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Title: Glycosaminoglycan mimicry by COAM reduces melanoma growth through chemokine induction and function
Authors: Piccard, Helene ×
Berghmans, Nele
Korpos, Eva
Dillen, Chris
Van Aelst, Ilse
Li, Sandra
Martens, Erik
Liekens, Sandra
Noppen, Sam
Van Damme, Jozef
Sorokin, Lydia
Opdenakker, Ghislain #
Issue Date: Aug-2012
Publisher: Wiley-Liss
Series Title: International Journal of Cancer vol:131 pages:E425-E436
Article number: 10.1002/ijc.26465
Abstract: Chlorite-oxidized oxyamylose (COAM), a glycosaminoglycan mimetic and potent antiviral agent, provided significant growth reduction of syngeneic murine B16-F1 melanoma tumors. A single early dose (100 µg, into the site of tumor cell inoculation) was sufficient to establish a persistent effect over 17 days (resected tumor volume of 78.3 mm(3) in COAM-treated mice compared to 755.2 mm(3) in the control cohort, i.e. 89.6% reduction of tumor volumes). COAM was a much better antitumoral agent than the polyanionic glycosaminoglycan heparin. COAM retained its antitumoral effect in lymphopenic mice, reinforcing the idea of myeloid cell involvement. Massive recruitment of myeloid cells into dermal air pouches in response to COAM and their increased presence in early-treated tumors indicated that mainly CD11b(+) GR-1(+) myeloid cells were attracted by COAM to exert antitumoral effects. Leukocyte chemotaxis was mediated by the chemokine system through the induction in B16-F1 cells of mouse granulocyte chemotactic protein-2/CXCL6 upon COAM treatment. COAM thus constitutes a novel tool to study the role of innate immune cells in the initial stages of tumor development and an example that innate immunostimulating glycosaminoglycan mimicry may be exploited therapeutically. © 2011 Wiley-Liss, Inc.
URI: 
ISSN: 0020-7136
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Immunobiology (Rega Institute)
Laboratory of Molecular Immunology (Rega Institute)
Laboratory of Virology and Chemotherapy (Rega Institute)
× corresponding author
# (joint) last author

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