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  • Articles: DFG German National Licenses  (2)
  • Histiocytosis X  (1)
  • Key wordsαvβ3  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Histiocytosis X arising in Hodgkin's disease: immunophenotypic characterization with a panel of monoclonal antibodies (1991)
    Springer
    Virchows Archiv 418 (1991), S. 369-373 
    Details
    ISSN: 1432-2307
    Keywords: Histiocytosis X ; Hodgkin's lymphoma ; Immunohistochemistry ; Intercellular adhesion molecule 1 ; Major histocompatibility complex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This report describes the antigenic profile of the proliferating cells of pulmonary histiocytosis X (HX) in a patient treated with chemotherapy for Hodgkin's lymphoma; the association of pulmonary HX and Hodgkin's disease has rarely been described in the literature. The histopathological diagnosis of HX was confirmed with the aid of monoclonal antibodies (mAbs) to CD4, CD1a, and polyclonal serum anti S-100 protein. The phenotype of HX cells has been analysed using a panel of mAbs against HLA class I A, B, C monomorphic determinants, locus A and B,β2-microglobulin, HLA class II distinct monomorphic determinants, DP, DQ, DR, intercellular adhesion molecule-1 (ICAM-1) and vitronectin receptors. Our results indicate that HX cells express HLA class I and II, including locus A, locus B and DP, DQ, DR, like their normal counterpart (represented by Langerhans cells) and detectable levels of ICAM-1 but not vitronectin receptors. We would like to stress the possibility of the association of HX and Hodgkin's lymphoma extending the immunophenotypic profile of HX cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01600168
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    αvβ3 expression on blood vessels and melanoma cells in primary lesions; differential association with tumor progression and clinical prognosis (2000)
    Springer
    Cancer immunology immunotherapy 49 (2000), S. 314-318 
    Details
    ISSN: 1432-0851
    Keywords: Key wordsαvβ3 ; Integrins ; Melanoma ; Blood vessels ; Prognosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The αvβ3 integrin has emerged as a key mediator in angiogenesis. Its role in tumor-induced angiogenesis is supported by its up-regulation in vivo in the vasculature of a number of different types of carcinoma. The potential clinical significance of αvβ3 expression on blood vessels in carcinomas is suggested by its association with tumor progression. Currently no information is available about the clinical significance of αvβ3 expression on the vasculature of lesions of melanocytic origin. Since we have previously found that αvβ3 expression on melanoma cells in primary lesions is associated with a poor prognosis, in the present study we have compared αvβ3 expression on blood vessels and on cells of melanocytic origin in nevi and in malignant melanoma lesions. In addition we have examined the lesions for expression of the αv subunit to gain information on the regulation of αvβ3 expression on endothelial cells and on cells of the melanocyte lineage. αvβ3 expression on endothelial cells and on melanocytic cells was a relatively sensitive and specific marker for malignant lesions. However, αvβ3 expression on endothelial cells in primary melanoma lesions was not associated with the prognosis of the disease. The αv subunit and the αvβ3 complex were differentially expressed on endothelial cells and on melanocytic cells, implying that different regulatory pathways control their expression. This finding may account for the differential clinical significance of αvβ3 expression on tumor vasculature and on melanoma cells we observed in our patient cohort. Lastly, αvβ3 may be a useful target for immunotherapeutic approaches in melanoma because of its high expression on the vasculature of all metastatic lesions tested and its restricted distribution in normal tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002620000124
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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