Kimbara S, Kondo S. Immune checkpoint and inflammation as therapeutic targets in pancreatic carcinoma. World J Gastroenterol 2016; 22(33): 7440-7452 [PMID: 27672267 DOI: 10.3748/wjg.v22.i33.7440]
Corresponding Author of This Article
Shunsuke Kondo, MD, PhD, Department of Experimental Therapeutics, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. shkondo@ncc.go.jp
Research Domain of This Article
Oncology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Sep 7, 2016; 22(33): 7440-7452 Published online Sep 7, 2016. doi: 10.3748/wjg.v22.i33.7440
Immune checkpoint and inflammation as therapeutic targets in pancreatic carcinoma
Shiro Kimbara, Shunsuke Kondo
Shiro Kimbara, Shunsuke Kondo, Department of Experimental Therapeutics, National Cancer Center Hospital, Tokyo 104-0045, Japan
Author contributions: Kimbara S and Kondo S contributed equally to this work.
Supported byJSPS Grant-in-Aid for Young Scientists (B), No. 268605371; AstraZeneca, Eli Lilly and Company, and Bayer AG (to Kondo S).
Conflict-of-interest statement: Shiro Kimbara have no conflict of interest associated with this manuscript. Shunsuke Kondo received research funding from AstraZeneca, Eli Lilly and Company, and Bayer AG.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Shunsuke Kondo, MD, PhD, Department of Experimental Therapeutics, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. shkondo@ncc.go.jp
Telephone: +81-3-35422511 Fax: +81-3-35423815
Received: March 26, 2016 Peer-review started: March 27, 2016 First decision: May 12, 2016 Revised: June 30, 2016 Accepted: August 1, 2016 Article in press: August 1, 2016 Published online: September 7, 2016 Processing time: 161 Days and 14.9 Hours
Core Tip
Core tip: Pancreatic adenocarcinoma is recognized as one of the most malignant neoplasms, and more efficacious treatment is desired earnestly. Recent research studies have revealed that the development and progression of pancreatic adenocarcinoma are highly influenced by immune responses, and inflammation is a critical promoter of the disease. In this article, we highlighted the emergence of immunosuppression-related signaling associated with immune checkpoint and inflammation, as a novel treatment target for cancer. Furthermore, the review demonstrated that the current focus on therapeutic strategies involving combination chemotherapy, immunotherapy, and anti-inflammation therapy might provide considerably more clinical benefits to patients than current therapies.
