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The Desmoid Tumor Research Foundation

January 2015

Antitumor effects of hyaluronan inhibition in desmoid tumors.

Author Information

Alexandra Briggs,Hira Rizvi,Justin D Buie,Laura Rosenberg,Monica M Bertagnolli,Nancy L Cho

Department of Surgery, Brigham and Women's Hospital, Boston, MA 02115, USA and Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USAnlcho@partners.org.,Department of Surgery, Brigham and Women's Hospital, Boston, MA 02115, USA and Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA.,Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA.

Publication

Summary

Desmoid tumors (DTs) are rare, mesenchymal tumors that exhibit features of an abundant wound healing process. Previously, we showed that mesenchymal stem cells (MSCs) are constituents of DTs and may contribute to desmoid tumorigenesis via activities associated with wound healing. Hyaluronan (HA) is a long-charged chain of repeating glucuronate and N-acetylglucosamine disaccharides that is synthesized by HA synthases (HAS) and degraded by hyaluronidases (HYAL). HA is secreted into the extracellular matrix by injured stroma and is important for normal tissue repair and neoplastic progression. Here, we investigated the presence of HA in DTs and the antitumor effects of the HA inhibitor, 4-methylumbelliferone (4-MU), on DT-derived mesenchymal cells.

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