

last: Thompson

first: Sharoni

last: Jacobs

first: Walter

last: Lee

first: Rahul

last: Mitra

first: Aysegul

last: Sahin

first: Gordon

middle: B

last: Mills

first: Melissa

last: Bondy


title: ChIP-chip of H3K9Ac in Drosophila at different time points of development

first: Kevin

last: White

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: H3K9Ac at 12 different time-points of Drosophila development.

Current Dataset:

[GSM386138..GSM386146]: ChIP-chip of H3K9AC in Drosophila embryos at 12-16 hours of development
[GSM386148..GSM386156]: ChIP-chip of H3K9AC in Drosophila L1 larvae
[GSM386158..GSM386166]: ChIP-chip of H3K9AC in Drosophila L2 larvae
[GSM386168..GSM386176]: ChIP-chip of H3K9AC in Adult female Drosophila
[GSM418290..GSM418298]: ChIP-chip of H3K9AC in Adult male Drosophila
[GSM442311..GSM442316]: ChIP-chip of H3K9AC in Drosophila embryos at 8-12 hours of development
[GSM442317..GSM442325]: ChIP-chip of H3K9AC in Adult male Drosophila - Set2
[GSM442326..GSM442334]: ChIP-chip of H3K9AC in Pupae
[GSM442335..GSM442343]: ChIP-chip of H3K9AC in L3
[GSM442344..GSM442352]: ChIP-chip of H3K9AC in Drosophila embryos at 20-24 hours of development
[GSM442353..GSM442361]: ChIP-chip of H3K9AC in Drosophila embryos at 4-8 hours of development
[GSM442362..GSM442370]: ChIP-chip of H3K9AC in Drosophila embryos at 0-4 hours of development

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: ChIP-chip of H3K4me3 in Drosophila at different time points of development

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays for H3K4me3 at 12 different time-points of Drosophila development.

Current Dataset:

[GSM385397..GSM385405]: ChIP-chip of H3K4me3 in Drosophila embryos at 12-16 hours of development
[GSM386032..GSM386040]: ChIP-chip of H3K4me3 in Drosophila embryos at 0-4 hours of development
[GSM386088..GSM386096]: ChIP-chip of H3K4me3 in Drosophila embryos at 4-8 hours of development
[GSM386097..GSM386105]: ChIP-chip of H3K4me3 in Drosophila embryos at 16-20 hours of development
[GSM386106..GSM386114]: ChIP-chip of H3K4me3 in Drosophila embryos at 20-24 hours of development
[GSM386115..GSM386123]: ChIP-chip of H3K4me3 in Drosophila L1 larvae
[GSM386125..GSM386133]: ChIP-chip of H3K4me3 in Drosophila L2 larvae
[GSM386996..GSM387004]: ChIP-chip of H3K4me3 in Adult Male
[GSM418254..GSM418262]: ChIP-chip of H3K4me3 in Drosophila embryos at 8-12 hours of development
[GSM442287..GSM442292]: ChIP-chip of H3K4me3 in Pupae
[GSM442293..GSM442301]: ChIP-chip of H3K4me3 in Adult Female
[GSM442302..GSM442310]: ChIP-chip of H3K4me3 in Drosophila L3 larvae

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: MSNP data for normal blood, normal bone marrow, CD34+ cells and placenta samples

status: Public on May 10 2008

first: Le

last: Jiang

address: 1130 St. Nicholas Ave

type:
Methylation profiling by SNP array
SNP genotyping by SNP array

summary:
A novel method for detecting genome-wide ASM (allele-specific methylation) was developed by modification of the Affymetrix 250K StyI SNP arrays.
Using this method, and the above mentioned samples, we consistently detected ASM in non-imprinted regions of the genome. Interestingly, ASM appears to be strongly correlated with the SNP sequences in cis.

overall_design: DNA from various sources (6 normal blood, 2 normal bone marrow, 2 CD34+ bone marrow, and 3 placenta samples) was genotyped and ASM was scored as an allele call conversion from 'AB' (heterozygous) to 'AA' or 'BB' (homozygous) in the StyI+HpaII genomic representation, compared to the StyI-only representation.  Each sample was subjected to 5 runs of genotyping on the 250K StyI array, including 2 StyI alone, 2 StyI+HpaII and 1 StyI+MspI.

first: Kristi

last: Kerkel

first: Benjamin

last: Tycko


title: c-Met confers protection against chronic liver tissue damage and fibrosis progression after bile-duct-ligation in mice

status: Public on Feb 18 2009

city: Wageningen

first: Guido

last: Hooiveld

address: HELIX, Stippeneng 4

department: Div. Human Nutrition & Health

country: Netherlands

institute: Wageningen University

summary: The HGF/c-Met system is an essential inducer of hepatocyte growth and proliferation. Although a fundamental role for the HGF receptor c-Met has been demonstrated in acute liver regeneration its cell specific role in hepatocytes during chronic liver injury and fibrosis progression has not been determined yet. In order to better characterize the role of c-Met in hepatocytes we generated a hepatocyte-specific c-Met knockout mouse (c-Met∆hepa) using the Cre-loxP system and studied its relevance after bile-duct ligation. Two strategies for c-Met deletion in hepatocytes were tested. Early deletion during embryonic development was lethal, while post-natal Cre-expression was successful leading to the generation of viable c-Met∆hepa mice. Bile-duct ligation in these mice resulted in extensive necrosis and lower proliferation rates of hepatocytes. Gene array analysis of c-Met∆hepa mice revealed a significant reduction of anti-apoptotic genes in c-Met deleted hepatocytes. These findings could be functionally tested as c-Met∆hepa mice showed a stronger apoptotic response after bile-duct ligation and Jo-2 stimulation. This phenotype was associated with increased expression of pro-inflammatory cytokines (TNF-a and IL-6) and an enhanced recruitment of neutrophils. Activation of these mechanisms triggered a stronger pro-fibrogenic response as evidenced by increased TGF-b1, a-SMA, collagen-1a mRNA expression and enhanced collagen-fiber staining in c-Met∆hepa mice.

overall_design: For gene array analysis c-MetDhepa and c-MetloxP/loxP controls were stimulated for 2 hours with 2µg recombinant mouse HGF.Three animals per group were treated in parallel, before and after i.p. injection of recombinant HGF or NaCl.

first: Arne

last: Giebeler

first: Christian

last: Klein

first: Mark

middle: V

last: Boekschoten

first: Malgorzata

last: Borowiak

first: Carmen

last: Birchmeier

first: Nikolaus

last: Gassler

first: Michael

last: Müller

last: Trautwein

first: Konrad

last: Streetz


title: In vivo gene expression in granulosa cells during pig terminal follicular development.

status: Public on Apr 30 2008

city: Castanet-Tolosan Cedex

first: Agnes

last: Bonnet

address: Chemin de Borde-Rouge  BP 52627

country: France

institute: INRA

summary:
The aim of this study is the identification of genes and gene networks involved in pig ovarian follicular development.
cDNA nylon micro-arrays (2849 sequenced clones) were designed from different libraries : four subtractive suppressive hybridization libraries (generated from small versus large and small versus medium follicles) and a pig multi-tissue cDNA library.
Granulosa cells were isolated from healthy follicles (small, medium or large), 24 h or 96 h after the end of a progestagen treatment. The RNA isolated from these cells was used to hybridize the micro-arrays and hybridisations were performed in duplicate. The images were quantified using Bzscan software and the data were managed with BASE software. Statistical analysis was performed using R software.
Keywords: cell type comparison

overall_design:
Granulosa cells were isolated from healthy follicles (small, medium or large). The RNA isolated from these cells was used to hybridize nylon micro-arrays. The arrays contained PCR products from 2848 pig cDNA clones (GPL3978), spotted in duplicate on two separate fields of the same membrane (last number 1 of the local ID corresponds to the left field and 2 corresponds to right field).
The data have been generated from 14 RNA follicle pools (five Large, five Medium and four Small follicles pools). For each follicle pool, 2 radioactive labellings were performed (before last number of the local ID corresponds to the duplicate number). Each membrane was exposed 6, 12 or 24 hours (depending on the saturation signal) to radioisotopic-sensitive imaging plates (BAS-2025, Fujifilm, Raytest France S.A.R.L., Courbevoie, France). The imaging plates were scanned thereafter with a phosphor imaging system at a 25 µm resolution (BAS-5000, Fujifilm, Raytest France S.A.R.L., Courbevoie, France). The images were quantified using semi-automated software, BZScan (Lopez F, Rougemont J, Loriod B, Bourgeois A, Loi L, Bertucci F, Hingamp P, Houlgatte R, and Granjeaud S. Feature extraction and signal processing for nylon DNA microarrays. BMC Genomics 5: 38, 2004). Fixed circle segmentation, i.e. a grid process with a fixed spot diameter was applied. The hybridization images were quantified by the extraction of the intensity for each spot. A new version of BZsan (AGscan solfware) is available at :
http://mulcyber.toulouse.inra.fr/projects/agscan/
The experimental data were managed using the free BASE software (Saal LH, Troein C, Vallon-Christersson J, Gruvberger S, Borg A, and Peterson C. BioArray Software Environment (BASE): a platform for comprehensive management and analysis of microarray data. Genome Biol 3: SOFTWARE0003, 2002.) modified by Sigenae team to accept radioactive experiments.
Finally, data consisted in (14 RNA x 2 labellings x 2 fields) 14 probes, 28 hybridisations, 42 images (14 images were filtred out for background too hight).

first: Bonnet

last: Agnès

first: Lê-Cao

last: Kim-Ann

first: Sancristobal

last: Magali

first: Benne

last: Françis

first: Robert-Granié

last: Cristèle

first: Law-So

last: Gilles

first: Fabre

last: Stephane

first: Besse

last: Philippe

first: De-Billy

last: Emmanuel

first: Quesnel

last: Elène

first: Hatey

last: François

first: Tosser-Klopp

last: Gwenola


title: ChIP-chip of H3K27me3 in Drosophila at different time points of development

first: Kevin

last: White

summary:
This is a dataset generated by the Drosophila Regulatory Elements modENCODE Project led by Kevin P. White at the University of Chicago. It contains ChIP-chip data on Agilent 244K dual-color arrays for antibody: H3K27me3 at 12 different time-points of Drosophila development.

Current Dataset:

[GSM384769..GSM384777]: ChIP-chip of H3K27me3 in Drosophila embryos at 0-4 hours of development
[GSM384778..GSM384786]: ChIP-chip of H3K27me3 in Drosophila embryos at 4-8 hours of development
[GSM384787..GSM384795]: ChIP-chip of H3K27me3 in Drosophila embryos at 12-16 hours of development
[GSM384797..GSM384805]: ChIP-chip of H3K27me3 in Drosophila embryos at 16-20 hours of development
[GSM384807..GSM384815]: ChIP-chip of H3K27me3 in Drosophila embryos at 20-24 hours of development
[GSM384817..GSM384825]: ChIP-chip of H3K27me3 in Drosophila L1 larvae
[GSM384826..GSM384834]: ChIP-chip of H3K27me3 in Drosophila L2 larvae
[GSM384839..GSM384847]: ChIP-chip of H3K27me3 in Drosophila pupae
[GSM385341..GSM385349]: ChIP-chip of H3K27me3 in Drosophila L3 larvae
[GSM418225..GSM418233]: ChIP-chip of H3K27me3 in Drosophila Adult male
[GSM418239..GSM418247]: ChIP-chip of H3K27me3 in Drosophila embryos at 8-12 hours of development
[GSM442006..GSM442014]: ChIP-chip of H3K27me3 in Drosophila Adult female

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and  http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf


title: Analysis of genetic changes in MCF10A series cells and MCFDCIS derived xenografts

status: Public on Mar 07 2008

first: Kornelia

last: Polyak

address: 450 Brookline Ave

summary:
MCF10A series is one of the few human models of breast tumor progression. A derivative of MCF10A cells is the MCFDCIS, which reproducibly forms comedo DCIS-like lesions that spontaneously progress to invasive tumors. We used this model to explore the relative importance of myoepithelial cells and stromal fibroblasts in the in situ to invasive breast carcinoma transition.
We use Affymetrix 11K XbaI or 250K StyI SNP arrays to analyze the MCF10A series cells and MCFDCIS derived xenografts for copy number changes and LOH (loss of heterozygosity).
Keywords: Cell line, xenografts of time course/co-injection groups, different cell types isolated from xenografts

overall_design: Cultured MCF10A series cells, xenografts formed from MCFDCIS cells at different time points and from different co-injection groups, and luminal (by Mucin1) and myoepithelial (by integrin beta6) cells magnetic beads-purified from MCFDCIS xenografts were processed for DNA purification. SNP array analysis was performed by the Dana-Farber Microarray Core using Affymetrix 11K XbaI or 250K StyI SNP arrays.

first: Min

last: Hu

first: Jun

last: Yao


title: Regulatory networks define phenotypic classes of human stem cell lines

status: Public on Aug 25 2008

city: Kiel

first: Franz-Josef

last: Mueller

state: Schleswig-Holstein

address: Niemannsweg 147

institute: Zentrum für Integrative Psychiatrie

summary:
Stem cells are defined as self-renewing cell populations that can differentiate into multiple distinct cell types.  However, hundreds of different human cell lines from embryonic, fetal, and adult sources have been called stem cells, even though they range from pluripotent cells, typified by embryonic stem cells, which are capable of virtually unlimited proliferation and differentiation, to adult stem cell lines, which can generate a far more limited repertory of differentiated cell types. The rapid increase in reports of new sources of stem cells and their anticipated value to regenerative medicine have highlighted the need for a general, reproducible method for classification of these cells.
We report here the creation and analysis of a database of global gene expression profiles (“Stem Cell Matrix”) that enables the classification of cultured human stem cells in the context of a wide variety of pluripotent, multipotent, and differentiated cell types. Using an unsupervised clustering method to categorize a collection of ~150 cell samples, we discovered that pluripotent stem cell lines group together, while other cell types, including brain-derived neural stem cell lines, are very diverse.
Using further bioinformatic analysis we uncovered a protein-protein network (“PluriNet”) that is shared by the pluripotent cells (embryonic stem cells, embryonal carcinomas, and induced pluripotent cells). Analysis of published data showed that the PluriNet appears to be a common characteristic of pluripotent cells, including mouse ES and iPS cells and human oocytes. Our results offer a new strategy for classifying stem cells and support the idea that pluripotence and self-renewal are under tight control by specific molecular networks.

Keywords: cell type comparison, clustering, classification, systems analysis, gene networks, protein-protein interactions, taxonomy, reference based classification

overall_design: In vitro stem cell preparations were first grouped with an unsupervised clustering mechanism and then we identified differentially expressed, connected subnetworks  by a systems analysis with differential MATISSE (Ulitsky & Schamir 2007), which integrated information on  a) co-expression patterns b) topological data from protein-protein interaction networks of the respective gene products and c) group memberships from the Stem Cell Matrix clustering step.

first: Louise

last: Laurent

first: Christina

last: Lu

first: Mahendra

last: Rao

first: Philip

last: Schwartz

first: Nils

middle: O

last: Schmidt

first: Jeanne

last: Loring

first: Scott

last: McKercher

first: Manfred

last: Westphal

first: Chrisa

last: Stubban

first: JeanPyo

last: Lee

first: Dustin

last: Wakeman

first: Rudolpho

last: Gonzales

first: In-Hyun

last: Park

first: George

last: Daley

first: Hyun-Sook

first: Shin

last: Moon

first: Katrin

last: Lamszus

first: Uwe

last: Kehler

first: Hildegard

last: Meissner

first: Helga

last: Dittmer

first: Svenja

last: Zapf

first: Maggie

last: Rosentraeger


title: Diffuse large B cell lymphomas

status: Public on Dec 08 2006

city: Amsterdam

first: Daoud

last: Sie

address: De Boelelaan 1117

institute: Vrije Universiteit Medical Center

summary:
Intrinsic resistance of lymphoma cells to apoptosis is a probable mechanism causing chemotherapy resistance and eventual fatal outcome in patients with diffuse large B cell lymphomas (DLBCL). We investigated whether microarray expression profiling of apoptosis related genes predicts clinical outcome in 46 patients with primary nodal DLBCL.

Unsupervised cluster analysis using genes involved in apoptosis (N=246) resulted in 3 separate DLBCL groups partly overlapping with GCB versus ABC like phenotype. One group with poor clinical outcome was characterized by high expression levels of pro-and anti-apoptotic genes involved in the intrinsic apoptosis pathway. A 2nd group, also with poor clinical outcome, was characterized by high levels of apoptosis inducing cytotoxic effector genes, possibly reflecting a cellular cytotoxic immune response. The 3rd group showing a favourable outcome was characterized by low expression levels of genes characteristic for both other groups.

Our results suggest that chemotherapy refractory DLBCL are characterized either by an intense cellular cytotoxic immune response or by constitutive activation of the intrinsic mediated apoptosis pathway with concomitant downstream inhibition of this apoptosis pathway. Consequently, strategies neutralizing the function of apoptosis-inhibiting proteins might be effective as alternative treatment modality in part of chemotherapy refractory DLBCL.
Keywords: expression profiling B lymphomas

overall_design: As an internal control for unsupervised clustering duplicate experiments were performed for 5 lymphoma samples (indicated as a and b, respectively), including isolation of mRNA from separate tissue samples at different days. Two tonsils with reactive follicular hyperplasia were included to compare the DLBCL with normal hyperplastic lymphoid tissue.

first: Jetty

last: Muris

first: Bauke

last: Ylstra

first: S

last: Cilessen

first: G

last: Ossenkoppele

first: J

last: Kluin-Nelemans

first: Paul

middle: P

last: Eijk

first: Ben

last: Nota

first: Marianne

last: Tijssen

first: Wim

last: de Boer

first: Mark

last: van de Wiel

last: van den IJssel

first: P

last: Janssen

last: de Bruin

first: H

last: van Krieken

first: Gerrit

last: Meijer

first: Chris

first: Joost

last: Oudejans


title: Expression data from A673 cell line treated with compounds at several doses and time points

status: Public on Mar 01 2007

first: Kimberly

last: Stegmaier

department: Department of Pediatric Oncology

institute: Dana-Farber Cancer Institute and Children’s Hospital Boston, Harvard Medical School

summary:
An increasing number of cancer-associated mutations have been identified. Unfortunately, little therapy today exploits these tumor-specific genetic lesions. Often, the resulting oncoproteins have been intractable to easy manipulation with current small molecule screening approaches. To overcome this impasse, we developed an expression-based approach to small molecule library screening. We applied this platform to the discovery of modulators of the activity of EWS/FLI, the Ewing sarcoma associated oncoprotein. Cytarabine (ARA-C) was identified as the top hit in a small molecule library screen. ARA-C modulates EWS/FLI by decreasing EWS/FLI protein level and has striking effects on cellular viability and transformation in in vitro and in vivo models of Ewing sarcoma. With poor outcomes for patients with relapsed Ewing sarcoma and the well established safety profile of ARA-C, clinical trials testing ARA-C in Ewing sarcoma are warranted. Expression data was created for A673 cells treated with ARA-C and two other compounds used to treat Ewing sarcoma (Puromycin and Doxorubicin) at two doses (EC50 and 2xEC50) and three time points (24 hours, 3 days, and 5 days).
Keywords: time course and dose response

overall_design: A673 cells were treated with ARA-C (at doses of EC50 and 2xEC50) or vehicle in triplicate and expression profiled at 24 hours, 3 days, and 5 days. To exclude the possibility that ARA-C's modulation of the EWS/FLI signature was simply a non-specific response to treatment with all cytotoxic agents, we asked whether other compounds known to kill Ewing sarcoma cells (Doxorubicin and Puromycin) would induce the EWS/FLI off genome-wide expression pattern. A673 cells were treated with Doxorubicin and Puromycin (at doses of EC50 and 2xEC50) and expression profiled at 24 hours, 3 days, and 5 days.

first: Jenny

last: Wong

first: Kenneth

middle: N

last: Ross

first: Kwan

middle: T

last: Chow

first: David

last: Peck

first: Renee

middle: D

last: Wright

first: Stephen

last: Lessnick

first: Andrew

last: Kung

first: Todd

last: Golub


title: Copy number alterations of 103 hepatocellular carcinomas with hepatitis C virus etiology

status: Public on Jun 22 2008

first: Derek

last: Chiang

summary:
To characterize the genetic alterations that instigate hepatitis C virus-induced hepatocellular carcinoma (HCC), we conducted an integrative genomic analysis of 103 HCCs.  Most tumors harbored 1q gain, 8q gain or 8p loss, with occasional alterations in 13 additional chromosome arms.  In addition to amplifications at 11q13 in 6 tumors, 4 tumors harbored focal gains at 6p21 incorporating VEGFA, which were confirmed in 4 of 113 HCC in an independent validation set.  Strikingly, this locus overlapped with copy gains in 4 of 371 lung adenocarcinomas.  Overexpression of VEGFA via 6p21 gain suggested a cell-nonautonomous mechanism of oncogene activation.  Hierarchical clustering of gene expression among 91 tumors identified 5 classes, including ‘Wnt-CTNNB1’, ‘proliferation’ and ‘interferon-related’ gene classes.  We also discovered a novel class defined by polysomy of chromosome 7, gains of which were associated with early tumor recurrence after resection.  These findings reveal key alterations in HCC pathogenesis and implicate potential therapeutic targets.
Keywords: disease state analysis

overall_design: 103 hepatocellular carcinomas and 95 adjacent cirrhotic, non-tumoral liver tissue were obtained at the time of surgical resection of orthotopic transplantation.

first: Augusto

last: Villanueva

first: Yujin

last: Hoshida

first: Judit

last: Peix

first: Philippa

last: Newell

first: Beatriz

last: Minguez

first: Amanda

last: Cozza

first: Diana

middle: J

last: Donovan

first: Swan

last: Thung

first: Manel

last: Sole

first: Victoria

last: Tovar

first: Clara

last: Alsinet

first: Alex

last: Ramos

first: Jordi

last: Barretina

first: Sasan

last: Roayaie

first: Myron

last: Schwartz

first: Vesna

last: Najfeld

last: Bruix

first: Vincenzo

last: Mazzaferro

first: Azra

last: Ligon

first: Samuel

last: Waxman

first: Scott

last: Friedman

first: William

middle: R

last: Sellers

first: Matthew

last: Meyerson

first: Josep

middle: M

last: Llovet


title: Prostaglandin E2 Receptor Subtype EP2- and EP4-regulated Gene Expression Profiling in Human Ciliary Smooth Muscle Cells

status: Public on Feb 24 2008

city: Los Angeles

first: Nils

middle: Werner Georg

last: Lambrecht

state: CA

address: 11301 Wilshire Blvd, Bldg.113, Rm.325A

department: Physiology

institute: UCLA

summary:
Changes of genome-wide mRNA transcription levels of human ciliary smooth muscle (hCSM) cells were determined by treating hCSM cells in culture with 200 nM of either an prostaglandin E2 receptor subtype EP2 or subtype EP4 selective agonist for 6 hours in comparison to untreated controls. This was followed by competitive hybridization of fluorescent Cy3 or Cy5 labeled cRNA probes derived from the treated versus untreated control total RNA samples onto an Agilent Human Whole Genome Expression oligonucleotide microarray.
Log 2 (LN) of the intra-slide ratios (RATIO, PRE_VALUE) of treated versus untreated samples was reported as VALUE in the sample files.
Keywords: prostaglandin E2 receptor agonists, subtype EP2, subtype EP4, hCSM

overall_design:
Human Ciliary Smooth Muscle Cell Culture:
Human ciliary smooth muscle (hCSM) cells were isolated from a female donor, received from the San Diego Eye Bank® (San Diego, CA) and cultured in DMEM with 10% fetal bovine serum and 0.5% penicillin/streptomycin according to the method reported previously by Woldemussie et al.
For transcriptome analysis, cells were used for experiments starting at passage 4. Three independent experiments at consecutive cell passages were performed. For each experiment 0.6 x 106 cells were plated onto 15 cm dishes in MEM D-Valine medium (PromoCell, Germany) supplemented with 10% FCS, L-glutamine and antibiotics/antimycotics. Cells were grown to ~80% confluency for 6 days, followed by starvation in absence of FCS and presence of 100 nM of the cyclooxygenase inhibitor indomethacin, 20 µg/ml fatty acid-free BSA and 4 µg/ml transferrin for 17 hours. Cells were then exposed for 6 hours to 200 nM of either the EP2 agonist AGN210937 or the EP4 agonist AGN202280 (Allergan, Irvine, CA) or the corresponding amount of DMSO in the absence of FCS and presence of transferrin.

Total RNA Extraction:
Total RNA was isolated using a RNA isolation kit (RNAqueous; Ambion, USA) which was followed by DNase I treatment (Turbo DNA-free; Ambion) and purification, according to the manufacturer’s protocols. RNA was quantitated using a spectrophotometer ND-1000 (Nanodrop Technologies, USA). RNA quality was assessed regarding purity and stability using a Bioanalyser 2100 (Agilent Technologies, USA). Extracted total RNA aliquots were snap-frozen in liquid nitrogen and stored at -800C for single use.

cRNA Labelling and Oligonucleotide Microarray Hybridization:
Total RNA was linearly amplified and labelled with Cy3 or Cy5 using a low RNA input Fluor Linear Amp Kit (Agilent Technologies, USA). Internal RNA controls from Agilent’s RNA Spike-in Kit were included, comprised of mixtures of 11 in vitro synthesized transcripts derived from the Adenovirus E1A transcriptome at various ratios. The final cRNA concentration of 500 ng total RNA used was typically 590-650 ng/μl and the Cy3- or Cy5-cytidine incorporation was 5.4 -6.0 pmol/μg cRNA as determined using the Nanodrop spectrophotometer ND-1000.
3.5 μg of Cy3 and Cy5 labeled cRNA (treated vs. untreated samples) were competitively hybridized to high-density DNA arrays from Agilent Technologies (Whole Human Genome Oligo Microarray 44K) for 17 hours at 650C according to the manufacturer’s protocol. Each set of three microarray experiments for triplicate analysis contained one dye swap experiment. All microarrays were scanned and the intensities normalized over background as well as to eliminate signal intensity-dependent bias from the ratio of the two channels (Lowess normalization) using a microarray scanner from Agilent Technologies including proprietary software. All microarray data sets were imported into the microarray data analysis software Genespring 7.3 (Agilent Technologies) followed by comparison of normalized intensities. Gene identities were updated according to Agilent’s latest list of gene annotations (G4112F, 07Feb07).
Consistency of microarray data quality was assessed by monitoring performance of the spiked internal RNA controls (330 microarray spots/array) at various ratios (Supplementary Data, Fig. S1), by carrying out a global analysis of all absolute fluorescent intensity values, and by analysis of negative control spots (314 microarray spots/array) for determination of detection thresholds.

first: Armin

last: Reitmair

first: Iskandar

last: Yakubov

first: George

last: Sachs

first: Wha-Bin

last: Im


title: Thiosulfate oxidation by Thiobacillus denitrificans under aerobic vs. denitrifying conditions

status: Public on Oct 06 2006

city: Livermore

first: Anu

last: Chakicherla

address: 7000 East Avenue, Mail Stop: L-446

institute: Lawrence Livermore National Lab

type: Expression profiling by genome tiling array

summary:
Beller, H. R., T. E. Letain, A. Chakicherla, S. R. Kane, T. C. Legler, and M. A. Coleman. 2006.  Whole-genome transcriptional analysis of chemolithoautotrophic thiosulfate oxidation by Thiobacillus denitrificans under aerobic vs. denitrifying conditions. Journal of Bacteriology 188:7005-7015.

Thiobacillus denitrificans is one of the few known obligate chemolithoautotrophic bacteria capable of energetically coupling thiosulfate oxidation to denitrification as well as aerobic respiration. As very little is known about the differential expression of genes associated with key chemolithoautotrophic functions (such as sulfur-compound oxidation and CO2 fixation) under aerobic versus denitrifying conditions, we conducted whole-genome, cDNA microarray studies to explore this topic systematically.  The microarrays identified 277 genes (approximately ten percent of the genome) as differentially expressed using Robust Multi-array Average statistical analysis and a 2-fold cutoff.  Genes upregulated (ca. 6- to 150-fold) under aerobic conditions included a cluster of genes associated with iron acquisition (e.g., siderophore-related genes), a cluster of cytochrome cbb3 oxidase genes, cbbL and cbbS (encoding the large and small subunits of form I ribulose 1,5-bisphosphate carboxylase/oxygenase, or RubisCO), and multiple molecular chaperone genes. Genes upregulated (ca. 4- to 95-fold) under denitrifying conditions included nar, nir, and nor genes (associated respectively with nitrate reductase, nitrite reductase, and nitric oxide reductase, which catalyze successive steps of denitrification), cbbM (encoding form II RubisCO), and genes involved with sulfur-compound oxidation (including two physically separated but highly similar copies of sulfide:quinone oxidoreductase and of dsrC, associated with dissimilatory sulfite reductase).  Among genes associated with denitrification, relative expression levels (i.e., degree of upregulation with nitrate) tended to decrease in the order nar > nir > nor > nos.  Reverse transcription, quantitative PCR analysis was used to validate these trends.
Keywords: bacterial metabolism

overall_design: After growth under either aerobic or denitrifying conditions (at least two successive transfers) with thiosulfate as the electron donor, triplicate cultures were harvested for RNA extraction.  The specific rates of thiosulfate oxidation were assessed in all cultures immediately before the harvesting of cells and were comparable under aerobic and denitrifying conditions.

first: Harry

last: Beller

first: Tracy

last: Letain

first: Staci

last: Kane

first: Tina

last: Legler

middle: A

last: Coleman


title: Characterization of the Drosophila genome at the nuclear lamina

status: Public on Aug 29 2006

first: Maarten

last: Fornerod

department: Gene Regulation

institute: Netherlands Cancer Institute

type: Genome binding/occupancy profiling by array

summary:
The nuclear lamina (NL) binds chromatin in vitro and is thought to function in its organisation, but genes that interact with the NL are unknown. Using an in vivo approach we identified 474 Drosophila genes that interact with B–type lamin, Lam. These genes are transcriptionally silent, late replicating, lack active histone marks, and are widely spaced. These factors collectively predict Lamin binding behavior, indicating the NL integrates variant and invariant chromatin features. Consistently, NE proximity is partly conserved between cell types and induction of gene expression or active histone marks reduces Lam binding. Lam target genes cluster in the genome, and these clusters are coordinately expressed during development. This genome-wide analysis gives clear insight into the nature and dynamic behavior of the genome at the NL.
Keywords: DamID and expression profiling

overall_design: DamID is based on the in vivo expression of a chimaeric protein consisting of a chromatin protein of interest fused to E. coli DNA adenine methyltransferase (Dam). Expression of low amounts of this fusion protein leads to preferential adenine methylation of DNA in the vicinity of native binding sites of the chromatin protein. Subsequently, adenine-methylated DNA fragments are isolated, labeled with a fluorescent dye, and hybridized to a microarray. Genomic binding sites of the protein can then be identified based on the methylation pattern. To correct for nonspecific binding of Dam, methylated DNA fragments from cells transfected with Dam alone served as a reference, and binding data are expressed as Dam-fusion:Dam methylation ratios. We performed DamID experiments using Drosophila Lam, encoded by the Dm0 gene, in Drosophila Kc167 cells, under various conditions. These conditions included wild-type Lam; a Lam deletion mutant of the C-terminal 4 amino acids of this protein, containing its nuclear membrane-targeting CaaX signal; cells grown in the presence of Ecdysone; cells grown in the presence of the deacetylase inhibitor trichostatin A (TSA). We also compared Lam binding profiles to mRNA expression profiles under normal conditions or in the presence of Ecdysone. For normal ("absolute") mRNA expression levels, mRNA-derived probe was hybridized against genomic DNA derived probe to correct for hybridization efficiency.

first: Helen

last: Pickersgill

first: Elzo

last: de Wit

first: Bernike

last: Kalverda

first: Wendy

last: Talhout

first: Bas

last: van Steensel


title: Time course response of Synechocystis PCC 6803 to dehydration/desiccation

status: Public on Sep 04 2006

city: Blacksburg

first: Malcolm

last: Potts

state: VA

address: W. Campus Drive

department: Biochemistry

institute: Virginia Tech

summary:
The responses of the transcriptome were monitored in Synechocysis PCC 6803 during a linear rate of evaporation of the culture to dryness (desiccation).  For each time point, total RNA were isolated from stressed and unstressed cells, reverse-transcribed, differentially labelled (dye swapped), hybridized together (stressed versus unstressed samples) and analyzed with DNA glass microarrays (two slides per each time point) (Custom-commercial array : CyanoCHIP version 2.0, TAKARA). To identify differentially expressed genes, the median of the normalized ratio of Cy5/Cy3 intensity was calculated for each spot of the replicated dye-swap. The results of the analysis were carefully examined to exclude the dye effect between the 2 Cy-swapped arrays.
Keywords: Dehydration, stress response, time course, transcription, cyanobacteria

overall_design:
Goal -
Compare the responses of cyanobacterium Synechocystis sp. PCC 6803 to UV-irradiation and dehydration/desiccation stress. The data here relate to dehydration/desiccation stress.

Origin of biological sample -
The axenic strain Synechocystis sp. PCC 6803 was obtained from the American Type Culture Collection (ATCC 27184). Special attention was given to maintain all the Synechocystis cultures under the same conditions to minimize environmental variation.

Brief description -
Ultraviolet (UV) light and desiccation stresses often co-occur in natural environments, making their combined effects important selective factors within microbial populations. The effects of these stresses on the cyanobacterium Synechocystis sp. PCC 6803 was assessed through transcriptional analyses using differential display and microarray assays.

Experimental factors and design -
Axenic Synechocystis cultures were grown at 25°C in BG-11 medium, on a rotary shaker at 70 rpm, at a photon flux density of 200 µmol photons m-2 s-1. At the midpoint of the exponential phase of growth (~ 10^6 to 10^7 cells ml-1),  25-ml aliquots  of axenic cultures were transferred to glass Petri dishes with covers and pre-adapted overnight.  The covers were removed and cultures were subjected to a linear rate of evaporation of (55% relative humidity maintained in the incubator). Samples were taken at 25, 20, 15, 12, 7, 3 and 0.5 ml of evaporated cultures and completely dried cultures; the latter corresponding to a total of 15 h of dehydration.
As controls, RNA was obtained from Synechocystis cells grown without dehydration.  Cells were disrupted with glass beads and RNA was extracted with a buffer of acidified phenol (65°C), sodium acetate pH 5.1, EDTA and sodium dodecyl sulfate), followed by ethanol precipitation. The RNA (10 µg) was annealed with 20 µg Random RT primer and reverse transcription into cDNA was achieved with Superscript II reverse transcriptase enzyme for 2h, at 42°C. The assay contained dGTP, dCTP, dATP and dTTP, each a final concentration of 0.5 mM. After hydrolysis of RNA with 0.1M NaOH and 10 mM EDTA, then neutralization, cDNAs were purified using a Quiagen QIAquick PCR purification kit as modified in the Genisphere 3DNA Array 350RP protocol.
Two experimental replicates of RNAs from time points 12 ml, and two experimental replicates from 0.5 ml, of dehydration, were used for hybridization to microarrays.

first: Laurence

last: Garczarek

first: Naren

last: Ramakrishan

first: Deept

last: Kumar

first: Richard

middle: F

last: Helm


title: Time course response of Synechocystis PCC 6803 to UV irradiation

summary:
The responses of the transcriptome of Synechocystis PCC 6803 to UV-irradiation were measured at time points over 36 h. Irradiation was provided by Sylvania soft white DuluzR compact fluorescent 23W bulbs (Osram Sylvania Ltd, Mississauga, Canada), a 20W RS UV-B medical light with a spectral maximum at 310 nm (model ‘TL’, Philips, Holland), and 15W black lights each with a spectral maximum at 368 nm (model F15T8-BL, General Electric, USA). Total quantum scalar irradiance was measured with a model QSL-100 meter (Biospherical Instruments Inc., San Diego, CA). The flux densities of the UV-A and UV-B components of the spectrum were measured with DIX series UV-B and 365A sensors, respectively, with a Spectroline DRC-100X digital radiometer (Spectronics Corporation, Westbury, NY). In these experiments full illumination represented a continuous photon flux density in the visible range of 330 μmol photons m-2 s-1, with UV-A and UV-B maxima of 3.8 x 10^6 and 0.8 x 10^6 mW m-2, respectively. All values reported were the incident fluxes within culture vessels at the immediate surface of the cell suspensions. Aliquot cultures (in duplicate) were harvested after 0, 15 min, 1 h, 3 h, 6 h, 12 h, 24 h and 36 h of UV-irradiation. For each time point, total RNA were isolated from stressed and unstressed cells, reverse-transcribed, differentially labelled (dye swapped), hybridized together (stressed versus unstressed samples) and analyzed with DNA glass microarrays (two slides per each time point) (Custom-commercial array : CyanoCHIP version 2.0, TAKARA). To identify differentially expressed genes, the median of the normalized ratio of Cy5/Cy3 intensity was calculated for each spot of the replicated dye-swap. The results of the analysis were carefully examined to exclude the dye effect between the 2 Cy-swapped arrays.
Keywords: UV-irradiation, desiccation, Synechocystis PCC 6803, cyanobacteria, time course, transcription

overall_design:
Goal -
Compare the responses of cyanobacterium Synechocystis sp. PCC 6803 to UV-irradiation and dehydration/desiccation stress.

Origin of biological sample -
The axenic strain Synechocystis sp. PCC 6803 was obtained from the American Type Culture Collection (ATCC 27184). Special attention was given to maintain all the Synechocystis cultures under the same conditions to minimize environmental variation.

Brief description -
Ultraviolet (UV) light and desiccation stresses often co-occur in natural environments, making their combined effects important selective factors within microbial populations. The effects of these stresses on the cyanobacterium Synechocystis sp. PCC 6803 was assessed through transcriptional analyses using differential display and microarray assays.

Experimental factors and design-
Axenic Synechocystis cultures were grown at 25°C in BG-11 medium, on a rotary shaker at 70 rpm, at a photon flux density of 200 µmol photons m-2 s-1. At the midpoint of the exponential phase of growth (~ 10^6 to 10^7 cells ml-1), 25-ml aliquots of the cell suspension were subjected to UV-irradiation (in 50-ml flasks) with a continuous photon flux density in the visible range of 330 µmol photons m-2 s-1. UV-A and UV-B maxima were 3.8 x 10^6  and 0.8 x 10^6  mW m-2, respectively. Cells were harvested after 0, 15 min, 1 h, 3 h, 6 h, 12 h, 24 h and 36 h of irradiation for disruption and rapid recovery of RNA.  As controls, RNA was obtained from Synechocystis cells grown without UV-irradiation.  Cells were disrupted with glass beads and RNA was extracted with a buffer of acidified phenol (65°C), sodium acetate pH 5.1, EDTA and sodium dodecyl sulfate), followed by ethanol precipitation. The RNA (10 µg) was annealed with 20 µg Random RT primer and reverse transcription into cDNA was achieved with Superscript II reverse transcriptase enzyme for 2h, at 42°C. The assay contained dGTP, dCTP, dATP and dTTP, each a final concentration of 0.5 mM. After hydrolysis of RNA with 0.1M NaOH and 10 mM EDTA, then neutralization, cDNAs were purified using a Quiagen QIAquick PCR purification kit as modified in the Genisphere 3DNA Array 350RP protocol.
Two experimental replicates of RNAs from time points 12 ml, and two experimental replicates from 0.5 ml, of dehydration, were used for hybridization to microarrays. Three experimental replicates of RNAs from time point 3h of UV-irradiation, and three experimental replicates from time point 36h of UV-irradiation, were used for hybridization to microarrays.

Quality contro-l
DNAse treatment (DNAse free, Ambion) was for 3 h at 37 °C. This treatment was sometimes repeated for 2 h until the absence of any detectable DNA was checked by the absence of product after 40 cycles of PCR amplification. The quality and purity of RNAs was judged by A254/280 (1.9 to 2.1) and by the integrity of 23S and 16S rRNA resolved through gel electrophoresis. The ribosomal subunits gave sharp and bright bands that were comparable among all samples.   The quality of the random primed cDNA samples was checked by SDS-PAGE after ligation of Cy3/Cy5 cap sequences. Test arrays were performed to determine the optimum hybridization and washing conditions of the TAKARA’s microarray chips.


title: Oligonucleotide-based arrayCGH

status: Public on Dec 19 2005

first: Daoud

last: Sie

type: Genome variation profiling by genome tiling array

summary:
Array-based comparative genomic hybridisation is a high-resolution method for measuring chromosomal copy number changes. Here we present a validated protocol using in-house spotted oligonucleotide libraries for array CGH. This oligo array CGH platform yields reproducible results and is capable of detecting single copy gains, multi-copy amplifications as well as homozygous and heterozygous deletions as small as 100 kb with high resolution. A human oligonucleotide library was printed on amine binding slides. Arrays were hybridised using a hybstation and analysed using BleuFuse feature extraction software, with over 95% of spots passing quality control. The protocol allows as little as 300 ng of input DNA without the need for amplification or target reduction and a 90% reduction of Cot1-DNA without compromising quality. High quality results have also been obtained with DNA from archival tissue. Finally, in addition to human oligo arrays, we have applied the protocol successfully to mouse oligo arrays. We believe that this oligo-based platform using “off-the-shelf” oligo-libraries provides an easy accessible alternative to BAC arrays for CGH, which is cost-effective, available at high resolution and easily implemented for any sequenced organism without compromising the quality of the results.
Keywords: comparative genomic hybridization, oligonucleotide,

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: 16 human and 2 mouse samples are analyzed on oligonucleotide arrays and some of them also on BAC arrays. Replicates are included in the series so that the total number of hybridizations is 30. Corresponding figure numbers: 1A/C: GSM73557, 1B/D: GSM75163, 2: GSM74521, 3: GSM73557, GSM75164, GSM75165, GSM75166, 4A: GSM75169, 4C: GSM75170, 5A: GSM75171, 6A: GSM75199, 6B: GSM75205, 7A:	GSM75209, 7B: GSM75175, GSM75174.

first: Paul

last: van den IJssel

first: Marianne

last: Tijssen

first: Suet-Feung

last: Chin

last: Eijk

first: Beatriz

last: Carvalho

first: Erik

last: Hopmans

first: Henne

last: Holstege

first: Jos

last: Jonkers

first: Gerrit

last: Meijer

first: Carlos

last: Caldas

first: Bauke

last: Ylstra


title: Effects of bGH treatment on rat primary hepatocytes

status: Public on May 04 2005

city: Stockholm

first: Amilcar

last: Flores

country: Sweden

institute: Karolinska Institute

summary:
Hepatocytes prepared from male livers where culture on matrigel before addition of bGH (50nM). RNA was prepared 24h and 48h later.
Keywords: time-course

first: Nina

last: Ståhlberg


title: Interspecies hybridization versus intra-species hybridization for Leishmania promastigote RNA.

status: Public on Mar 10 2006

city: West Lafayette

first: Timothy

last: Holzer

state: IN

address: 175 S. University St.

institute: Purdue University

summary:
We examined the Leishmania mexicana transcriptome to identify differentially regulated mRNAs using high-density whole-genome oligonucleotide microarrays designed from the genome data of a closely related species, Leishmania major. This experiment appears as Fig. 1 of the associated publication.
Keywords: RNA expression profiling

sample_organism:
Leishmania major
Leishmania mexicana

overall_design: Two biological replicates of promastigote RNA from each species, L. major and L. mexicana, were hybridized to L. major arrays and analyzed.

first: James

last: Forney

first: W

last: McMaster


title: Expression profiling reveals differential gene expression Leishmania mexicana

summary:
We examined the Leishmania mexicana transcriptome to identify differentially regulated mRNAs using high-density whole-genome oligonucleotide microarrays designed from the genome data of a closely related species, Leishmania major. Statistical analysis on array hybridization data representing 8156 predicted coding regions revealed 288 genes (3.5% of all genes) whose steady-state mRNA levels meet criteria for differential regulation between promastigotes and lesion-derived amastigotes. Interestingly, sample comparison of promastigotes to axenic amastigotes resulted in only 17 genes (0.2%) that meet the same statistical criteria for differential regulation. The reduced number of regulated genes is a consequence of an increase in the magnitude of the transcript levels in cells under axenic conditions. The expression data for a subset of genes was validated by quantitative PCR. Our studies show that interspecies hybridization on microarrays can be used to analyze closely related protozoan parasites, that axenic culture conditions may alter amastigote transcript abundance, and that there is only a relatively modest change in abundance of a few mRNAs between morphologically distinct promastigote and amastigote cultured cells. Leishmania may represent an alternative paradigm for eukaryotic differentiation with minimal contributions from changes in mRNA abundance.
Keywords: RNA expression profiling

overall_design: This expression profiling study was performed with L. mexicana RNA samples hybridized to L major oligonucleotide arrays. There are three biological replicates for all axenic cultures. All lesion-derived amastigote samples are technical replicates.


title: Time course of PBL derived avian macrophages stimulated with whole Ecoli or LPS

status: Public on Sep 24 2004

city: Newark

first: Calvin

last: Keeler

state: DE

department: Animal and Food Sciences

institute: University of Delaware

summary:
This series compares gene expression in chicken peripheral blood lymphocyte (PBL) derived macrophages following stimulation with either XL10 E. coli or S. typh LPS over an 8 hour time course (0,1,2,4,and 8 hours). For the late time points, the stimuli were removed after 2 hours and fresh media was added for the remaining time.

Keywords: time-course

first: Travis

middle: W

last: Bliss


title: TP12 adult with emb 3

status: Public on Dec 31 2003

city: New Haven

first: Valerie

last: Reinke

state: CT

address: 333 Cedar St

department: Genetics

institute: Yale University School of Medicine

summary:
Timepoint 12 wild type adult with emb 3 vs mixed stage reference
Keywords: other


title: TP11 adult with emb 2

summary:
Timepoint 11 wild type adult with emb 2 vs mixed stage reference
Keywords: other


title: TP09 adult

summary:
Timepoint 09 wild type adult vs mixed stage reference
Keywords: other


title: A molecular neuroethological approach for identifying and characterizing a melody of behaviorally regulated genes

status: Public on Apr 11 2006

city: Durham

first: Osceola

last: Whitney

address: Research Drive, Bryan Research Building, Room 401E

department: Neurobiology

institute: Duke University Medical Center

summary:
Songbirds possess one of the most accessible neural systems for the study of brain mechanisms of behavior. However, neuroethological studies in songbirds have been limited by the lack of high-throughput molecular resources and gene manipulation tools. To overcome this limitation, here we generated a resource of full-length cDNAs for gene expression analyses and gene manipulation in songbirds. We constructed 21 regular, normalized, and subtracted full-length cDNA libraries from brains of songbirds in 57 behavioral and developmental conditions in an attempt to clone as much of the brain transcriptome as possible. From these libraries ~14,000 transcripts were isolated, representing an estimated 4,738 genes, or ~40% of the genes expressed in the brain. With these cDNAs, we created a novel draft transcriptome database and large scale songbird brain cDNA microarrays. We used the arrays to reveal a set of 33 genes regulated in brain vocal nuclei by singing behavior. These genes clustered into 4 anatomical and 6 temporal brain expression patterns. Their functions spanned broad range of cellular and molecular categories, including signal transduction, trafficking, structural, and synaptically released molecules. With the full-length cDNAs, we over-expressed proteins of representative singing-regulated genes in vocal nuclei in the absence of singing, using a lentiviral vector system. This resource now allows investigators to comprehensively study molecular neuroethological mechanisms of behavior.
Keywords: songbird, zebra finch, transcriptome, learned vocalization, immediate early genes, lentivirus

overall_design: For the HVC there are 3 replicates of a dual Cy-dye experiement; samples GSM103451 and GSM103453 are dye swaped technical replicates.  Sample GSM103740 is a biological replicate. For the RA there are 4 replicates of a dual Cy-dye experiement; samples GSM103741 and GSM103742 are dye swaped technical replicates.  Samples GSM103743 and GSM103744 are biological replicates. For the Area X there are 4 replicates of a dual Cy-dye experiement; samples GSM103748 and GSM103750 are technical replicates.  Samples GSM103749 and GSM103751 are biological replicates. For the lateral MAN there are 3 replicates of a dual Cy-dye experiement; samples GSM103745 and GSM103746 are technical replicates. Sample GSM103747 is a biological replicate. HVC, RA, Area X or MAN cDNA from singing and quiet zebra finches was labeled with either Cy5 or Cy3 and hybridized to the array.

first: Kazuhiro

last: Wada

first: Erich

last: Jarvis


title: TP10 adult with embs 1

summary:
Timepoint 10 wild type adults with embs 1 vs mixed stage reference
Keywords: other


title: TP06 late L4/young adult

summary:
Timepoint 06 wild type late L4/young adults vs mixed stage reference
Keywords: other


title: TP07 early young adult

summary:
Timepoint 07 wild type early young adult vs mixed stage reference
Keywords: other


title: TP05 late L4

summary:
Timepoint 05 wild type late-L4 larvae vs mixed stage reference
Keywords: other


title: TP04 early L4

summary:
Timepoint 04 wild type early L4 larvae vs mixed stage reference
Keywords: other


title: TP08 late young adult

summary:
Timepoint 08 wild type late young adult vs mixed stage reference
Keywords: other


title: TP03 late L3/early L4

summary:
Timepoint 03 wild type late-L3/early L4 larvae vs mixed stage reference
Keywords: other


title: TP02 late-L3

summary:
Timepoint 02 wild type late-L3 larvae vs mixed stage reference
Keywords: other


title: oocytes vs sperm

summary:
fem-1(lf) oocytes only vs fem-3(gf) sperm only
Keywords: other


title: no germline males vs reference

summary:
no germline glp-4 adult males vs mixed stage reference
Keywords: other


title: adult males vs reference

summary:
wild type adult males vs mixed stage reference
Keywords: other


title: TP01 mid-L3

summary:
Timepoint 01 wild type mid-L3 larvae vs mixed stage reference
Keywords: other


title: wt L4

summary:
wild type L4 vs mixed stage reference
Keywords: other


title: wt L3

summary:
wild type L3 vs mixed stage reference
Keywords: other


title: wt L2

summary:
wild type L2 vs mixed stage reference
Keywords: other


title: wt adults

summary:
wild type adult vs mixed stage reference
Keywords: other


title: glp-4 L4

summary:
glp-4 L4 vs mixed stage reference
Keywords: other


title: glp-4 L2

summary:
glp-4 L2 vs mixed stage reference
Keywords: other


title: glp-4 L3

summary:
glp-4 L3 vs mixed stage reference
Keywords: other


title: Anti-inflammatory compounds in SCI

status: Public on Oct 03 2003

city: Piscataway

first: Ronald

middle: P.

last: Hart

state: NJ

address: 604 Allison Rd Rm B430

department: Cell Biology & Neuroscience

institute: Rutgers University

summary:
A screen of 5 anti-inflammatory compounds for their effects in explanted, cultured rat spinal cord slices.  All injured (explanted) cords are cultured for 4 hrs.
Keywords: ordered

first: Jonathan

middle: Z

last: Pan

first: Rebecka

last: Jornsten


title: Multiplex three dimensional brain gene expression mapping in a mouse model of Parkinson's disease

status: Public on Mar 29 2002

first: Vanessa

middle: Marie

last: Brown

address: 650 Charles E. Young Dr. South, CHS 23-151

department: Department of Molecular & Medical Pharmacology

summary:
Voxelation is a novel technology designed to produce high throughput, three-dimensional imaging of gene expression patterns in the brain. In these experiments, mouse brains were dissected into 40 voxels, or cubes, by cutting 10 serial coronal sections and transecting each coronal section into fourths. Using microarrays, the gene expression pattern of 9000 genes was acquired for both a normal and a pharmacological model of Parkinson's disease (PD) mouse brain.
The mice used in these experiments were C57BL/6J males 10-24 weeks in age.
Keywords = voxelation, 3-D gene expression, Parkinson's disease
Keywords: other

first: Alex

last: Ossadtchi

first: Arshad

middle: H

last: Khan

first: Simon

last: Yee

first: William

last: Melega

last: Cherry

first: Richard

last: Leahy

first: Desmond

last: Smith


title: glp-4 adults

summary:
glp-4 adults vs mixed stage reference
Keywords: other