Biological and Pharmaceutical Bulletin
The Pharmaceutical Society of Japan, established in 1880, is one of Japan’s oldest and most distinguished academic societies. The Society currently has around 18,000 members. It publishes three monthly scientific journals. Chemical and Pharmaceutical Bulletin (Chem. Pharm. Bull.) began publication in 1953 as Pharmaceutical Bulletin. It covers chemistry fields in the pharmaceutical and health sciences. Biological and Pharmaceutical Bulletin (Biol. Pharm. Bull.) began publication in 1978 as the Journal of Pharmacobio-Dynamics. It covers various biological topics in the pharmaceutical and health sciences. A fourth Society journal, the Journal of Health Science, was merged with Biol. Pharm. Bull. in 2012. Yakugaku Zasshi (Japanese for “Pharmaceutical Science Journal”) has the longest history, with publication beginning in 1881. Yakugaku Zasshi is published mostly in Japanese, except for some articles related to clinical pharmacy and pharmaceutical education, which are published in English.
The main aim of the Society’s journals is to advance the pharmaceutical sciences with research reports, information exchange, and high-quality discussion. The average review time for articles submitted to the journals is around one month for first decision. The complete texts of all of the Society’s journals can be freely accessed through J-STAGE. The Society’s editorial committee hopes that the content of its journals will be useful to your research, and also invites you to submit your own work to the journals.

Chairman of Committee
Ken-ichi Hosoya
Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama



Read more
Published by The Pharmaceutical Society of Japan  
9,693 registered articles
(updated on January 16, 2019)
Online ISSN : 1347-5215
Print ISSN : 0918-6158
1.694
2017 IMPACT FACTOR
JOURNALS PEER REVIEWED FREE ACCESS FULL-TEXT HTML ADVANCE PUBLICATION
Featured article
Volume 42 (2019) Issue 1 Pages 57-65
Forced Expression of CXCL10 Prevents Liver Metastasis of Colon Carcinoma Cells by the Recruitment of Natural Killer Cells
Norihito Kikuchi, Jiabin Ye, Jotaro Hirakawa, Hiroto Kawashima

CXC chemokine ligand 10 (CXCL10) is a CXC chemokine family protein that transmits signals by binding to its specific receptor, CXCR3. CXCL10 is also known as an interferon-γ-inducible chemokine involved in various biological phenomena, including chemotaxis of natural killer (NK) cells and cytotoxic T lymphocytes, that suppress tumor growth and inhibition of angiogenesis. In this study, we examined the effects of forced expression of CXCL10 in a murine colon carcinoma cell line (CT26) on growth and metastasis in syngeneic mice. We first established CT26 cells that were stably expressing murine CXCL10 (CT26/CXCL10) and compared their growth with their parental CT26 cells in vitro and in vivo. The in vitro growth of the CT26/CXCL10 and CT26 cells was comparable, whereas the in vivo growth of the CT26/CXCL10 cells in the skin was strongly suppressed. Liver metastasis of the CT26/CXCL10 cells was also significantly suppressed after intra-splenic implantation. Removal of NK cells by the administration of anti-asialo GM1 antibody canceled the suppression of subcutaneous growth and liver metastasis of CT26/CXCL10 cells. Immunofluorescence clearly showed that abundant NKp46-positive NK cells were recruited into the liver metastatic lesions of the CT26/CXCL10 cells, consistent with specific NK cell migration towards the culture supernatant from the CT26/CXCL10 cells in the chemotaxis assay using transwells. These findings indicate that CXCL10 prevents in vivo growth and metastasis of colon carcinoma cells by recruiting NK cells, suggesting that forced expression of CXCL10 in the colon tumors by gene delivery should lead to a favorable clinical outcome.
Read more
Editor’s picks

CXC chemokine ligand (CXCL) 10 is a chemokine that binds to CXCR3 expressed on natural killer (NK) cells and cytotoxic T lymphocytes. In this paper, Kikuchi et al. showed that forced expression of CXCL10 in murine colon carcinoma CT26 cells prevents their in vivo proliferation and liver metastasis by recruiting NK cells, suggesting that forced expression of CXCL10 in the colon tumors by gene delivery should lead to a favorable clinical outcome.

View the past featured articles
Most viewed articles Dec.2018
Share this page
Select past volume & issue
Favorites & Alerts
Journal news & Announcements
  • Biol. Pharm. Bull. Vol. 41 No. 10
    Current Topics: Transporter Research Yields New Discoveries in Life Sciences
Predecessor

The annual reports of the Public Health Division of the Pharmaceutical Society of Japan

Eisei kagaku

Journal of Health Science

Journal of Pharmacobio-Dynamics

feedback
 Top