Filtered selection coupled with support vector machines generate functionally relevant prediction model for colorectal cancer. In this study, we built a model that uses Support Vector Machine (SVM) to classify cancer and normal samples using Affymetrix exon microarray data obtained from 90 samples of 48 patients diagnosed with CRC. From the 22,011 genes, we selected the 20, 30, 50, 100, 200, 300 and 500 genes most relevant to CRC using the Minimum-RedundancyMaximum-Relevance (mRMR) technique. With these gene sets, an SVM model was designed using four different kernel types (linear, polynomial, radial basis function and sigmoid).
Filtered selection coupled with support vector machines generate a functionally relevant prediction model for colorectal cancer.
Sex, Age, Specimen part, Disease stage
View SamplesFine control of macrophage activation is required to prevent inflammatory disease, particularly at barrier sites such as the lung. However, the dominant mechanisms that regulate pulmonary MFs during inflammation are currently poorly understood. Here we show that airway MFs are substantially less able to respond to the canonical type-2 cytokine IL-4, which underpins allergic disease and parasite worm infections, than lung tissue or peritoneal cavity MFs. We reveal that MF hypo-responsiveness to IL-4 is dictated by the lung environment, though independent of the host microbiota or the prominent lung extracellular matrix components surfactant protein D and mucin 5b. Rather, compared to cavity MFs, airway MFs display severely dysregulated metabolism. Strikingly, upon removal from the lung, alveolar MFs regain IL-4 responsiveness in a process dependent upon glycolysis. Thus, we propose that impaired glycolysis within the pulmonary niche is a central determinant for regulation of MF responsiveness during type-2 inflammation. Overall design: The 13 analysed samples belong to 6 different groups, each group consisted of 2 or 3 samples. The groups consist of 3 separate macrophage populations, from either control or IL-4 complex treated mice. Each individual sample was generated from 3-5 pooled biological replicate mice.
The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation.
Treatment, Subject
View SamplesRegulation of gene expression at the post-transcriptional level plays an indispensable role during TGFbeta-induced EMT and metastasis. This regulation involves a transcript-selective translational regulatory pathway in which a ribonucleoprotein (mRNP) complex, consisting of heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) and eukaryotic elongation factor 1A1 (eEF1A1), binds to a 3-UTR regulatory BAT (TGF activated translation) element and silences translation of Dab2 and ILEI mRNAs, two transcripts which are involved in mediating EMT. TGFbeta activates a kinase cascade terminating in the phosphorylation of hnRNP E1, by isoform-specific stimulation of protein kinase B/Akt2, inducing the release of the mRNP complex from the 3-UTR element, resulting in the reversal of translational silencing and increased expression of Dab2 and ILEI transcripts.
Establishment of a TGFβ-induced post-transcriptional EMT gene signature.
Specimen part
View SamplesPhosphate is essential for healthy bone growth and plays an essential role in fracture repair. Although phosphate deficiency has been shown to impair fracture healing, the mechanisms involved in impaired healing are unknown. More recently, studies have shown that the effect of phosphate deficiency on the repair process varied based on the genetic strain of mice, which is not characterized.
Hypophosphatemia Regulates Molecular Mechanisms of Circadian Rhythm.
Sex, Specimen part, Time
View SamplesTimed sleep restriction designed to mimic human shift work was performed over a 2 week period in mice. On the final day, tissues were collected at 6 hour intervals to exmaine the effects of sleep restriction on circadian gene expression.
Circadian desynchrony promotes metabolic disruption in a mouse model of shiftwork.
Sex, Specimen part, Treatment, Time
View SamplesThe molecular mechanisms by which individuals subjected to environmental heat stress either adapt or develop heat-related complications are not well understood. We analysed the changes in blood mononuclear gene expression patterns in human volunteers exposed to an extreme heat in a sauna (temperature of 78 6 C).
A Model of Exposure to Extreme Environmental Heat Uncovers the Human Transcriptome to Heat Stress.
Sex, Age, Specimen part, Treatment, Subject, Time
View SamplesMature B cells leave the bone marrow as naïve B cells and migrate to the secondary lymphoid organs where they encounter the antigen for the first time. This interaction stimulates B cells to rapidly grow and form characteristic histological structures called germinal center. In the germinal centers, B cells are targeted by mechanisms of genetic editing of the immunoglobulin loci, namely somatic hypermutation and class switch recombination, undergo selection for high affinity immunoglobulin receptors and are committed to differentiate into memory B cells or plasma cells. GCs display two histological areas the dark and the light zone that have been characterized as functionally distinct compartments through which B cells recycle multiple times during the germinal center reaction. Overall design: Naïve, germinal center and memory B cells were isolated from three independent donors each.
MEF2B Instructs Germinal Center Development and Acts as an Oncogene in B Cell Lymphomagenesis.
Specimen part, Subject
View SamplesThe 24R,25-dihydroxyvitamin D metabolite (24R,25D) has long been suspected of participating to bone fracture repair. We used Cyp24a1-deficient mice, unable to produce 24R25D, to observe gene expression in callus tissue compared to that of control littermates.
Optimal bone fracture repair requires 24R,25-dihydroxyvitamin D3 and its effector molecule FAM57B2.
Age, Specimen part, Treatment, Time
View SamplesExpression data from CD34+ hematopoietic cells transduced with control or anti-SLPI shRNA, serum starved and treated with G-CSF.
A lack of secretory leukocyte protease inhibitor (SLPI) causes defects in granulocytic differentiation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas.
Specimen part
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