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Immunological targets for cancer therapy: new recognition

Authors Shurin MR 

Received 23 October 2018

Accepted for publication 24 October 2018

Published 21 November 2018 Volume 2018:7 Pages 83—85

DOI https://doi.org/10.2147/ITT.S191821

Checked for plagiarism Yes



Michael R Shurin1,2

1Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA; 2Department of Immunology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA

During the last decade, we have witnessed exhilarating progress in the expansion of immunotherapeutic approaches to cancer treatment. In part, this has been because of discovery and development of antibodies which can block immune inhibitory receptors unleashing antitumor immune responses – the so-called checkpoint inhibitors. Blocking cancer progression by eliminating brakes on immune effector cells in the tumor environment has jointly earned James P Allison, PhD (Department of Immunology, MD Anderson Cancer Center, University of Texas, Houston, TX, USA) and Tasuku Honjo, MD, PhD (Graduate School of Medicine, Kyoto University, Kyoto, Japan) the Nobel Prize in Physiology or Medicine in 2018. Whereas the concept of cancer immunosurveillance dates back more than 100 years, the study of Allison’s and Honjo’s teams over the past few decades not only confirmed the idea but also converted it into an effective immunotherapeutic tactic, which dramatically improved outcomes for some cancer patients.
 

Disclosure

The author reports no conflicts of interest in this work.

References

1.

Ishida Y, Agata Y, Shibahara K, Honjo T. Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death. EMBO J. 1992;11(11):3887–3895.

2.

Leach DR, Krummel MF, Allison JP. Enhancement of antitumor immunity by CTLA-4 blockade. Science. 1996;271(5256):1734–1736.

3.

Kwon ED, Hurwitz AA, Foster BA, et al. Manipulation of T cell costimulatory and inhibitory signals for immunotherapy of prostate cancer. Proc Natl Acad Sci U S A. 1997;94(15):8099–8103.

4.

Nishimura H, Nose M, Hiai H, Minato N, Honjo T. Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor. Immunity. 1999;11(2):141–151.

5.

Freeman GJ, Long AJ, Iwai Y, et al. Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation. J Exp Med. 2000;192(7):1027–1034.

6.

Hodi FS, Mihm MC, Soiffer RJ, et al. Biologic activity of cytotoxic T lymphocyte-associated antigen 4 antibody blockade in previously vaccinated metastatic melanoma and ovarian carcinoma patients. Proc Natl Acad Sci U S A. 2003;100(8):4712–4717.

7.

Iwai Y, Terawaki S, Honjo T. PD-1 blockade inhibits hematogenous spread of poorly immunogenic tumor cells by enhanced recruitment of effector T cells. Int Immunol. 2005;17(2):133–144.

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