Minimum information about a microarray experiment (MIAME)—toward standards for microarray data

Brāzma, Alvis; Hingamp, Pascal; Quackenbush, John; Sherlock, Gavin; Spellman, Paul T.; Stoeckert, C. J.; Aach, John; Ansorge, Wilhelm; Ball, Catherine A.; Causton, Helen C.; Gaasterland, Terry; Glenisson, Patrick; Holstege, Frank C.P.; Kim, Irene F.; Markowitz, Victor; Matese, John C.; Parkinson, Helen; Robinson, Alan J.; Sarkans, Ugis; Schulze-Kremer, Steffen; Stewart, Jason; Taylor, Ron; Vilo, Jaak; Vingron, Martin

doi:10.1038/ng1201-365

Cited by 3,600 publications

(2,221 citation statements)

References 11 publications

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“…Image and data files, array layout, as well as all relevant information according to the MIAME guidelines (Minimum Information About a Microarray Experiment [20]) were transferred into the Expressionist Refiner Array (Genedata AG, Basel, Switzerland). To exclude artefacts near background range, all spots were eliminated when sample or reference intensity was less than 50 or less than the local background.…”

Section: Discussionmentioning

confidence: 99%

JAK2-negative ET patients do not display constitutively active JAK/STAT signaling

Schwemmers

Will

Waller

et al. 2007

Experimental Hematology

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Objective-Presence of the JAK2 V617F mutation in only 40-60% of patients with Essential Thrombocythemia (ET) underscores the heterogeneity of this myeloproliferative disorder (MPD). Several distinct mutations, either in JAK2 (exon 12) or in c-Mpl (W515L) have been described in subsets of other MPDs, Polycythemia vera (PV) and Idiopathic Myelofibrosis (IMF). Analogous to JAK2 V617F , these mutations cause constitutive JAK2 and STAT activation. It has therefore been proposed that constitutive activation of the JAK/STAT pathway underlies the molecular etiology of all MPDs. We investigated the alternative hypothesis that distinct alterations, separate from the JAK/ STAT signal transduction pathway, underlie a subset of JAK2 V617F -negative ET.Methods-cDNA microarrays and qRT-PCR were used to compare gene expression in 40 ET patients with and without the JAK2 V617F mutation.Results-Unsupervised clustering of gene expression patterns in ET patients revealed two distinct subclasses of patients. These subclasses differed in presence or absence of the JAK2 V617F mutation. Patients lacking the JAK2 V617F mutation displayed significantly lower expression of the JAK/STAT target genes Pim-1 and SOCS2. In addition, JAK2 V617F -negative patients showed lower levels of STAT3 phosphorylation.Conclusions-These data demonstrate that a large proportion of JAK2 V617F -negative ET patients do not display constitutive JAK/STAT signaling. Hence, we propose that alterations in different signal transduction pathways can lead to the clinical phenotype of ET. Elucidation of novel ETinducing changes will facilitate both a molecular classification of ET and the development of rationally designed therapies.

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Section: Discussionmentioning

confidence: 99%

JAK2-negative ET patients do not display constitutively active JAK/STAT signaling

Schwemmers

Will

Waller

et al. 2007

Experimental Hematology

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“…Experimental procedures and data analysis followed recommended standards [16]. Total RNA from ten preparations per cell type, isolated from different placentas, was pooled [17].…”

Section: Methodsmentioning

confidence: 99%

Insulin control of placental gene expression shifts from mother to foetus over the course of pregnancy

et al. 2005

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Aims/hypothesis: The human placenta is a complex organ situated at the interface between mother and foetus that separates maternal from foetal blood. The placental surfaces exposed to the two bloodstreams are different, i.e. trophoblasts and endothelial cells are in contact with the maternal and foetal circulation, respectively. Both cell types produce high insulin receptor levels. The aim of the present study was to test the hypothesis that spatiotemporal changes in insulin receptor expression in trophoblasts from first trimester to the endothelium at term shift the control of insulin-dependent processes from mother to foetus. Methods: Global microarray analysis of primary trophoblasts from first trimester and term human placentas and endothelial cells from term human placentas cultured under hyperinsulinaemic and control conditions identified different sets of regulated genes in trophoblasts and endothelial cells. Results: Insulin effects on placental gene expression underwent developmental changes from trophoblasts in the first trimester to endothelial cells at term that were paralleled by changes in levels of activated insulin receptors. The changes in gene regulation were both quantitative (i.e. magnitude of effect) and qualitative (i.e. specific genes affected and direction of regulation). Conclusions/interpretation: This spatio-temporal shift in insulin sensitivity throughout pregnancy allows maternal and foetal insulin to regulate different processes within the placenta at different gestational stages, facilitated by compartmentalisation of the insulin response. Thus, by altering the levels and function of insulin receptors in space and time, control of insulin-dependent processes in the human placenta will change from mother to foetus throughout gestation. This will be of particular interest in conditions associated with altered maternal or foetal insulin levels, i.e. diabetes mellitus or intrauterine growth restriction.

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“…Second, the one problem we don't have is a shortage of omega-3-even if it turns out to be the nutritional wonder that some tout it being, which is now in doubt 1 . Not only is it found naturally in readily available foods like walnuts, flaxseed and fish, but it can be found in supplements and nutritionally supplemented foods like Smart Balance Maximizing state and federal spending while minimizing conflicts peanut butter, oil and margarine.…”

Section: Ron Edgar and Tanya Barrettmentioning

confidence: 99%

“…Early transgenic projects in pigs demonstrated an important proof of concept, but creating omega-3-enhanced pigs seems to come from the "because we can" school of justification. Even if the benefits of dietary omega-3 were incontrovertible (which they're not) 1 , and even if the only sources of omega-3 were animal based (which they aren't), the rationale for creating these genetically modified (GM) pigs is specious at best. Thus, in their paper, Lai et al write, "The only way to enrich the tissues of mammals with n-3 fatty acids has been dietary provision of n-3 fatty acids.…”

Section: Ron Edgar and Tanya Barrettmentioning

confidence: 99%

Why the omega-3 piggy should not go to market

Fiester

2006

Nat Biotechnol

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Minimum information about a microarray experiment (MIAME)—toward standards for microarray data

Cited by 3,600 publications

References 11 publications

JAK2-negative ET patients do not display constitutively active JAK/STAT signaling

JAK2-negative ET patients do not display constitutively active JAK/STAT signaling

Insulin control of placental gene expression shifts from mother to foetus over the course of pregnancy

Why the omega-3 piggy should not go to market

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