Search Results - (Author, Cooperation:L. Bjorge)
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1Latest Papers from Table of Contents or Articles in PressA. I. Ojesina ; L. Lichtenstein ; S. S. Freeman ; C. S. Pedamallu ; I. Imaz-Rosshandler ; T. J. Pugh ; A. D. Cherniack ; L. Ambrogio ; K. Cibulskis ; B. Bertelsen ; S. Romero-Cordoba ; V. Trevino ; K. Vazquez-Santillan ; A. S. Guadarrama ; A. A. Wright ; M. W. Rosenberg ; F. Duke ; B. Kaplan ; R. Wang ; E. Nickerson ; H. M. Walline ; M. S. Lawrence ; C. Stewart ; S. L. Carter ; A. McKenna ; I. P. Rodriguez-Sanchez ; M. Espinosa-Castilla ; K. Woie ; L. Bjorge ; E. Wik ; M. K. Halle ; E. A. Hoivik ; C. Krakstad ; N. B. Gabino ; G. S. Gomez-Macias ; L. D. Valdez-Chapa ; M. L. Garza-Rodriguez ; G. Maytorena ; J. Vazquez ; C. Rodea ; A. Cravioto ; M. L. Cortes ; H. Greulich ; C. P. Crum ; D. S. Neuberg ; A. Hidalgo-Miranda ; C. R. Escareno ; L. A. Akslen ; T. E. Carey ; O. K. Vintermyr ; S. B. Gabriel ; H. A. Barrera-Saldana ; J. Melendez-Zajgla ; G. Getz ; H. B. Salvesen ; M. Meyerson
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-01-07Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Adenocarcinoma/genetics/virology ; Carcinoma, Squamous Cell/genetics/virology ; Case-Control Studies ; Cell Cycle Proteins/genetics ; Core Binding Factor beta Subunit/genetics ; DNA Copy Number Variations/genetics ; DNA Mutational Analysis ; DNA-Binding Proteins/genetics ; E1A-Associated p300 Protein/genetics ; Exome/genetics ; F-Box Proteins/genetics ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Genome, Human/*genetics ; Genomics ; HLA-B Antigens/genetics ; Humans ; Mitogen-Activated Protein Kinase 1/genetics ; Mutation/*genetics ; NF-E2-Related Factor 2/genetics ; Papillomaviridae/genetics/physiology ; Papillomavirus Infections/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-ets ; Receptor, ErbB-2/genetics ; Transcription Factors/genetics ; Transcriptome/genetics ; Tumor Suppressor Protein p53/genetics ; Ubiquitin-Protein Ligases/genetics ; Uterine Cervical Neoplasms/*genetics/virology ; Virus Integration/geneticsPublished by: -
2Articles: DFG German National LicensesKRISTOFFERSEN, E. K. ; ULVESTAD, E. ; BJØRGE, L. ; AARLI, Å. ; MATRE, R.
Oxford, UK : Blackwell Publishing Ltd
Published 1994Staff ViewISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: We have previously produced a MoAb, B1D6, against a plaeental FcR. The antigen isolated using F(ab')2-fragments of B1D6 exhibits Fc-binding properties with low affinity for IgG. The antigen is a single-chained glycoprotein with a molecular weight of approximately 37 kDa and a pi of about 7.0-8.5. Amino acid sequences from enzymatic digests of the antigen indicated that it is annexin II. Immunoreactivity using anti-annexin antisera and purified placental annexin II have further established the specificity of BID6 to annexin II. The B1D6 epitope appears to be intramembraneous and intracellular on placental syncytiotrophoblasts, monoeytes and other cells investigated.Type of Medium: Electronic ResourceURL: -
3Articles: DFG German National LicensesStaff View
ISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: The vulnerability of tumour cells to complement-mediated immune attack is regulated by membrane associated molecules. Recently, we have shown that the expression of the membrane attack complex inhibitor CD59 is enhanced on colonic adenocarcinoma cells compared to normal colonic epithelial cells. CD59 was shown, in the same study, to protect the tumour cells from complement-mediated lysis. Levamisole (LMS), used in conjunction with 5-fluorouracil as adjuvant therapy, reduces the incidence of colon cancer relapse following surgical resection. This led to our investigation of the effect of LMS on CD59 expression and function on the human colorectal cell lines HT29 and Caco-2. When cultured in the presence of 10 μM LMS, the cells reduced their expression of CD59 in a time-dependent manner. LMS treated HT29 ceils were more sensitive to lysis by complement than control cells, and the reduction in CD59 expression was shown to be partly responsible for this. A reduction in CD59 expression will augment complement-mediated immune surveillance and may contribute to LMSs anti-tumour activity in vivo.Type of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesBJØRGE, L. ; JENSEN, T. SKEIE ; ULVESTAD, E. ; VEDELER, C. A. ; MATRE, R.
Oxford, UK : Blackwell Publishing Ltd
Published 1995Staff ViewISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: CD59 is a 18–25kDa glycoprotein which, by inhibiting the formation of the membrane attack complex, protects homologous cells from complement mediated damage. We have described recently the expression and complement regulatory function of CD59 on colonic adenocarcinoma cells both in vivo and in vitro. In this study we have examined the influence of cytokines on the expression and complement regulatory function of CD59 on the colonic adenocarcinoma cell line HT29. CD59 expression on the HT29 cells was up–regulated after stimulation by mononuclear cells activated by mixed lymphocyte reaction and by culture supernatants from activated mononuclear cells. Similarly, a dose–dependent increase in CD59 expression was observed after stimulation with both tumour necrosis factor-γ and interleukin-1β. A dose–dependent increase in the level of CD59 expression was also seen using low concentrations of interferon-γ (IFN-γ), while CD59 expression on cells cultured with high IFN-γ concentrations was comparable to non–stimulated cells. Cytokine treated cells were more resistant to lysis by homologous complement than non–stimulated cells, and the increase in CD59 expression was shown to be partially responsible for this. The present data strengthen the role of CD59 as a possible participant in tumour escape.Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesStaff View
ISSN: 1432-0851Keywords: Key words Complement ; CD55 (DAF) ; CD46 (MCP) ; Cancer biologySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract To avoid destruction by complement, normal and malignant cells express membrane glycoproteins that restrict complement activity. These include decay-accelerating factor (DAF, CD55), membrane cofactor protein (MCP, CD46) and protectin (CD59), which are all expressed on colonic adenocarcinoma cells in situ. In this study we have characterised the C3/C5 convertase regulators DAF and MCP on the human colonic adenocarcinoma cell line HT29. DAF was found to be a glycosyl-phosphatidylinositol-anchored 70-kDa glycoprotein. Blocking experiments with F(ab′)2 fragments of the anti-DAF monoclonal antibody BRIC 216 showed that DAF modulates the degree of C3 deposition and mediates resistance to complement-mediated killing of the cells. The expression and function of DAF were enhanced by tumour necrosis factor α (TNFα) and interleukin-1β (IL-1β). Cells incubated with interferon γ (IFNγ) did not alter their DAF expression. Two MCP forms were expressed, with molecular masses of approximately 58 kDa and 68 kDa, the lower form predominating. MCP expression was up-regulated by IL-1β, but not by TNFα or IFNγ. Expression of DAF and MCP promotes resistance of colonic adenocarcinoma cells to complement-mediated damage, and represents a possible mechanism of tumour escape.Type of Medium: Electronic ResourceURL: -
6Articles: DFG German National LicensesHarms, L. ; Bock, A. ; JÄnisch, W. ; Valdueza, J. ; Weber, J. ; Link, I. ; Keyser, J. ; Goossens, A. ; Wilczak, N. ; Vedeler, C. ; Bjorge, L. ; Uvestad, E. ; Conti, G. ; Williams, K. ; Ginsberg, L. ; Rafique, S. ; Rapoport, S. I. ; Gershfeld, N. L. ; Meilleure, G. ; Crevits, L. ; Faiss, J. H. ; Heye, N. ; Blanke, J. ; Sackmann, A. ; Kastrup, O.
Springer
Published 1994Staff ViewISSN: 1432-1459Source: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: