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Status: Bibliographieeintrag

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Verfasst von:Podar, Klaus [VerfasserIn]   i
 Zimmerhackl, Alexander [VerfasserIn]   i
 Fulciniti, Mariateresa [VerfasserIn]   i
 Tonon, Giovanni [VerfasserIn]   i
 Hainz, Ursula [VerfasserIn]   i
 Tai, Yu-Tzu [VerfasserIn]   i
 Vallet, Sonia [VerfasserIn]   i
 Halama, Niels [VerfasserIn]   i
 Jäger, Dirk [VerfasserIn]   i
 Olson, Dian L. [VerfasserIn]   i
 Sattler, Martin [VerfasserIn]   i
 Chauhan, Dharminder [VerfasserIn]   i
 Anderson, Kenneth C. [VerfasserIn]   i
Titel:The selective adhesion molecule inhibitor Natalizumab decreases multiple myeloma cell growth in the bone marrow microenvironment
Titelzusatz:therapeutic implications
Verf.angabe:Klaus Podar, Alexander Zimmerhackl, Mariateresa Fulciniti, Giovanni Tonon, Ursula Hainz, Yu-Tzu Tai, Sonia Vallet, Niels Halama, Dirk Jäger, Dian L. Olson, Martin Sattler, Dharminder Chauhan and Kenneth C. Anderson
E-Jahr:2011
Jahr:19 September 2011
Umfang:11 S.
Fussnoten:Gesehen am 02.01.2023
Titel Quelle:Enthalten in: British journal of haematology
Ort Quelle:Oxford [u.a.] : Wiley-Blackwell, 1955
Jahr Quelle:2011
Band/Heft Quelle:155(2011), 4, Seite 438-448
ISSN Quelle:1365-2141
Abstract:Recent advances regarding the introduction of anti-adhesion strategies as a novel therapeutic concept in oncology hold great promise. Here we evaluated the therapeutic potential of the new-in-class-molecule selective-adhesion-molecule (SAM) inhibitor Natalizumab, a recombinant humanized IgG4 monoclonal antibody, which binds integrin-α4, in multiple myeloma (MM). Natalizumab, but not a control antibody, inhibited adhesion of MM cells to non-cellular and cellular components of the microenvironment as well as disrupted the binding of already adherent MM cells. Consequently, Natalizumab blocked both the proliferative effect of MM-bone marrow (BM) stromal cell interaction on tumour cells, and vascular endothelial growth factor (VEGF)-induced angiogenesis in the BM milieu. Moreover, Natalizumab also blocked VEGF- and insulin-like growth factor 1 (IGF-1)-induced signalling sequelae triggering MM cell migration. In agreement with our in vitro results, Natalizumab inhibited tumour growth, VEGF secretion, and angiogenesis in a human severe combined immunodeficiency murine model of human MM in the human BM microenvironment. Importantly, Natalizumab not only blocked tumour cell adhesion, but also chemosensitized MM cells to bortezomib, in an in vitro therapeutically representative human MM-stroma cell co-culture system model. Our data therefore provide the rationale for the clinical evaluation of Natalizumab, preferably in combination with novel agents (e.g. bortezomib) to enhance MM cytotoxicity and improve patient outcome.
DOI:doi:10.1111/j.1365-2141.2011.08864.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1111/j.1365-2141.2011.08864.x
 DOI: https://doi.org/10.1111/j.1365-2141.2011.08864.x
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Antibodies, Monoclonal, Humanized
 Bone Marrow Cells
 Cell Adhesion
 Cell Growth Processes
 Cell Line, Tumor
 Cell Movement
 Disease Models, Animal
 Endothelial Cells
 Fibronectins
 Humans
 Immunohistochemistry
 Integrin alpha4
 Male
 Mice
 Mice, SCID
 Multiple Myeloma
 Natalizumab
 Neovascularization, Pathologic
 Signal Transduction
 Tumor Microenvironment
 Vascular Endothelial Growth Factor A
 Xenograft Model Antitumor Assays
K10plus-PPN:1830186884
Verknüpfungen:→ Zeitschrift

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