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  • 1
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2307
    Keywords: CD44 ; Leucocyte-endothelial cell adhesion molecule-1 ; B-lymphocytes ; B-cell neoplasms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lymphocytes leave the blood via post-capillary venules by binding initially to their specialized endothelium. CD44 is a 80–90 kDa hyaluronate-binding glycoprotein involved in binding to endothelium of high endothelial venules (HEV). LECAM-1 is a 75–85 kDa glycoprotein with lectin activity interacting with human peripheral lymph node vascular addressin (PNAd) on HEV. This immunohistochemical study shows that CD44 and LECAM-1 are essentially coordinately expressed on B-lymphocytes. The mode and level of CD44/ LECAM-1 expression dissect the peripheral B-cell development into stages that are closely linked to morphologically defined B-cell compartments. Although statistically correlated in B-cell leukaemias (p〈0.0009) and extranodal B-cell lymphomas (p〈0.003), expression of both molecules was less stringently coordinated in 127 B-cell neoplasms examined. B-cell chronic lymphocytic leukaemia, hairy cell leukaemia and mantle zone lymphoma were CD44/LECAM-1 positive, thus corresponding to their reactive counterparts. Correspondingly, follicular centre cell-derived lymphomas were devoid of both markers. Conversely, CD44 and LEC-AM-1 were infrequently detectable in extranodal malignant B-cell neoplasms, irrespective of their maturational state. Presence versus absence of CD44 and LECAM-1, alone or together, determined neither the leukaemic versus aleukaemic state nor the nodal versus extranodal tumour-forming phenotype of a B-cell tumour.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 419 (1991), S. 7-28 
    ISSN: 1432-2307
    Keywords: Soft tissue tumours ; Phenotyping ; Cell surface molecules
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study is aimed at the characterization of soft tissue tumours (STT) by means of cell surface molecules. To achieve this, normal mesenchymal tissues were extensively examined for expression of leucocyte differentiation (CD) antigens and HLA molecules. The panel of antigens finally examined in STT comprised CD10, CD13, CD24, CD34, CD36, CD56, CD57, HLA-A,B,C,β 2-microglobulin, HLA-DR, -DP, and -DQ and the HLA-D-associated invariant chain (Ii). STT were determined by conventional histomorphological and immunohistochemical criteria. The immunohistological analysis was based on serial frozen sections, one of which was used to demonstrate CD53 antigen. This very broadly distributed leuco/histiocyte-restricted antigen allowed for the distinction between the background of interstitial “stromal” cells and the neoplastic population. In some STT, the expression pattern of the cell surface molecules corresponded to that in their non-neoplastic counterparts. The majority of STT, however, showed considerable changes in the cell surface immunophenotype compared to their cells of origin. These alterations consisted mainly in an aberrant induction/neoexpression and, to a much lesser extent, in an aberrant down-regulation/loss of cell surface antigens. Nevertheless, some immunophenotype configurations are described which, for the time being, can be considered to be useful supplements in the differential diagnosis of this complex class of tumours. The data also indicate considerable changes in cell surface antigen expression occurring in the course of neoplastic transformation of mesenchymal cells. Detailed analysis of alterations in the functional repertoire of neoplastic mesenchymal cells might provide new insights into the biology of STT, possibly leading to new concepts for therapeutic intervention.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2307
    Keywords: β1 Integrins ; Immunohistochemistry ; Breast tissue ; Prognostic parameters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β1 Integrins were examined immunohisto-chemically in normal and mastopathic mammary glands, 12 benign tumours and 90 carcinomas of the breast using monoclonal antibodies againstβ1 andα1 toβ6 subunits. When compared with epithelial cells of non-neoplastic mammary glands and of benign tumours, carcinoma cells showed considerable quantitative changes in the pattern ofα2,α3 andα6 subunit expression. In contrast, the distribution pattern ofβ1,α1,α4 andα5 antigens corresponded to the situation observed in non-neoplastic mammary gland epithelium in most instances. An abnormal expression ofα2 was found in 71.0% of the carcinomas ranging from a remarkably low number ofα2-positive tumour cells in 27.5% of the cases to a complete absence of theα2 molecule in 43.5% of the carcinomas. Of the carcinomas 39.9% exhibited quantitative changes inα3 expression with an abnormally low content ofα3-positive neoplastic cells in 15.4% and a complete absence of this molecule in 24.5% of the cases. Expression ofα6 was abnormal in 73.2% of the carcinomas, consisting in a greater number ofα6-negative tumour cells in 31.9% and in a complete absence ofα6 in 41.3% of the tumours. The abnormally low expression/absence ofα2 andα3 subunits correlated with oestrogen receptor negativity (P〈0.033 andP〈0.04, respectively). In addition, abnormally low expression/absence ofα2 correlated with poor differentiation of the tumours (P〈 0.014). The quantitative changes in the expression pattern ofβ1-associatedα subunits in breast carcinomas may cause a disturbed cell-cell and/or cell-matrix interaction that increases the invasive and migratory property of the tumour cells.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-7373
    Keywords: malignant gliomas ; oncogenes ; growth factors ; gene amplification ; EGF receptor ; ERBB2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The objective of the present study was to determine the frequency of amplifications of three different members of theerbB gene family in human glioblastoma multiforme (GBM). We investigated 47 glial tumors (37 GBM WHO grade IV, 5 anaplastic astrocytomas WHO III and 5 astrocytomas WHO II) by Southern and Western analysis, and immunocytochemistry. Gene amplification oferbB genes in human malignant gliomas was restricted to the EGF receptor (EGFR) gene,erbB-1. We found amplification of the EGFR gene in 49% (18/37) of GBM but not in the astrocytomas WHO II/III. TheerbB-2 anderbB-3 genes showed no amplification in the tumor specimens investigated in this study. At the protein level we found overexpression of the EGF receptor in 86% (32/37) by Western analysis and in 92% (34/37) by immunocytochemistry. Expression of the ERBB2 protein was present in 54% (20/37) but immunoreactivity was much weaker than for EGF receptor and in most cases barely detectable by Western analysis and immunocytochemistry. The ERBB3 protein was not expressed in the glial tumors investigated in this study. Of the threeerbB genes only gene amplification and overexpression of the EGF receptor seems to have an impact on tumor progression of human gliomas. Our data from immunohistochemistry indicate that ERBB2 expression in GBM is closely correlated with EGF receptor levels and is therefore not useful as an independent prognostic parameter.
    Type of Medium: Electronic Resource
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