Author
An-Sofie De Weer
Bio: An-Sofie De Weer is an academic researcher from Ghent University Hospital. The author has contributed to research in topics: Normalization (statistics) & Database normalization. The author has an hindex of 2, co-authored 2 publications receiving 875 citations.
Papers
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TL;DR: It is demonstrated that the mean expression value outperforms the current normalization strategy in terms of better reduction of technical variation and more accurate appreciation of biological changes.
Abstract: Gene expression analysis of microRNA molecules is becoming increasingly important. In this study we assess the use of the mean expression value of all expressed microRNAs in a given sample as a normalization factor for microRNA real-time quantitative PCR data and compare its performance to the currently adopted approach. We demonstrate that the mean expression value outperforms the current normalization strategy in terms of better reduction of technical variation and more accurate appreciation of biological changes.
952 citations
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TL;DR: There was an error in the name of the 13th author and the correct name is Florence Nguyen-Khac.
Abstract: There was an error in the name of the 13th author. The correct name is Florence Nguyen-Khac.
3 citations
Cited by
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TL;DR: Findings are discussed with a specific focus on the clinical utility of cell-free nucleic acids as blood biomarkers for cancer screening, prognosis and monitoring of the efficacy of anticancer therapies.
Abstract: 1described the presence of cell-free nucleic acid (cfNA) in human blood for the first time. This attracted little attention in the scientific community and it was not until 1994 that the importance of cfNA was recognized as a result of the detection of mutated RAS gene fragments in the blood of cancer patients 2,3 (TIMELINE). In 1996, microsatellite alterations on cell-free DNA (cfDNA) were shown in cancer patients 4
2,427 citations
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TL;DR: This work reviews the major considerations for carrying out and interpreting results of miRNA-profiling studies and suggests several approaches that can be considered for effective use.
Abstract: MicroRNAs (miRNAs) are small RNAs that post-transcriptionally regulate the expression of thousands of genes in a broad range of organisms in both normal physiological contexts and in disease contexts. miRNA expression profiling is gaining popularity because miRNAs, as key regulators in gene expression networks, can influence many biological processes and also show promise as biomarkers for disease. Technological advances have spawned a multitude of platforms for miRNA profiling, and an understanding of the strengths and pitfalls of different approaches can aid in their effective use. Here, we review the major considerations for carrying out and interpreting results of miRNA-profiling studies.
1,465 citations
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TL;DR: It is shown that miR-9, which is upregulated in breast cancer cells, directly targets CDH1, the E-cadherin-encoding messenger RNA, leading to increased cell motility and invasiveness, and a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis
Abstract: β-catenin signalling, which contributes to upregulated expression of the gene encoding vascular endothelial growth factor (VEGF); this leads, in turn, to increased tumour angiogenesis. Overexpression of miR-9 in otherwise non-metastatic breast tumour cells enables these cells to form pulmonary micrometastases in mice. Conversely, inhibiting miR-9 by using a ‘miRNA sponge’ in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin. Metastases are responsible for more than 90% of cancer-related mortality. These secondary growths arise through a multistep process that begins when cancer cells within primary tumours break away from neighbouring cells and invade the basement membrane 1 . This local invasion may frequently be triggered by contextual signals that carcinoma cells receive from the nearby stroma, causing them to undergo an epithelial–mesenchymal transition (EMT) 2 . Subsequently, metastasizing cells enter the circulation either directly or through lymphatics. Size constraints in the microvasculature cause many of these cells to be arrested at distant sites, where they may extravasate and enter the foreign tissue parenchyma. There they may remain dormant or, with low efficiency, proliferate from occult micrometastases to form angiogenic, clinically detectable metastases. The absence of EMT-inducing signals in the foreign microenvironment may cause such disseminated cells to revert to an epithelial phenotype by means of a mesenchymal–epithelial transition. Critical regulators of the metastatic process include both proteins and miRNAs 3,4
1,238 citations
01 Feb 2010
TL;DR: In this article, the authors uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasissuppressing protein E-cadherin.
Abstract: β-catenin signalling, which contributes to upregulated expression of the gene encoding vascular endothelial growth factor (VEGF); this leads, in turn, to increased tumour angiogenesis. Overexpression of miR-9 in otherwise non-metastatic breast tumour cells enables these cells to form pulmonary micrometastases in mice. Conversely, inhibiting miR-9 by using a ‘miRNA sponge’ in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin. Metastases are responsible for more than 90% of cancer-related mortality. These secondary growths arise through a multistep process that begins when cancer cells within primary tumours break away from neighbouring cells and invade the basement membrane 1 . This local invasion may frequently be triggered by contextual signals that carcinoma cells receive from the nearby stroma, causing them to undergo an epithelial–mesenchymal transition (EMT) 2 . Subsequently, metastasizing cells enter the circulation either directly or through lymphatics. Size constraints in the microvasculature cause many of these cells to be arrested at distant sites, where they may extravasate and enter the foreign tissue parenchyma. There they may remain dormant or, with low efficiency, proliferate from occult micrometastases to form angiogenic, clinically detectable metastases. The absence of EMT-inducing signals in the foreign microenvironment may cause such disseminated cells to revert to an epithelial phenotype by means of a mesenchymal–epithelial transition. Critical regulators of the metastatic process include both proteins and miRNAs 3,4
1,124 citations
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TL;DR: Transplantation of both white and brown adipose tissue—brown especially—into ADicerKO mice restores the level of numerous circulating miRNAs that are associated with an improvement in glucose tolerance and a reduction in hepatic Fgf21 mRNA and circulating FGF21.
Abstract: Adipose tissue is a major site of energy storage and has a role in the regulation of metabolism through the release of adipokines. Here we show that mice with an adipose-tissue-specific knockout of the microRNA (miRNA)-processing enzyme Dicer (ADicerKO), as well as humans with lipodystrophy, exhibit a substantial decrease in levels of circulating exosomal miRNAs. Transplantation of both white and brown adipose tissue-brown especially-into ADicerKO mice restores the level of numerous circulating miRNAs that are associated with an improvement in glucose tolerance and a reduction in hepatic Fgf21 mRNA and circulating FGF21. This gene regulation can be mimicked by the administration of normal, but not ADicerKO, serum exosomes. Expression of a human-specific miRNA in the brown adipose tissue of one mouse in vivo can also regulate its 3' UTR reporter in the liver of another mouse through serum exosomal transfer. Thus, adipose tissue constitutes an important source of circulating exosomal miRNAs, which can regulate gene expression in distant tissues and thereby serve as a previously undescribed form of adipokine.
1,025 citations