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Träfflista för sökning "WFRF:(Engström Wilhelm) "

Sökning: WFRF:(Engström Wilhelm)

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2.
  • Engström, Wilhelm (författare)
  • Effects of Insulin-like Growth Factor Binding Protein 7 on Apoptosis in Human Teratocarcinoma Cells In Vitro
  • 2010
  • Ingår i: Anticancer Research. - International Institute of Anticancer Research (IIAR). - 0250-7005 .- 1791-7530. ; 30, s. 911-914
  • Tidskriftsartikel (refereegranskat)abstract
    • Human teratocarcinoma cells (Tera-2) deprived of serum undergo programmed cell death which can be counteracted by simultaneous addition of IGF-II. This protective effect of IGF-II was specific in the sense that addition of IGF-binding protein 7 (IGFBP-7) resulted in an increased apoptotic rate almost comparable to that of the classical IGFBPs. Autoradiographic analysis of incorporated tritiated thymidine indicated that the proportion of S-phase cells was comparable, irrespective of total cell numbers. This further suggests that IGF-II rescues cells from apoptosis and that IGFBP-7 is a specific antagonist.
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3.
  • Engström, Wilhelm (författare)
  • Expression of JNK-interacting Protein JIP-1 and Insulin-like Growth Factor II in Wilms Tumour Cell Lines and Primary Wilms Tumours
  • 2009
  • Ingår i: Anticancer Research. - International Institute of Anticancer Research (IIAR). - 0250-7005 .- 1791-7530. ; 29, s. 2467-2472
  • Tidskriftsartikel (refereegranskat)abstract
    • JNK-interacting protein 1 (JIP-1) is an important scaffolding protein in the JNK signalling pathway. It is also believed to play a role in the mediation of mitogenic messages from the plasma membrane to the cell interior. Previous studies suggest that the JIP-gene is co-regulated with the insulin-like growth factor II (IGF II) gene, thereby contributing to the growth stimulatory effects of this potent growth factor. The striking coexpression of these two genes was found in murine fetuses as well as in primary human embryonic tumours. When six primary Wilms tumours were examined, the two genes showed a high degree of co-variation in the sense that high expression of IGF II was followed by high expression of JIP-1 and vice versa. However, when the human Wilms tumour cell line WCCS-1 was examined, a very modest intrinsic expression of IGF 11 was accompanied by a moderate expression of JIP-1. When exogenous IGF H was added, which has previously been shown to induce apoptosis in this cell line, the JIP-1 expression increased. These data suggest that JIP-1 has a more complex role in the regulation of proliferation as well as programmed cell death.
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4.
  • Engström, Wilhelm (författare)
  • Role of fibroblast growth factors in elicitation of cell responses
  • 2014
  • Ingår i: Cell Proliferation. - Wiley: 12 months. - 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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5.
  • Engström, Wilhelm (författare)
  • The Expression of the Insulin-like Growth Factor II, JIP-1 and WT1 Genes in Porcine Nephroblastoma
  • 2009
  • Ingår i: Anticancer Research. - International Institute of Anticancer Research (IIAR). - 0250-7005 .- 1791-7530. ; 29, s. 4999-5003
  • Tidskriftsartikel (refereegranskat)abstract
    • c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP-1) is an important scaffolding protein in the JNK signalling pathway. It is also believed to play a role in the mediation of mitogenic messages from the plasma membrane to the cell interior. Previous studies have suggested that the JIP gene is co-regulated with the insulin-like growth factor II (IGF-II) gene, thereby contributing to the growth stimulatory effects of this potent growth factor. The striking co-expression of these two genes has been found in murine foetuses as well as in primary human embryonic tumours. When six primary Wilms tumours (nephroblastomas) from pig were examined, the two genes showed a high degree of co-variation in the sense that high or low expression of IGF-II and high or low expression of JIP-1 ocurred together. By contrast the expression of a third Wilms tumour related gene, WT1, was completely uncorrelated to the expression of IGF-II and JIP. In this respect, porcine nephroblastomas resemble human Wilms tumours. This further suggests that JIP-1 may play a role in the regulation of IGF-II-driven tumour cell proliferation.
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6.
  • Engström, Wilhelm, et al. (författare)
  • The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling
  • 2015
  • Ingår i: Carcinogenesis. - Oxford University Press (OUP): Policy B - Oxford Open Option B. - 0143-3334 .- 1460-2180. ; 36, s. S38-S60
  • Forskningsöversikt (refereegranskat)abstract
    • The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.
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7.
  • Engström, Wilhelm (författare)
  • The RECK Gene and Biological Malignancy-Its Significance in Angiogenesis and Inhibition of Matrix Metalloproteinases
  • 2014
  • Ingår i: Anticancer Research. - International Institute of Anticancer Research (IIAR). - 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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9.
  • Engström, Wilhelm (författare)
  • The WT1 Gene - Its Role in Tumourigenesis and Prospects for Immunotherapeutic Advances
  • 2014
  • Ingår i: In Vivo. - International Institute of Anticancer Research (IIAR). - 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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10.
  • Eriksson, Staffan, et al. (författare)
  • Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead
  • 2015
  • Ingår i: Carcinogenesis. - Oxford University Press (OUP): Policy B - Oxford Open Option B. - 0143-3334 .- 1460-2180. ; 36, s. S254-S296
  • Forskningsöversikt (refereegranskat)abstract
    • Low-dose exposures to common environmental chemicals that are deemed safe individually may be combining to instigate carcinogenesis, thereby contributing to the incidence of cancer. This risk may be overlooked by current regulatory practices and needs to be vigorously investigated.Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.
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