120
views
0
recommends
+1 Recommend
1 collections
    8
    shares

      To submit to Bentham Journals, please click here

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Use of Lentinan for Treating Gastric Cancer

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Natural compounds containing fungal β-glucans have been used to improve general health for thousands of years in China and Japan. Lentinan, the backbone of β-(1, 3)-glucan with β-(1, 6) branches, is one of the active ingredients purified from Shiitake mushrooms and has been approved as a biological response modifier for the treatment of gastric cancer in Japan. Despite recent advances in chemotherapeutic agents, unresectable or recurrent gastric cancer remains an incurable disease, with survival rates being far from satisfactory. Recent clinical studies have shown that chemo-immunotherapy using lentinan prolongs the survival of patients with advanced gastric cancer, as compared to chemotherapy alone. In addition, trastuzumab, an antibody against HER2/neu growth factor receptor, has been used for the treatment of gastric cancer in combination with cytotoxic chemotherapeutic agents. Lentinan may exert a synergistic action with anti-cancer monoclonal antibodies to activate complement systems through the mechanism of antibody-dependent cellular cytotoxicity and complement dependent cytotoxicity. Because a better understanding of its biological activities should enable us to use lentinan more efficiently in the treatment of gastric cancer, immunological effects provided by β-glucans, a possible mode of action of lentinan, and its clinical application including future potential uses are discussed in the present review.

          Related collections

          Most cited references84

          • Record: found
          • Abstract: found
          • Article: not found

          Dectin-1: a signalling non-TLR pattern-recognition receptor.

          Dectin-1 is a natural killer (NK)-cell-receptor-like C-type lectin that is thought to be involved in innate immune responses to fungal pathogens. This transmembrane signalling receptor mediates various cellular functions, from fungal binding, uptake and killing, to inducing the production of cytokines and chemokines. These activities could influence the resultant immune response and can, in certain circumstances, lead to autoimmunity and disease. As I discuss here, understanding the molecular mechanisms behind these functions has revealed new concepts, including collaborative signalling with the Toll-like receptors (TLRs) and the use of spleen tyrosine kinase (SYK), that have implications for the role of other non-TLR pattern-recognition receptors in immunity.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Dectin-1 Is A Major β-Glucan Receptor On Macrophages

            Zymosan is a β-glucan– and mannan-rich particle that is widely used as a cellular activator for examining the numerous responses effected by phagocytes. The macrophage mannose receptor (MR) and complement receptor 3 (CR3) have historically been considered the major macrophage lectins involved in the nonopsonic recognition of these yeast-derived particles. Using specific carbohydrate inhibitors, we show that a β-glucan receptor, but not the MR, is a predominant receptor involved in this process. Furthermore, nonopsonic zymosan binding was unaffected by genetic CD11b deficiency or a blocking monoclonal antibody (mAb) against CR3, demonstrating that CR3 was not the β-glucan receptor mediating this activity. To address the role of the recently described β-glucan receptor, Dectin-1, we generated a novel anti–Dectin-1 mAb, 2A11. Using this mAb, we show here that Dectin-1 was almost exclusively responsible for the β-glucan–dependent, nonopsonic recognition of zymosan by primary macro-phages. These findings define Dectin-1 as the leukocyte β-glucan receptor, first described over 50 years ago, and resolves the long-standing controversy regarding the identity of this important molecule. Furthermore, these results identify Dectin-1 as a new target for examining the immunomodulatory properties of β-glucans for therapeutic drug design.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Syk-dependent cytokine induction by Dectin-1 reveals a novel pattern recognition pathway for C type lectins.

              Pattern-recognition receptors (PRRs) detect molecular signatures of microbes and initiate immune responses to infection. Prototypical PRRs such as Toll-like receptors (TLRs) signal via a conserved pathway to induce innate response genes. In contrast, the signaling pathways engaged by other classes of putative PRRs remain ill defined. Here, we demonstrate that the beta-glucan receptor Dectin-1, a yeast binding C type lectin known to synergize with TLR2 to induce TNF alpha and IL-12, can also promote synthesis of IL-2 and IL-10 through phosphorylation of the membrane proximal tyrosine in the cytoplasmic domain and recruitment of Syk kinase. syk-/- dendritic cells (DCs) do not make IL-10 or IL-2 upon yeast stimulation but produce IL-12, indicating that the Dectin-1/Syk and Dectin-1/TLR2 pathways can operate independently. These results identify a novel signaling pathway involved in pattern recognition by C type lectins and suggest a potential role for Syk kinase in regulation of innate immunity.
                Bookmark

                Author and article information

                Journal
                Anticancer Agents Med Chem
                Anticancer Agents Med Chem
                CMCACA
                Anti-Cancer Agents in Medicinal Chemistry
                Bentham Science Publishers
                1871-5206
                1875-5992
                June 2013
                June 2013
                : 13
                : 5
                : 681-688
                Affiliations
                [1 ]Department of Medical Oncology, Nagoya Memorial Hospital, Nagoya 468-8520, Japan
                [2 ]Department of Clinical Oncology, Nagoya Memorial Hospital, Nagoya 468-8520, Japan
                [3 ]Department of Gastroenterology, Nagoya Graduate School of Medicine, Nagoya 466-8550
                Author notes
                [* ]Address correspondence to this author at the Department of Medical Oncology, Nagoya Memorial Hospital, 4-305 Hirabari, Tenpaku-ku, Nagoya, 468-8520, Japan; Tel: +81-52-804-1111; Fax: +81-52-803-8830; E-mail: kina@ 123456hospy.or.jp
                Article
                CMCACA-13-681
                10.2174/1871520611313050002
                3664515
                23092289
                2b36c21a-95f2-4571-a80f-47d6eb1ae787
                © 2013 Bentham Science Publishers

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 June 2012
                : 23 August 2012
                : 17 October 2012
                Categories
                Article

                Oncology & Radiotherapy
                gastric cancer,β-glucan,lentinan.
                Oncology & Radiotherapy
                gastric cancer, β-glucan, lentinan.

                Comments

                Comment on this article