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Träfflista för sökning "WFRF:(Engström Wilhelm) srt2:(2014)"

Sökning: WFRF:(Engström Wilhelm) > (2014)

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1.
  • Engström, Wilhelm, et al. (författare)
  • Epigenic regulation of the IGF2/H19 locus
  • 2014
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 34, s. 5895-5895
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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2.
  • Engström, Wilhelm (författare)
  • Role of fibroblast growth factors in elicitation of cell responses
  • 2014
  • Ingår i: Cell Proliferation. - : Wiley. - 0960-7722 .- 1365-2184. ; 47, s. 3-11
  • Tidskriftsartikel (refereegranskat)abstract
    • Fibroblast growth factors (FGFs) are signalling peptides that control important cell processes such as proliferation, differentiation, migration, adhesion and survival. Through binding to different types of receptor on the cell surface, these peptides can have different effects on a target cell, the effect achieved depending on many features. Thus, each of the known FGFs elicits specific biological responses. FGF receptors (FGFR 1-5) initiate diverse intracellular pathways, which in turn lead to a variety of results. FGFs also bind the range of FGFRs with a series of affinities and each type of cells expresses FGFRs in different qualitative and quantitative patterns, which also affect responses. To summarize, cell response to binding of an FGF ligand depends on type of FGF, FGF receptor and target cell, all interacting in concert. This review aims to examine properties of the FGF family and its members receptors. It also aims to summarize features of intracellular signalling and highlight differential effects of the various FGFs in different circumstances.
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4.
  • Engström, Wilhelm (författare)
  • The RECK Gene and Biological Malignancy-Its Significance in Angiogenesis and Inhibition of Matrix Metalloproteinases
  • 2014
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 34, s. 3867-3873
  • Forskningsöversikt (refereegranskat)abstract
    • The RECK (reversion-inducing cysteine-rich protein with Kazal motifs) gene is a relatively newly discovered gene with important implications in cancer biology. RECK is normally expressed in all cells of the body and has an important role in the balance between destructive and constructive features of the extracellular matrix (ECM). The RECK protein is a membrane-bound glycoprotein that inhibits matrix metalloproteinases with the function of breaking-down the ECM. There is a significant correlation between RECK gene expression and the formation of new vessels, presumably via the mediation of vascular endothelial growth factor (VEGF), which is an important and powerful inducer of angiogenesis.. Research has shown that down-regulation of RECK is caused by the rat sarcoma oncogene (RAS), which is also a common cause of tumor development in the early stages. For a tumor to progress and gain characteristics that classifies it as malignant, the degradation of the ECM and mobilization of new blood vessels are essential functions. If the tumor is inhibited with respect to these functions, it will cease to grow. RECK is, therefore, a potential tumor inhibitor but also a prognostic marker available at early clinical stages.
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5.
  • Engström, Wilhelm (författare)
  • The WT1 Gene - Its Role in Tumourigenesis and Prospects for Immunotherapeutic Advances
  • 2014
  • Ingår i: In Vivo. - 0258-851X. ; 28, s. 675-681
  • Forskningsöversikt (refereegranskat)abstract
    • The Wilms Tumour 1 (WT1) gene is a complex gene which was originally linked to suppression of cancer in kidneys. Studies of WT1-knockout mice confirmed the important role of WT1 in the pathogenesis of Wilms' tumour, a tumour which accounts for 95% of all childhood renal tumours. In such cases, the WT1 gene acts as a tumour-suppressor gene. Subsequent research has shown that the WT1 gene in many other cases acts as an oncogene, most prominently in leukaemia and lung cancer (even though these cancer forms can emerge as a result of many other aetiological factors). Since WT1 acts as an oncogene in many different organs, it is of great importance to evaluate how and when the WT1 gene and protein act. This information can then be used to develop immunotherapy to stabilize and treat different malignant diseases. Both phase I and phase II studies have been carried out on candidate vaccines with varying but overall promising results. The immune response does not always correlate with the clinical response, however, and the efficacy of the treatment is often limited. Further development is, therefore, needed to understand how vaccines can be improved, so that they, can hopefully fulfil a clinical role in the future.
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6.
  • Nordin, Matilda, et al. (författare)
  • Epigenetic regulation of the Igf2/H19 gene cluster
  • 2014
  • Ingår i: Cell Proliferation. - : Wiley. - 0960-7722 .- 1365-2184. ; 47, s. 189-199
  • Tidskriftsartikel (refereegranskat)abstract
    • Igf2 (insulin-like growth factor 2) and H19 genes are imprinted in mammals; they are expressed unevenly from the two parental alleles. Igf2 is a growth factor expressed in most normal tissues, solely from the paternal allele. H19 gene is transcribed (but not translated to a protein) from the maternal allele. Igf2 protein is a growth factor particularly important during pregnancy, where it promotes both foetal and placental growth and also nutrient transfer from mother to offspring via the placenta. This article reviews epigenetic regulation of the Igf2/H19 gene-cluster that leads to parent-specific expression, with current models including parental allele-specific DNA methylation and chromatin modifications, DNA-binding of insulator proteins (CTCFs) and three-dimensional partitioning of DNA in the nucleus. It is emphasized that key genomic features are conserved among mammals and have been functionally tested in mouse. The enhancer competition model', the boundary model' and the chromatin-loop model' are three models based on differential methylation as the epigenetic mark responsible for the imprinted expression pattern. Pathways are discussed that can account for allelic methylation differences; there is a recent study that contradicts the previously accepted fact that biallelic expression is accompanied with loss of differential methylation pattern.
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  • Resultat 1-6 av 6

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