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  • By Author: Samii, Madjid x
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Wolf O. Luedemann, Marcos S. Tatagiba, Sami Hussein and Madjid Samii

✓ The authors report the case of a 27-year-old woman with an arthrogryposis multiplex congenita (AMC) associated with atlantoaxial subluxation. To the authors' knowledge, this is the first report of its kind. The authors review the literature with reference to dysraphic abnormalities associated with atlantoaxial subluxation and with AMC. The patient presented with severe tetraparesis following a minor traffic accident. She underwent a procedure in which transoral decompression and dorsal stabilization were performed and, postoperatively, made a good clinical outcome. The authors stress the need for diagnostic neuroimaging of the craniocervical junction in patients with AMC.

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Roger Breyer, Sami Hussein, Dorel L. Radu, Klaus-Martin Pütz, Sven Gunia, Hartmut Hecker, Madjid Samii, Gerhard F. Walter and Alexandru C. Stan

Object. Glioblastoma multiforme (GBM) invasiveness is a complex process that involves recognition and attachment of GBM cells to particular extracellular matrix (ECM) molecules before migrating into proteolytically modified matrix and inducing angiogenesis. The CD44 molecule, which is a transmembrane adhesion molecule found on a wide variety of cells including GBM, has been suggested as the principal mediator of migration and invasion. The aim of the present study was to demonstrate whether an antibody specific to the standard form of CD44 (CD44s, 85–90 kD) might prevent invasion and thus disrupt progression of C6 GBM in vivo.

Methods. Immunostaining demonstrated homogeneous expression of CD44s on the surface of C6 GBM cells and tumors. Flow cytometric analysis demonstrated binding saturation of anti-CD44s monoclonal antibody (mAb) to the receptor at 1 µg/5 × 105 cells. Blocking of CD44s in vitro resulted in a dose-dependent progressive (up to 94 ± 2.7%; mean ± standard deviation [SD]) detachment of C6 cells from ECM-coated culture. Blocking of CD44s in vivo resulted in significantly reduced C6 brain tumors (3.6 ± 0.4% [SD])—measured as the quotient: tumor surface (mm2)/brain surface (mm2) × 100—compared with untreated (19.9 ± 0.9%) or sham-treated (19.2 ± 1.1 to 19.3 ± 2.5% [SD]) rats. Disruption of C6 GBM progression correlated with an improved food intake; treated rats were significantly less cachectic (166.6 ± 16.4 g [SD]) than those that were untreated (83 ± 2.7 g [SD]) or sham-treated (83.4 ± 1.1 to 83 ± 2.2 g [SD]) rats.

Conclusions. The authors conclude that CD44s-targeted treatment with specific mAb may represent an effective means for preventing progression of highly invasive GBMs.

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Roger Breyer, Sami Hussein, Dorel L. Radu, Klaus-Martin Pütz, Sven Gunia, Hartmut Hecker, Madjid Samii, Gerhard F. Walter and Alexandru C. Stan

Glioblastoma multiforme (GBM) invasiveness is a complex process that involves recognition and attachment of GBM cells to particular extracellular matrix (ECM) molecules prior to migrating into proteolytically modified matrix and inducing angiogenesis. The CD44, which is a transmembrane adhesion molecule found on a wide variety of cells including GBM, has been suggested as the principal mediator of migration and invasion. The aim of the present study was to demonstrate whether an antibody specific to the standard form of CD44 (CD44s, 85-90 kDa) might prevent invasion and thus disrupt progression of C6 GBM in vivo.

Immunostaining demonstrated homogenous expression of CD44s on the surface of C6 GBM cells and tumors. Flow cytometric analysis demonstrated binding saturation of anti-CD44s mAb to the receptor at 1 μg/5 X 105 cells. Blocking of CD44s in vitro resulted in a dose-dependent progressive (up to 94 ± 2.7%; mean ± standard deviation [SD]) detachment of C6 cells from ECM-coated culture surfaces. Blocking of CD44s in vivo resulted in significantly reduced C6 brain tumors (3.6 ± 0.4% [SD])--measured as the quotient: tumor surface (mm2)/brain surface (mm2) X 100--as compared with untreated (19.9% ± 0.9%) or sham-treated rats (19.2 ± 1.1% to 19.3 ± 2.5% [SD]). Disruption of C6 GBM progression correlated with an improved food intake; treated rats were significantly less cachectic (166.6 ± 16.4 g [SD]) than those that were untreated (83.0 ± 2.7 g [SD]) or sham-treated (83.4 ± 1.1 g to 83.0 ± 2.2 g [SD]) rats.

The authors conclude that CD44s-targeted treatment with specific mAb may represent an effective means for preventing progression of highly invasive GBMs.