title: Effect of LH replacement on luteal transcriptome following CET-induced luteolysis

city: Bangalore

first: priyanka

last: samji

state: Karnataka

address: Malleswaram

department: Molecular Reproduction Development and Genetics

country: India

institute: Indian Institute of Science

summary:
A large body of evidence suggests that the development and maintenance of corpus luteum (CL) in primates requires the action of LH. Earlier, using CET-induced luteolysis model, we demonstrated changes in luteal transcriptome suggesting nuclear actions of LH in the primate CL. To further demonstrate the role of LH in maintenance of primate CL, replacement studies were carried out and it was observed that administration of a single injection of rhLH was sufficient to restore the progesterone to pre-CET treatment levels and prevent the CET-induced luteolysis. To elucidate the molecular mechanisms underlying the rescue of CL function, we used LH-replacement model to study immediate early changes in gene expression at a global level (Affymetrix oligonucleotide microarray) following LH replacement in CET-treated monkeys and to evaluate if the changes in gene expression mediated by LH-withdrawal can be reversed by LH replacement. Results demonstrated up-and down-regulation of various genes following LH replacement and suggested that LH-withdrawal induced changes in gene expression are reversible at least for some genes.
Keywords: CL, CET, rhLH

overall_design: Female monkeys receiving CET treatment on day 7 of luteal phase were administered 20 IU/kg BW of rhLH or PBS (0.5 ml) i.v. at 24 h post CET treatment and blood samples were collected before and after rhLH/PBS treatments. To study changes in gene expression associated with LH replacement following inhibition of endogenous LH secretion by CET, CL was collected at 8 h (n=2) following LH replacement from female monkeys treated previously with CET for 24 h. Monkeys receiving CET on day 7 of luteal phase and 1X PBS at 24 h following CET treatment served as control (n=2) for the present study. Corpora lutea following different treatments were cut into small quarters and snap frozen in liquid nitrogen.

first: Priyanka

last: Samji

first: Jayaram

last: Puttaiah

first: Medhamurthy

last: Rudraiah


title: Identification of luteinizing hormone regulated genes in the primate corpus luteum

status: Public on Jun 07 2007

summary:
Corpus luteum (CL) is an ephemeral gland whose main function is to secrete progesterone required for the establishment and maintenance of pregnancy. It is very well established that development and maintenance of CL function in primates requires action of luteinizing hormone (LH) but the extent and mechanism by which LH contributes to the maintenance of CL function through out the luteal phase is not known. To study the nuclear actions mediated by LH, we evaluated global genomic changes in CL of monkeys treated with GnRH receptor antagonist to inhibit pituitary LH secretion. Affymetrix microarray analysis was performed on RNA samples from CL obtained from VEH or CET treated monkeys. Results demonstrate that LH regulates expression of a number of genes which might be important for maintenance of CL structure and function.
Keywords: CL, LH, CET, gene expression

overall_design: A single s.c. injection of GnRH receptor antagonist, Cetrorelix (CET), administered at a dose of 150 µg/kg BW has been shown to induce luteolysis. For the purpose of microarray analysis, VEH (5.25% glucose) or CET (treatment) was injected to female monkeys on day 7 of luteal phase and CL collected at 24 h post treatment (n=3) was cut into small quarters and snap frozen in liquid nitrogen. To minimize between animal variations, CL for both VEH and CET treatments were collected from the same monkeys.


title: Identification of Genetic Variants Contributing to Cisplatin-Induced Cytotoxicity using a Genome-wide Approach

status: Public on Jun 06 2007

city: Chicago

first: Eileen

last: Dolan

state: IL

address: 5841 S. Maryland

department: Medicine

country: USA

institute: University of Chicago

summary:
Cisplatin, a platinating agent commonly used in treating several cancers is associated with nephrotoxicity, neurotoxicity and ototoxicity that have hindered its utility. To gain a better understanding of the genetic variants associated with cisplatin induced toxicity, we present a step-wise approach integrating genotypes, gene expression and sensitivity of HapMap cell lines to cisplatin. Cell lines derived from 30 trios of European descent (CEU) and 30 trios of African descent (YRI) were utilized to develop a preclinical model to identify genetic variants and gene expression that contribute to cisplatin induced cytotoxicity in two different populations. Cytotoxicity was determined as cell growth inhibition at increasing concentrations of cisplatin for 48 h. Gene expression on 176 HapMap cell lines (87 CEU and 89 YRI) was determined using the Affymetrix GeneChip® Human Exon 1.0 ST Array. We identified 6, 2 and 9 representative SNPs that contribute to cisplatin-induced cytotoxicity through their effects on 8, 2 and 16 gene expressions in the combined, CEPH and Yoruban populations, respectively. These genetic variants contribute to 27, 29 and 45% of the overall variation in cell sensitivity to cisplatin in the combined, CEPH and Yoruban populations, respectively. Our whole genome approach can be used to elucidate expression quantitative trait loci contributing to a wide range of cellular phenotypes.
Keywords: exon array

overall_design: Gene expression on 176 HapMap cell lines.

first: R

middle: S

last: Huang

first: Shiwei

last: Duan

first: Sunita

middle: J

last: Shukla

first: Emily

middle: O

last: Kistner

first: Tyson

middle: A

last: Clark

first: Tina

middle: X

last: Chen

first: Anthony

middle: C

last: Schweitzer

first: John

middle: E

last: Blume

first: M


title: Identification of target genes of myostatin loss-of-function in the muscle of bovine fetuses

status: Public on Jul 17 2007

city: Saint-Genès-Champanelle

first: Isabelle

last: CASSAR-MALEK

address: Theix

department: Centre de Clermont-Fd/Theix

country: France

institute: INRA

summary:
Myostatin is a highly conserved Transforming Growth Factor beta family member which negatively regulates muscle development. Double-muscled (DM) cattle have a loss-of-function mutation in their myostatin gene responsible for a hypermuscular phenotype mainly due to hyperplasia. Thus these animals represent a good model for understanding the mechanisms at the origin of muscular hypertrophy. In order to identify individual genes or networks that may be myostatin targets, we looked for genes differentially expressed between DM and normal (NM) animals (n=3 per group) in the semitendinosus muscle (a hypertrophied muscle in DM animals) at 260 days of fetal development (intensive muscle biochemical differentiation). The experiment was carried out using muscle-dedicated high density oligonucleotide arrays of around 6,000 muscle specific genes.
A great number of genes was found to be differentially expressed according to the genetic type (some with a change higher than 5-fold), and according to the zygosity of the myostatin mutation. They belonged to various functional categories. The genes down-regulated in DM fetuses corresponded mainly to genes encoding extracellular matrix proteins, slow contractile proteins and ribosomal proteins. On the other hand, the genes up-regulated in DM fetuses were involved mainly in the regulation of transcription, cell cycle/apoptosis, translation, or DNA metabolism. These data singled out features indicating that DM muscle had shifted towards a more glycolytic metabolism, had an altered extracellular matrix composition (e.g. down-regulation of COL1A1, COL1A2, and up-regulation of collagen IV) and a decreased adipocyte differentiation (down-regulation of C1QTNF3). Altered gene expression in the three major muscle compartments (e.g. fibers, connective tissue and intramuscular adipose tissue) is in agreement with the well known characteristics of DM cattle. In addition, novel potential targets of the myostatin gene were identifed. Thus, the myostatin loss-of-function mutation affected several physiological processes involved in the development and the determinism of the functional characteristics of the muscle tissue.
Keywords: Double-muscled, myostatin loss-of-function, bovine fetuses

overall_design: Transcriptomic profiling of Semitendinosus (ST) muscle of three double-muscled fetuses were analyzed relative to three conventional fetuses. Each individual sample was compared to a reference pool. Four chips were hybridized per sample comparison.

last: Cassar-Malek

first: Florent

last: Passelaigue

first: Carine

last: Bernard

first: Jean

last: Léger

first: Jean-François

last: Hocquette


title: Differential antigen processing by dendritic cell subsets in vivo

status: Public on Dec 01 2006

city: New York

first: Diana

last: Dudziak

state: NY

address: 1230 York Avenue

institute: The Rockefeller University

summary:
Dendritic cells (DCs) process and present self and foreign antigens to induce tolerance or immunity. In vitro models suggest that induction of immunity is controlled by regulating the presentation of antigen, but little is known about how DCs control antigen presentation in vivo. To examine antigen processing and presentation in vivo we specifically targeted antigens to the two major subsets of DCs using chimeric monoclonal antibodies. Unlike CD8+ DCs that express the cell surface protein CD205, CD8- DCs, which are positive for the 33D1 antigen, are specialized for presentation on MHC class II. This difference in antigen processing is intrinsic to the DC subsets and associated with increased expression of proteins associated with MHC processing.
Keywords: cell type comparison of wildtype and Flt3L melonom spleen DCs and splenic B cells, CD4 and CD8 T cells

overall_design: This study includes data from cell sort purified dendritic cells, B cells and CD4 and CD8 T cells. The genearray was performed to identify the transmembrane molecule recognized by the antibody 33D1. The antibody 33D1 binds specifically to CD8-CD11cHigh DCs in the spleen. Therfore the data set was reduced in this way that all molecules that are expressed either in CD8=CD11cHigh DCs, B cells and T cells were diminished of the CD8+CD11cHigh DC data set. This Genearray was also used to analyze MHC class I and MHC class II associated moelcules as the DC subsets differ in the antigen presentation. Each Series consists of 3 individuall samples


title: Expression analysis of Cupriavidus metallidurans CH34 in presence of heavy metals

status: Public on Mar 16 2007

city: MOL

first: Natalie

last: Leys

state: Please select one below:

address: 200, boeretang

department: Institute for Environment, Health & Safety

country: Belgium

summary:
Cupriavidus metallidurans CH34 is a metal resistant beta-proteobacterium. The genome of this bacterium contain many genes involved in heavy metal resistance. Gene expression of C. metallidurans was studied after the addition of of Zn(II), Cd(II), Cu(II), Ni(II), Pb(II), Hg(II) or Co(II).
Keywords: Heavy metal stress response

overall_design:
Cultures of C. metallidurans CH34 were grown at 30°C until OD reached 0.6 (mid- exponential phase cultures).
Heavy metals (0.8 mM of Zn(II), 0.5 mM of Cd(II), 0.1 mM of Cu(II), 0.6 mM of Ni(II), 0.4 mM of Pb(II), 5 uM of Hg(II) and 0.5 mM of Co(II)) were added to the culture for 30 minutes induction time.
Total RNA was extracted, reverse-transcribed and labeled with Cy3-dCTP for the control (without metal) and with Cy5-dCTP for each conditions (challenged with one metal).
Labeled cDNA were (control and one condition) added to a spotted slide for overnight hybridization at 42°C.
Slides were scanned with a laser at 532 and 635 nm.

first: Sébastien

last: MONCHY

first: Mohammed

last: BENOTMANE

first: Max

last: MERGEAY


title: Expression data of S. mutans in semi synthetic medium with 0.5% sucrose

status: Public on Sep 01 2006

city: Braunschweig

first: Robert

last: Geffers

address: Inhoffenstr. 7

department: Dep. Molecular Bacteriology

country: Germany

institute: HCI - Helmholtz Centre for Infection Research

summary:
The autoinducer-2 (AI-2) group of signalling molecules represent a new type of cell-cell communication since they are produced by many phylogenetic groups of bacteria as the by product of a metabolic transformation carried out by the luxS enzyme. To separate the metabolic function of the luxS enzyme from the signalling role of AI-2, we carried out a global transcriptome analysis of a luxS null mutant of Streptococcus mutans UA159, an important cariogenic bacterium and crucial component of the dental plaque biofilm community. The data revealed fundamental changes in gene expression affecting 585 genes (appr. 30 % of the genome) which could not be restored by chemically synthesized DPD, the precursor of AI-2, and which are therefore related to the metabolic function of the luxS enzyme in the activated methyl cycle. All functional classes of enzymes were affected, including genes known for their pleiotropic effects in S. mutans, consistent with the impaired biofilm formation of the luxS deficient strain which could not be restored by added AI-2. At the same time, 59 genes were found whose transcription clearly responded to the addition of AI-2. Some of them were related to protein synthesis, stress, and cell division and so were probably indirectly controlled by AI-2. However, three density dependent transcriptional regulators were identified which were directly regulated by AI-2, since their transcription was stimulated repeatedly by
its addition. Moreover, three specific components of membrane transport systems were upregulated after addition of AI-2, suggesting they might be involved in its uptake. Finally, a global regulatory protein, the δ subunit of the RNA polymerase (rpoE) was induced 147fold by AI-2, representing the largest differential gene expression observed in our analysis. The data show for the first time a signalling role of AI-2 on the cellular level in Gram positive bacteria.
Keywords: time course

overall_design: S. mutans UA159 wild type was cultured anaerobically in BM medium containing 0.5% sucrose at 37°C, and the samples were collected at the following optical densities of the culture: 0.05, 0.1, 0.2, 0.3, 0.5, 0.7, 0.9 and 1.2. To obtain the same amount of RNA from each growth stage, the volumes of the samples withdrawn ranged from 200 ml (OD600 = 0.05) to 2.5 ml (OD600 = 1.2). The samples were fixed using RNA Protect Bacterial Reagent (Qiagen, Hilden, Germany). For each time point, two biological and two technical replicates were measured. Signal intensities were averaged among the technical replicates. In addition, normalized signal intensities from gene replicates were averaged and transformed into relative signal log2 ratios (SLR), whereby single averaged signal intensities were compared to the average of time 0 group signal intensities. Genes were selected that SLR differed by more than two over the entire time course.

first: Helena

last: Sztajer

first: André

last: Lemme

first: Stefan

last: Schulz

first: Ramiro

last: Vilchez

first: Georg

last: Conrads

first: Irene

last: Wagner-Dobler


title: S. coelicolor Wild Type R5- Medium Time-course Study

status: Public on Jun 08 2007

city: Minneapolis

first: Karthik

middle: P

last: Jayapal

state: MN

address: 421 Washington Ave SE

department: Chemical Engineering and Materials Science

institute: University of Minnesota

summary:
Many biological processes are intrinsically dynamic, incurring profound changes at both molecular and physiological levels. Systems analyses of such processes incorporating large-scale transcriptome or proteome profiling can be quite revealing. Although consistency between mRNA and proteins is often implicitly assumed in such studies, instances of divergent trends are frequently observed indicating the existence of post-transcriptional regulation. Here, we present a comparative transcriptome and proteome analysis of growth and stationary phase adaptation in Streptomyces coelicolor, taking the time-dynamics of process into consideration. These processes are of immense interest in streptomycetes as they encompass the physiological transformations eliciting biosynthesis of many naturally occurring therapeutic agents. A shotgun proteomics approach based on mass spectrometric analysis of isobaric stable isotope labeled peptides iTRAQ(TM) enabled identification and rapid quantification of approximately 14% of the theoretical proteome of S. coelicolor. Independent principal component analyses of this and DNA microarray-derived transcriptome data revealed that the prominent patterns in both protein and mRNA domains are surprisingly well correlated. Despite this general consensus, by employing a systematic concordance analysis we estimated that over 30% of the analyzed genes likely exhibited significantly divergent patterns, of which nearly one-third displayed even opposing trends. Integrating this data with biological information, we discovered that certain groups of functionally related genes were co-regulated independently as mRNA and/or proteins despite observations of apparent mRNA-protein discordance. This clearly suggests that post-transcriptional regulatory mechanisms are prominent even amongst prokaryotes while reaffirming the plausibility of such mechanisms acting in a concerted fashion at a protein complex or sub-pathway level.
Keywords: Time course

overall_design: Time-course study involved analysis of 8 samples (7h, 11h, 14h, 16h, 22h, 26h, 34h, 38h). Of these, 14h, 22h, 26h and 38h were analyzed in duplicate arrays. All arrays used cDNA labeled with Alexa647 and gDNA labeled with Cy3.

first: Wei-Shou

last: Hu


title: Alzheimer's disease and the normal aged brain (steph-affy-human-433773)

status: Public on Jul 10 2006

city: Phoenix

first: Winnie

last: Liang

state: AZ

address: 445 N. Fifth Street

institute: Translational Genomics

summary:
Information about the genes that are preferentially expressed during the course of Alzheimer’s disease (AD) could improve our understanding of the molecular mechanisms involved in the pathogenesis of this common cause of cognitive impairment in older persons, provide new opportunities in the diagnosis, early detection, and tracking of this disorder, and provide novel targets for the discovery of interventions to treat and prevent this disorder. Information about the genes that are preferentially expressed in relationship to normal neurological aging could provide new information about the molecular mechanisms that are involved in normal age-related cognitive decline and a host of age-related neurological disorders, and they could provide novel targets for the discovery of interventions to mitigate some of these deleterious effects.
Aim 1. Collect brain samples from three Alzheimer’s Disease Centers (ADCs) for subsequent gene expression profiling. Individuals will be stratified with respect to diagnostic groups (using both clinical and neuropathological criteria), age groups, and APOE genotype. 150 individual brains will be sampled from the Arizona ADC, the Duke University ADC, and the Washington University ADC. Miniscule sample sizes (200 um of sectioned tissue) from six brain regions that are histopathologically or metabolically relevant to AD and aging will be collected, ensuring that this proposal does not deplete the national resource. Frozen and fixed samples will be sent to Phoenix, sectioned in a standardized fashion, and then returned. Aim 2. Tissue heterogeneity will be eliminated prior to expression profiling by performing laser capture microscopy on all brain regions. Aim 3. Expression profile LCM-captured cells on the Affymetrix U133 Plus 2.0 array (~55,000 transcripts), and quickly provide these data to the community at large. Aim 4. Identify pathogenic cascades related to each of the clinico-pathologic correlates using unsupervised and supervised analyses coupled with a hypothesis-driven approach. Aim 5. Validation of the expression correlates at the protein and functional levels.
Scientific progress in the last few years has improved our understanding of AD and raised the hope of identifying treatments to halt the progression and prevent the onset of this disorder. For instance, researchers have begun to characterize the cascade of molecular events which lead to the major histopathological features of the disorder: neuritic plaques, which contain extra-cellular deposits of amyloid beta-peptides (Abeta); neurofibrillary tangles, which contain the hyperphosphorylated form of the intracellular, microtubule-associated protein, tau; and a loss of neurons and synapses. These molecular events provide targets for the development of promising new treatments. For example, A-beta has been postulated to trigger a cascade of events that are involved in the pathogenesis of AD. This proposal hopes to provide new information about the genes that are preferentially expressed in the development of AD histopathology, including the over-expression of APP, amyloid-induced neurotoxicity, and hyperphosphorylation of tau, as well as bring clarity to the metabolic abnormalities that seem to play a role in dementia and AD development and pathology.
We will perform LCM on 6 brain regions with about 14 biological replicates per brain region.  The brain regions are as follows: 1) entorhinal cortex 2) hippocampus 3) medial temporal gyrus 4) posterior cingulate 5) superior frontal gyrus and 6) primary visual cortex.  We will collect layer III pyramidal cells from the white matter in each region, isolate total RNA from LCMed cell lysates, and perform double round amplification of each sample for array analysis.
Keywords: other

first: Dietrich

last: Stephan


title: Treatment-specific changes in gene expression discriminate in vivo drug response in human leukemia cells

status: Public on Apr 21 2003

city: Memphis

first: William

last: Evans

state: TN

address: 332 N. Lauderdale St.

department: Pharmaceutical Sciences

institute: St.Jude Children's Research Hospital

summary:
To elucidate the genomics of cellular responses to cancer treatment, we analyzed the expression of over 9,600 human genes in acute lymphoblastic leukemia cells before and after in vivo treatment with methotrexate and mercaptopurine given alone or in combination. Based on changes in gene expression, we identified 124 genes that accurately discriminated among the four treatments. Discriminating genes included those involved in apoptosis, mismatch repair, cell cycle control and stress response. Only 14% of genes that changed when these medications were given as single agents also changed when they were given together. These data indicate that lymphoid leukemia cells of different molecular subtypes share common pathways of genomic response to the same treatment, that changes in gene expression are treatment-specific and that gene expression can illuminate differences in cellular response to drug combinations versus single agents.
Keywords: other

first: M

middle: H

last: Cheok

first: W

last: Yang

first: Ching-Hon

last: Pui

first: J

middle: R

last: Downing

first: C

last: Cheng

middle: V

last: Relling


title: Metastatic potential of melanomas defined by specific gene expression profiles with no BRAF signature (Philadelphia).

status: Public on Jun 27 2006

city: Zürich

first: Keith

last: Hoek

address: private

country: Switzerland

institute: Currently unaffilliated

summary:
The molecular biology of metastatic potential in melanoma has been studied many times previously and changes in the expression of many genes have been linked to metastatic behaviour. What is lacking is a systematic characterization of the regulatory relationships between genes whose expression is related to metastatic potential.  Such a characterization would produce a molecular taxonomy for melanoma which could feasibly be used to identify epigenetic mechanisms behind changes in metastatic behaviour. To achieve this we carried out three separate DNA microarray analyses on a total of 86 cultures of melanoma.  Significantly, multiple testing correlation revealed that previous reports describing correlations of gene expression with activating mutations in BRAF or NRAS were incorrect and that no gene expression patterns correlate with the mutation status of these MAPK pathway components. Instead, we identified three different sample cohorts (A, B and C) and found that these cohorts represent melanoma groups of differing metastatic potential. Cohorts A and B were susceptible to TGFbeta-mediated inhibition of proliferation and had low motility.  Cohort C was resistant to TGFb and demonstrated high motility. Meta-analysis of the data against previous studies linking gene expression and phenotype confirmed that cohorts A and C represent transcription signatures of weakly and strongly metastatic melanomas, respectively. Gene expression co-regulation suggested that signalling via TGFbeta-type and Wnt pathways underwent considerable change between cohorts. These results suggest a model for the transition from weakly to strongly metastatic melanomas in which TGFbeta-type signalling upregulates genes expressing vasculogenic/extracellular matrix remodeling factors and Wnt signal inhibitors, coinciding with a downregulation of genes downstream of Wnt signalling.
Keywords: class discovery study (differential metastatic potential)

overall_design: In this data set 29 melanoma cultures were analyzed.

first: Natalie

last: Schlegel

first: Patricia

last: Brafford

first: Antje

last: Sucker

first: Selma

last: Ugurel

first: Rajiv

last: Kumar

first: Barbara

middle: L

last: Weber

first: Katherine

last: Nathanson

first: David

last: Phillips

first: Meenhard

last: Herlyn

first: Dirk

last: Schadendorf

first: Reinhard

last: Dummer


title: Gene expression data from somites of E9.5 mouse embryos

status: Public on Dec 01 2010

city: paris

first: mounia

last: lagha

address: 25 rue du Dr Roux

institute: Institut Pasteur

summary: We used microarrays to identify Pax3 targets during myogenesis in the mouse embryo

overall_design: Mouse embryos were genotyped Pax3GFP/+ or Pax3PAX3-FKHR/GFP and dissected at E9.5 under a fluorescent binocular. Somites were dissected from the interlimb region and the more hypaxial domain separated from the neural tube and the epaxial extremity of the somites. GFP positive cells were then sorted by flow cytometry before RNA extraction and hybridization on Affymetrix microarrays. We also sorted GFP negative cells.

first: Mounia

last: Lagha

first: Takahiko

last: Sato

first: Béatrice

last: Regnault

first: Frédéric

last: Relaix

first: Margaret

last: Buckingham


title: natural variation affy data

status: Public on Dec 31 2004

city: Delhi

first: Srinivasan

last: Ramachandran

email: ramu@igib.res.in, ramucbt@yahoo.com

state: Delhi

address: Mall Road (Near Delhi University Campu)

department: Functional Genomics Unit

institute: Institute of Genomics and Integrative Biology

summary:
Natural variation in gene expression among healthy human individuals has been largely unexplored. In order to understand the genetic basis of variation in gene expression between normal human individuals, we need to obtain genome-wide expression data from various populations. Studies in monozygotic twins could enable us to estimate the size of the contribution of genetic and environmental factors to the natural variation in gene expression. In this work, we report the gene expression analysis of 5 pairs of monozygotic twins and 3 unrelated individuals
Normal healthy twin pairs were recruited for the study. Three more normal individuals including two females and one male were recruited. First, labeled products were hybridized with the Affymetrix GeneChip Test3 arrays. If the results were judged satisfactory, hybridization was subsequently carried out with the HG U95A arrays as per manufacturer's instructions. Arrays were hybridized at 45°C for 16 hours. The array was then washed using an automated Gene Chip Fluidics Station 400. After washing, the array was stained with streptavidin-phycoerythrin and scanned with a HP Gene Array Scanner. The data was analyzed using Gene Chip Software for expression analysis (MAS 5). All Gene Chip experiments were performed at the Weizmann Institute of Science, Rehovot, Israel.
Following comparisons were carried out:
1.	Between female identical twin pair (GSM14480 and GSM14481; GSM29053 and GSM 29054; GSM 29055 and GSM 29056)
2.	Between male identical twin pair (GSM14478 and GSM14479; GSM 29057 and GSM 29058)
3.	Between unrelated female individuals (include GSM14483, GSM20645 also but exclude comparisons within same twin pairs)
4.	Between unrelated male individuals (include GSM14477 but exclude comparisons between same twin pairs)

Keywords: repeat sample

first: Anu

last: Sharma

first: Vineet

middle: K

first: Shirley

last: Saban

first: Doron

last: Lancet

first: Samir

last: Brahmachari


title: Metastatic potential of melanomas defined by specific gene expression profiles with no BRAF signature.

first: Keith

last: Hoek

summary:
The molecular biology of metastatic potential in melanoma has been studied many times previously and changes in the expression of many genes have been linked to metastatic behaviour. What is lacking is a systematic characterization of the regulatory relationships between genes whose expression is related to metastatic potential.  Such a characterization would produce a molecular taxonomy for melanoma which could feasibly be used to identify epigenetic mechanisms behind changes in metastatic behaviour. To achieve this we carried out three separate DNA microarray analyses on a total of 86 cultures of melanoma.  Significantly, multiple testing correlation revealed that previous reports describing correlations of gene expression with activating mutations in BRAF or NRAS were incorrect and that no gene expression patterns correlate with the mutation status of these MAPK pathway components. Instead, we identified three different sample cohorts (A, B and C) and found that these cohorts represent melanoma groups of differing metastatic potential. Cohorts A and B were susceptible to TGFbeta-mediated inhibition of proliferation and had low motility.  Cohort C was resistant to TGFb and demonstrated high motility. Meta-analysis of the data against previous studies linking gene expression and phenotype confirmed that cohorts A and C represent transcription signatures of weakly and strongly metastatic melanomas, respectively. Gene expression co-regulation suggested that signalling via TGFbeta-type and Wnt pathways underwent considerable change between cohorts. These results suggest a model for the transition from weakly to strongly metastatic melanomas in which TGFbeta-type signalling upregulates genes expressing vasculogenic/extracellular matrix remodeling factors and Wnt signal inhibitors, coinciding with a downregulation of genes downstream of Wnt signalling.

This SuperSeries is composed of the SubSeries listed below.

overall_design:
Refer to individual Series

Zurich: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4840
Philadelphia: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4841
Mannheim: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4843

first: Natalie

last: Schlegel

first: Patricia

last: Brafford

first: Antje

last: Sucker

first: Selma

last: Ugurel

first: Rajiv

last: Kumar

first: Barbara

last: Weber

first: Katherine


title: Expression Data from Burkitt Lymphoma Patients

status: Public on Jul 05 2006

city: Bethesda

first: Sandeep

last: Dave

state: MD

address: 9000 Rockville Pike

institute: National Cancer Institute

summary:
Burkitt Lymphoma patient samples using gene expression to create a molecular definition of the disease. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
Keywords: clinical history design

overall_design: Samples were obtained from patients with Burkitt lymphoma and gene expression profiling was used to create a molecular definition of the disease. The molecular definition was then used to predict the disease in an independent set of patients with atypical Burkitt lymphoma and diffuse large B cell lymphoma.


title: Metastatic potential of melanomas defined by specific gene expression profiles with no BRAF signature (Zürich).

overall_design: In this (Zürich) data set three melanocyte cultures and twelve melanoma cultures were analyzed.

last: Nathanson

first: David

last: Phillips

first: Meenhard

last: Herlyn

first: Dirk

last: Schadendorf

first: Reinhard

last: Dummer


title: Molecular markers of breast cancer progression in a MMTV-PyMT hyperplasia transplant mouse model of breast cancer

status: Public on Jul 06 2007

city: Indianapolis

first: Hosein

last: Kouros-Mehr

state: IN

address: 533 Merrill St.

department: Oncology

institute: Eli Lilly

summary:
The primary cause of mortality in breast cancer is metastasis, a process which is still poorly understood.  To study the process of breast cancer metastasis, we isolated focal hyperplasias from the MMTV-PyMT transgenic breast cancer model and transplanted to syngeneic hosts.  The transplants underwent stereotyped progression to adenoma, early carcinoma, and late carcinoma at 5, 8 and 18 weeks post-transplant, respectively.   We compared the gene expression profiles of adenomas and late carcinomas by microarray.  Analysis of the data revealed that the most differentially expressed gene family between adenomas and late carcinomas were luminal differentiation genes, among them GATA-3.  In this report, we characterized the role of GATA-3 in breast cancer.
Keywords: spotted oligonucleotide

overall_design: Single hyperplasias were isolated from pubertal MMTV-PyMT x B-actin-GFP mice and transplanted into syngeneic hosts.  Total RNA from adenomas (5 week outgrowths) were compared to late carcinomas (18 week outgrowths).

first: Zena

last: Werb