116 research outputs found

    Recombinant humanised anti-HER2/neu antibody (Herceptin®) induces cellular death of glioblastomas

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    Glioblastoma multiforme (GBM) remains the most devastating primary tumour in neuro-oncology. Targeting of the human epithelial receptor type 2 (HER2)-neu receptor by specific antibodies is a recent well-established therapy for breast tumours. Human epithelial receptor type 2/neu is a transmembrane tyrosine/kinase receptor that appears to be important for the regulation of cancer growth. Human epithelial receptor type 2/neu is not expressed in the adult central nervous system, but its expression increases with the degree of astrocytoma anaplasia. The specificity of HER2/neu for tumoral astrocytomas leads us to study in vitro treatment of GBM with anti-HER2/neu antibody. We used human GBM cell lines expressing HER2/neu (A172 express HER2/neu more than U251MG) or not (U87MG) and monoclonal humanised antibody against HER2/neu (Herceptin®). Human epithelial receptor type 2/neu expression was measured by immunohistochemistry and flow cytometry. Direct antibody effect, complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity were evaluated by different cytometric assays. We have shown, for the first time, the ability of anti-HER2/neu antibodies to induce apoptosis and cellular-dependent cytotoxicity of HER2/neu-expressing GBM cell lines. The results decreased from A172 to U251 and were negative for U87MG, in accordance with the decreasing density of HER2/neu receptors

    Chromatolytic neurons in lateral geniculate body in Werdnig-Hoffmann disease.

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    In a case of Werdnig-Hoffmann disease, we have observed pathologic changes in the neuronal cell bodies of the lateral geniculate nucleus. These changes are similar to those seen in lower motor neurons and dorsal root ganglia. As the lateral geniculate nucleus and its projections are entirely central, this observation raises questions as to the possible etiologic role of root entry zone glial bundles in the evolution of neuronal alterations in severe spinal muscular atrophy
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