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  • 2005-2009
  • 2000-2004  (1)
  • 1990-1994  (1)
  • Glioblastoma  (1)
  • Meningioma  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Neurosurgical review 23 (2000), S. 39-44 
    ISSN: 1437-2320
    Keywords: Key words Anaplastic astrocytoma ; Dissemination ; E-cadherin ; Glioblastoma ; N-cadherin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Cadherins are Ca2+-dependent cell adhesion molecules that play an important role in tissue construction and morphogenesis in multicellular organisms. Because in recent years there have been reports of cadherin involvement in tumor metastasis, we conducted an immunostain for E-cadherin and N-cadherin monoclonal antibodies in paraffin-embedded surgical specimens of primary and recurrent lesions in 13 cases of glioblastoma and nine cases of anaplastic astrocytoma. No expression of E-cadherin was detected in the tumor cells. On the other hand, expression of N-cadherin was observed in malignant astrocytic tumor cells, but the N-cadherin positive rate tended to be less at the time of recurrence. Decreased expression of N-cadherin was detected at the time of recurrence in 11 of the 13 cases in the glioblastoma group. Cerebrospinal fluid (CSF ) dissemination and extracranial metastasis were observed in nine (81.8%) of these 11 patients. Therefore, we tried to analyze the clinical backgrounds and the N-cadherin positive rates by statistics. We concluded that decreased expression of N-cadherin at the time of recurrence correlates with dissemination in malignant astrocytic tumors.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Meningioma ; venous stasis ; brain oedema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Many factors have been suggested as possible mechanisms for the development of peritumoural oedema in meningioma. Venous compression by the tumour is thought to be one factor, but reports presenting a direct relationship between venous compression and the formation of oedema are rare. We have recently observed 6 meningioma patients in whom venous stasis contributed to peritumoural oedema. The stasis was due to 1) compression of an adjacent cortical vein by the tumour with stasis at the site of compression and/or its distal portion. 2) compression of adjacent brain by the tumour with prolonged perfusion and delayed venous return (visualized as pial staining in the capillary and venous phases), and 3) presence of an early draining vein linked to a nearby cortical vein with stasis at its periphery. Venous compression and stasis seem to be related not only to the formation of peritumoural oedema but also to the occurrence of haemorrhagic infarction after the resection of meningiomas.
    Type of Medium: Electronic Resource
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