| 1. |
- Bergman, Daniel, et al.
(författare)
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Insulin-Like Growth Factor 2 in Development and Disease: A Mini-Review
- 2013
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Ingår i: Gerontology. - : S. Karger AG. - 0304-324X .- 1423-0003. ; 59, s. 240-249
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Forskningsöversikt (refereegranskat)abstract
- Background: Insulin-like growth factor 2 (IGF2) is a protein hormone known to regulate cell proliferation, growth, migration, differentiation and survival. The gene is parentally imprinted in the sense that transcripts are almost exclusively derived from the paternal allele. Loss of imprinting of the IGF2 gene is a recurrent observation in growth disorders that combine overgrowth with a variety of malignant tumours. Moreover, IGF2 has been proposed to play a role in the development of a variety of seemingly unrelated cancers that play an important role in geriatric medicine, e.g. breast cancer, colon cancer and lung cancer. Finally, IGF2 has been implicated in cardiovascular disease, since, for example, IGF2 has been shown to influence the size of atherosclerotic lesions. Objective: To summarize current knowledge about IGF2, its interactions with binding proteins and receptors and connections with key diseases. Methods: The contents of this paper were based on reviews of existing literature within the field. Results: There is a substantial amount of research linking IGF2 to growth disorders, cancer and to a much lesser degree cardiovascular disease. Some of the studies on IGF2 and tumour growth have yielded conflicting results, for instance regarding its effect on apoptosis. Conclusion: Today, our knowledge on how IGF2 is composed and interacts with receptors has come a long way. However, there is comparatively little information on how IGF2 affects tumour growth and cardiovascular diseases such as atherosclerosis. Thus, further research will be needed to elucidate the impact of IGF2 on key diseases. Copyright (C) 2012 S. Karger AG, Basel
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| 2. |
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| 3. |
- Engström, Wilhelm
(författare)
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Effects of Insulin-like Growth Factor Binding Protein 7 on Apoptosis in Human Teratocarcinoma Cells In Vitro
- 2010
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 30, s. 911-914
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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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| 4. |
- Engström, Wilhelm, et al.
(författare)
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Epigenic regulation of the IGF2/H19 locus
- 2014
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 34, s. 5895-5895
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 5. |
- Engström, Wilhelm
(författare)
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Expression of JNK-interacting Protein JIP-1 and Insulin-like Growth Factor II in Wilms Tumour Cell Lines and Primary Wilms Tumours
- 2009
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 29, s. 2467-2472
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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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| 6. |
- Engström, Wilhelm
(författare)
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Role of fibroblast growth factors in elicitation of cell responses
- 2014
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Ingår i: Cell Proliferation. - : Wiley. - 0960-7722 .- 1365-2184. ; 47, s. 3-11
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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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| 7. |
- Engström, Wilhelm
(författare)
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The Expression of the Insulin-like Growth Factor II, JIP-1 and WT1 Genes in Porcine Nephroblastoma
- 2009
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 29, s. 4999-5003
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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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| 8. |
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| 9. |
- Engström, Wilhelm, et al.
(författare)
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The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling
- 2015
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Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 36, s. S38-S60
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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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| 10. |
- Engström, Wilhelm
(författare)
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The RECK Gene and Biological Malignancy-Its Significance in Angiogenesis and Inhibition of Matrix Metalloproteinases
- 2014
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Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 34, s. 3867-3873
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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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