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  • Antigen-Antibody Interaction  (1)
  • Carcinoembryonic antigen  (1)
  • 1
    ISSN: 1432-2307
    Keywords: Carcinoembryonic antigen ; Monoclonal antibodies ; Pancreatic tumours ; Immunoreactivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The expression of CEA and related antigens in formalin-fixed paraffin-embedded tissues of normal pancreas and different pancreatic neoplasms was studied immunocytochemically using three monoclonal antibodies (MAbs) recognizing different epitopes on CEA and related antigens. Additionally, a number of extrapancreatic malignancies were tested. The epitope recognized by MAb 250 (present on CEA and NCA 95) was expressed in all but one pancreatic ductal adenocarcinoma and ampullary carcinoma (42/43). The MAb 431 defined epitope (present only on CEA) was less frequently found (27/43). MAb 374, defining an epitope on CEA, NCA 95 and NCA 55 proved to be nearly as sensitive tive as MAb 250, but also reacted with normal duct epithelium. In contrast, MAb 250 and MAb 431 discriminated clearly between reactive duct lesions and malignant duct changes. Moreover, these MAbs differentiated between pancreatic duct carcinomas and nonduct type carcinomas as well as benign pancreatic tumours. In duct type carcinomas, the strongest staining was observed in well differentiated tumours. No discrimination was possible between pancreatic carcinomas and other adenocarcinomas of the gastrointestinal tract nor between most of the lung carcinomas and some other malignancies, specified below. MAb 250 and MAb 431 failed to react with hepatocellular carcinomas, renal cell carcinomas, carcinoids, sarcomas and melanomas. The findings suggest that paraffin-embedded tissues of pancreatic duct type carcinomas, in contrast to nonduct type tumours and normal ducts, are distinguished by the presence of a CEA and NCA 95 related epitope.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 58 (1980), S. 543-550 
    ISSN: 1432-1440
    Keywords: Immunkomplexe ; Antigen-Antikörper-Wechselwirkung ; Komplement ; Hagemanfaktor ; Immune Complexes ; Antigen-Antibody Interaction ; Complement ; Hageman Factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Immune complexes (IC) may be pathophysiologically active in correlation with the nature and size of the antigen, the type and the quality of the antibody, and the concentration of both. Those parameters are decisive for the composition and the lattice structure of IC. Pathogenic effects are induced: by complement activation and generation of biologically active C′ split products via the classical and the alternative pathway, by interaction with Fc and complement receptors resulting in exocytosis of lysosomal contents including degradative enzymes, cationic proteins, vasoactive amines and mediators effective on lymphocytes and macrophages; by direct and indirect activation of the Hageman factor followed by stimulation of the kinin, coagulation and fibrinolysis system; and by modulation of the immune response via the afferent and the efferent branch. All those mechanisms seem to be involved in the induction of lesions along the vessel wall in the various privileged organs.
    Notes: Zusammenfassung Die pathophysiologische Rolle von Immunkomplexen (IC) ist abhängig von deren Zusammensetzung und Vernetzungsgrad. Entscheidend für diese Parameter sind Art und Größe des Antigens, Klasse und Bindungsqualität des Antikörpers und die Konzentration beider Anteile. Pathogene Auswirkungen der IC werden hervorgerufen - durch Aktivierung von Komplement Über den klassischen und den alternativen Weg und der Bildung von biologisch aktiven Komplementspaltprodukten, - durch Wechselwirkung mit Fc und Komplementrezeptoren, was wiederum zur Exozytose lysosomaler Substanzen inklusiv kataboler Enzyme, kationischer Proteine, vasoaktiver Amine und Mediatoren, wirksam auf Lymphozyten und Makrophagen, führt. - durch direkte und indirekte Aktivierung des Hagemanfaktors, gefolgt von der Stimulation des Kinin-, Gerinnungs- und Fibrinolysesystems, - und durch Beeinflussung der Immunantwort über den afferenten und den efferenten Weg. All diese Mechanismen scheinen an der Entstehung von Läsionen entlang der Gefäßwand in den jeweiligen disponierten Organen beteiligt zu sein.
    Type of Medium: Electronic Resource
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