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Sökning: L773:0250 7005 OR L773:1791 7530

  • Resultat 51-60 av 656
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51.
  • 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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52.
  • 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. - 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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53.
  • 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. - 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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54.
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55.
  • 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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56.
  • Eriksson, David, et al. (författare)
  • Apoptotic signalling in HeLa Hep2 cells following 5 Gy of cobalt-60 gamma radiation
  • 2009
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 29:11, s. 4361-4366
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The apoptotic signalling pathways involved in the delayed type of apoptosis occurring in HeLa Hep2 cells following radiation were investigated. MATERIALS AND METHODS: HeLa Hep2 cells were exposed to 5 Gy of cobalt-60 radiation. The activation of caspase-2, caspase-8, caspase-9 and effector caspase-3 was investigated by caspase assay plates and Western blots. Cleavage of poly (ADP-ribose) polymerase (PARP) was analysed on Western blots. HeLa Hep2 cells were irradiated with or without preincubation with inhibitors of protein synthesis (cycloheximide, CHX) and caspases, followed by TUNEL staining and caspase assay plate evaluation. RESULTS: Initiator caspases-2, -8, -9, and effector caspase-3, were found to be activated and PARP cleaved following irradiation. CHX completely inhibited the caspase activation and the associated apoptosis. Pretreatment with caspase-2 inhibitor indicated that caspase-2 was involved in the execution of the apoptosis. CONCLUSION: Activation of the apoptotic signalling pathways following irradiation of HeLa Hep2 cells includes components from the intrinsic as well as the extrinsic pathways and seems to require de novo protein synthesis.
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57.
  • Eriksson, Mathilda, et al. (författare)
  • Utilization of a right-handed coiled-coil protein from archaebacterium Staphylothermus marinus as a carrier for cisplatin
  • 2009
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 29:1, s. 11-18
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The nano-sized right-handed coiled-coil (RHCC) protein, originating from the archaebacterium Staphylothermus marinus, is stable at high salt concentrations, high temperatures, high pressures and extremes of pH. Its crystal structure reveals four hydrophobic cavities which can incorporate heavy metals. Nano-sized compounds have been used to carry cytotoxic drugs to tumours, avoiding delivery to healthy tissue, in part due to enhanced permeability in tumour blood vessels (enhanced permeability and retention effect). MATERIALS AND METHODS: The ability of RHCC to carry the platinum-containing chemotherapeutic drug cisplatin to cells, while retaining the cytotoxic potential was tested both in vitro and in vivo. RESULTS: RHCC was able to bind and enter cells in vitro and was not severely toxic or immunogenic in mice. Moreover, RHCC incorporated cisplatin, without inhibiting the cytotoxic potential of the drug against tumour cell lines in vitro or in vivo. CONCLUSION: RHCC can be used as a carrier of cisplatin without abrogating the effect of the drug.
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58.
  • Ernstson, Avalon, et al. (författare)
  • Detection of HPV mRNA in Self-collected Vaginal Samples Among Women at 69-70 Years of Age
  • 2019
  • Ingår i: Anticancer research. - : Anticancer Research USA Inc.. - 1791-7530 .- 0250-7005. ; 39:1, s. 381-386
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND/AIM: Cervical cancer is associated with poorer diagnosis among the elderly and pap-smear screening has a lower sensitivity. Self-sampling for detection of high-risk human papillomavirus (hr-HPV) may be an alternative screening method. The aim of this study was to analyze the response rate to vaginal HPV self-sampling and the HPV mRNA prevalence among women 69-70 years. MATERIALS AND METHODS: An HPV self-sampling kit was sent to 1,000 women 69-70 years whom had not taken a cervical smear in ≥5 years. The samples were analyzed by the Aptima HPV mRNA assay. HPV-positive women were recalled for a follow-up examination. RESULTS: The self-sample response rate was 43.3%. The HPV mRNA prevalence was 6.2%. All HPV-positive women attended follow-up. CONCLUSION: HPV self-sampling was accepted among older women. Although the HPV mRNA prevalence was 6.2%, no high-grade cytological abnormalities were found. Larger studies are needed to elucidate hr-HPV self-sampling as a tool to identify older women at risk of cervical cancer.
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59.
  • Evertsson, Sofia, 1972-, et al. (författare)
  • Microsatellite instability and MBD4 mutation in unselected colorectal cancer
  • 2003
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 23:4, s. 3569-3574
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: We investigated the prognostic significance of microsatellite instability (MSI) and the association with clinicopathological factors in colorectal cancer, and further identified MBD4 mutations and their clinicopathological significance.PATIENTS AND METHODS: MSI was analyzed in 201 colorectal cancers. Sequencing analysis of MBD4 was performed in 26 MSI and 28 microsatellite stable (MSS) tumors.RESULTS: Twenty-seven tumors (13.4%) were MSI but did not correlate with improved survival. MSI was significantly correlated with proximal colon tumors (p < 0.001), poor differentiation or mucinous type (p = 0.005) and multiple tumors (p = 0.04). MBD4 mutations were found in 15% MSI but not in MSS tumors. The mutated cases showed female overrepresentation, proximal site and poorly-differentiated/mucinous type.CONCLUSION: MSI was not correlated with survival, but shared other features associated with MSI in colorectal cancer as demonstrated by others. The clinicopathological variables associated with the MBD4 mutations were probably the reflection of MSI features.
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60.
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